The American beef industry is mostly to blame for causing the American beef consumer to stampede at the first hint of Bovine Spongiform Encephalopathy (BSE or Mad Cow Disease). It did it by adamantly and very publicly banning the importation of beef from any country with a reported case of Mad Cow Disease. Then it told the American consumer that these actions were required in order to protect not only the people, because they believe BSE can cause variant Creutzfeldt-Jacob Disease (or vCJD) in humans, but also the U.S. cattle herds from exposure to this dreaded brain-wasting, deadly disease.
The National Cattleman’s Beef Association (NCBA) and its lapdogs, the Beef Checkoff and the many individual state checkoffs such as the Texas Beef Council, did little to play down the dangers of Mad Cow Disease and did everything it could to get the consumer focused on the invincibility of our country’s cattle industry and the safety and sanctity of the U.S. beef they eat.
To protect us all, they and their well-lobbied politicians set up onerous import bans against the cattle and beef from affected countries, and some of the bans lasted for years. Consequently, the American consumer has been taught that all beef products from any country with even one case of Mad Cow Disease should be shunned for at least a year or so for their own safety. One bite of tainted beef and they will die for sure.
Consumers Told to Quit Eating Beef
Well, the United States beef industry is no longer invincible. We’ve got another confirmed case of Mad Cow Disease in our 100-million head herd of healthy cattle. Now other countries are banning our beef because all, or at least some, of it must be contaminated, right? One bite of American beef and you’re a dead duck. So what should the American consumer do? You’ve got it. He should quit eating American beef for at least a year. That’s not my idea, that’s the NCBA speaking.
By and large, the average American is so far out of touch with reality that it’s incomprehensible. Whether he’s an agricultural producer or a city slicker, more often than not his comprehension of the Big Picture can only be defined as being as dumb as a sack of hammers. Neither group (country hick or city slicker) knows the other, and they really don’t want to strike up an acquaintance. They aren’t neighbors, they never see each other, they don’t understand each other’s jargons and accents, and both believe the other side is always taking advantage of him. For sure they don’t know much about life. The community disintegration caused by Big Business, the vulnerability of our nation’s financial system, the consistency of human nature, and the simplicity of nature is way beyond what they learned in school. Oh, they know how to use cellular phones, computers, and other modern gizmos, but that’s rote, not wisdom. Shockingly, neither group even knows how to grow and raise food. They buy everything they eat in grocery stores.
Since nearly all Americans are in the “sack of hammers” category, they live in the world of denial. That’s right. When they hear the truth and it differs from their fantasies, myths, hand-me-down knowledge, and superstitions, they reject it immediately. They know they know better—just like a 12-year-old. If you repeat the truth, they know they know better—just like an 18-year-old. That’s my best definition of living in denial.
So what’s the problem here with this Mad Cow Disease thing? From what I’ve learned, the grand total of all the people who ate tainted beef from all over the world ever since the disease was first detected 15 years ago or so is about 143 unfortunate souls. Let’s see now. Every day, Americans jump in their vehicles and drive wherever. And every week about 750 of them are killed because they rode in a vehicle. Many more end up maimed for life. Would you rather eat beef or take a ride in a car?
I used to know the head meat butcher in a Safeway store in Oregon. He told me that when the first Mad Cow thing hit the news, he had 20 calls from folks who wanted to return their standing rib roasts they’d bought for Christmas dinner. You’ve got it; they were going to drive to his store to get their money back. The odds were stacked against them from that very moment. They had a greater chance of dying driving to the store than eating the beef they were taking back!
I’m not trying to play down the Mad Cow thing. If livestock management (feeds fed) are the problem, then our industry should do everything it can to make the appropriate changes. And yes, the consumers’ reactions to Mad Cow Disease that most cattlemen are anguishing over today are of their industry’s own making. In its desire to sell more of its cheap, convenient, and predictable meat products to the American consumer, the industry made some horrible marketing choices with the perceptions they’ve created. Today they are backfiring.
What’s Killing Americans?
Ironically, the concerns for Mad Cow Disease are common knowledge, yet only a grand total of about 200 people have died worldwide for all of detectable time. That pales in significance when compared with the number of Americans killed in traffic accidents every week. The number killed in traffic accidents involving just deer exceeds 200 annually! (The world's annual death toll from all types of traffic accidents is incredibly high.) But get this. The number of folks dying early or suffering immeasurably from obesity, diabetes, cancer, heart disease, mental disorders, arthritis, lupus, allergies, osteoporosis, and other body-failing “diseases” make the automobile accident list look like child’s play.
Why should I bring this up? Well, eating grain causes those maladies. And eating livestock products from critters fed grain also causes those maladies. I’m not talking about heresy and old wive’s tales. I’m talking about peer-reviewed scientific research that’s been published in scientific journals.
Think about it for a minute. The masses were stampeded over the risks of dying from eating beef because the American cattle industry reported another case of Mad Cow Disease. Yet the risks of their dying from Mad Cow Disease are lower than being struck by lightning. On the other hand, they live comfortably with the 70% chance of dying early or from suffering in ill health from eating too much grain and grain-fed livestock products.
The madness of crowds is a wonder to behold.
Slanker's Grass-Fed Meats
There is one man who did considerable work on BSE and his observations are something everyone should at least ponder. He is Mark Purdey. I first started reading his works many years ago before he died. To give you an idea about his take on our country's first case of Mad Cow, I've reproduced a report he issued on December 30, 2003. The headline above is a link to Wikipedia which lists links to many of Purdey's reports. He is a brilliant man and his work was gaining fame internationally until his premature death. The media, our government, and our leading educators have not been very sympathetic regarding his theories.
A brief statement by Mark Purdey – UK TSE researcher and lecturer.
Despite increasing evidence that the "mad cow" group of diseases stem from environmental as opposed to infectious origins, the first reported case of BSE in the USA has been met with a furore of hyper-infectious hysteria. Whilst the arrival of the disease in North America should not be treated lightly, the epidemiological track record of the BSE outbreaks in Europe suggests that there is no need for the panic.
One of the key neuro-pathological markers that have enabled researchers to diagnose BSE, has focused upon the presence of a malformed version of the prion protein – a native brain protein which is present in all healthy mammals, and performs a functional role in mediating the circadian rhythm.
Various researchers have established a hypothesis on the origins of TSEs (the BSE group of diseases) which is based on the unproven assumption that this malformed "prion" serves as the infectious agent that is responsible for the cause of BSE. Furthermore, it has been suggested that the feeding of the ground down remains of TSE affected sheep to cattle served as the vehicle for transmitting these infectious prions into the European cattle herd, and causing BSE. But many major flaws have arisen in the established theory, such as the exportation of thousands of tons of the UK’s BSE incriminated cattle feeds to countries all over the world. Despite those countries receiving this feed throughout the 1960s, 70s, 80s and 90s, their cattle populations have remained BSE-free to date. So how can micro doses of the feed cause BSE?
Furthermore, why have tens of thousands of BSE outbreaks continued to emerge in European cattle that have been born after their respective bans on the meat and bone meal going into cattle feeds?
Recent UK lab research has demonstrated that an intermediate toxic factor – which causes the normal prion protein to transform into its abnormal prion form – is the actual causal agent; thereby indicating that the malformed prion represents little more than a "tombstone" legacy that is a "hang over" from the toxic TSE disease process.
The Metal Detective
For fifteen years I have carried out geo-chemical analyses of the ecosystems (soil, water, vegetation, etc.) to gauge the levels of 46 metals and their radioactive/magnetic susceptibility status in every sizeable TSE cluster hotspot around the world. This has involved travelling to Japan, New Guinea, Canada, USA, Europe, Iceland, etc, in order to pinpoint the common toxic denominator that is exclusively shared by all of these isolated cluster locations.
This work has identified that a package of toxic environmental factors underpins the pathogenesis of TSEs, where the simultaneous exposure to a copper deficient food chain and rogue radioactive metal pollutants brings about the malformation of the prion protein, with a consequent break down in the way that the brain deals with incoming surges of electromagnetic radiation – eg; light and sound waves, etc.
The normal prion protein actually binds up with copper in the healthy brain, where this metal performs a role in the conduction of incoming electromagnetic energy along the circadian circuits – in order to regulate various essential physiological processes under daylight/darkness control. But once the problem of copper deficiency surfaces via the food chain, then the prion protein is unable to find its normal copper co-partner and is rendered susceptible to binding up with certain rogue "foreign" metals that serve as undesirable substitutes at the protein’s vacant copper bonds.
My studies have shown that TSEs will develop in environments where metals such as manganese and silver are at high level – as a result of various natural or artificial sources of pollution. These can get taken up into the animal via contaminated foods or atmospheres, and, under certain circumstances, can flood past the blood/brain barrier where they are free to bind onto any copper depleted prion proteins. This triggers off the progressive chain of events that leads to the development of the so called sporadic, traditional strain of TSE which usually surfaces in the susceptible members of the local mammalian populations during the later stages of middle age.
Mad Cow Melt Down.
But my research has further identified the presence of the more virulent radioactive metals, such as strontium 90 and barium, in the ecosystems where the clusters of the more aggressive modern strains of TSE, like BSE and vCJD, have emerged in younger mammals. Lab studies have shown that these radioactive metals can also bind into the prion protein-ferritin complexes in the brain.
In this respect, it can be explained why the 1986 outbreak of BSE in Europe – largely confined to the UK – emerged in those areas where exclusively high doses of a systemic acting organo-dithiophosphate insecticide had been compulsorily used for the treatment of warble fly since the early 1980s. This chemical acts as a copper chelator, where its two free sulphurs locked onto copper in the brains treated cows, thereby starving the prion proteins of their crucial copper co-partners. And once the radioactive metals rained down over the pastures of NW Europe after the Chernobyl blow out in April 1986, the prion proteins of those copper depleted cattle were vulnerable to bonding up with these rogue radioactive substitutes.
When the prion protein has attached itself to a radioactive metal in place of copper, it is easy to envision how the brain is subjected to a steady, self perpetuating state of "melt down." These foreign substitute metals will fail to act in the overall best interests of the organism, particularly since the invasive metal is in ferrimagnetic/radioactive form. In this respect, the prion protein becomes much like a trojan horse which trucks around the circadian circuits of the brain carrying its lethal radioactive cargo of metallic missiles on board – a fire power capacity that is potentially capable of detonating a deleterious chain reaction of free radical mediated neuro-degeneration – a well recognised toxicological phenomena that results from the radioactive decay and ferri-magnetic fields that are emitted by any radioactive metal that gets lodged into biological tissue. TSE ensues.
The US Wasting Lands.
During the autumn and spring of 2002/2003, I carried out a series of analyses in the ecosystems supporting the clusters of TSE that had emerged across the USA and Canada. My resulting data indicated that all of these clusters are located in areas where copper is virtually absent in the food chain. Furthermore, I identified the presence of high levels of certain radioactive metal species in those environments, which had invariably resulted from toxic discharges vented out of the military munitions production/testing ranges or oil/gas well sites that were centrally located within all of these cluster environments.
In this respect, the lone case of BSE that has emerged in Washington state, has probably stemmed from the fact that this cow had been imported from the copper deficient pastures of Alberta Canada into an area where the most intensive radioactive metal pollution has occurred in the USA – around the Hanford plutonium nuclear processing plant.
Mark Purdey - 30th December 2003