|REACTIONS OF A KINDLY NATURE|
"Michelle Bowen, 29, died a slow painful death which ended in a coma three weeks after giving birth to her son via emergency caesarean section. Stephen Churchill, a student, started feeling depressed and dizzy last year, then sank into a living nightmare of terrifying hallucinations; he was dead in 12 months at age 19. Peter Hall, 20, showed the first signs of depression around Christmas, 1994; within twelve months he couldn't walk, talk, or do anything for himself. They all died of Creutzfeldt-Jakob disease, a relentlessly progressive and invariably fatal dementia which usually attacks people in their sixties. Cases such as these involving people under age 30 were until recently exceedingly rare.An uproar ensued when a leading British neuropathologist Bernard Tomlinson announced he refused to feed his children hamburgers out of fear that they might contract this disease from infected beef. On Wednesday, March 20, 1996, Sir Tomlinson's fears were validated. The British government announced that "exposure to a cattle disease called Bovine Spongiform Encephalopathy was the most likely explanation of these deaths and seven other recently diagnosed cases of Creutzfeldt-Jakob Disease among British young people." Michael Greger 1By year's end British citizens will have consumed the meat of 750,000 mad cows. That's the number of diseased critters that will slip through the jerry-rigged system meant to contain Mad Cow Disease - about ten pounds per person in the form of roasts, sausages, meat pies and other assorted beef scraps. Since the first indication in 1985 that something was amok in the beef and dairy industry, government officials and government scientists world wide have done their best to confuse and downplay the grim ramifications of this emerging disease. How serious is Mad Cow Disease? Many people may already be infected with this gruesome malady, and even though it should be front page news you'll never read what I'm about to tell you in your local newspaper.
Mad Cow Disease made headlines on March 22, 1996: "Deaths cause British panic over 'Mad Cow Disease'." 2
Newspapers across the USA announced a drastic slump in British beef prices and the plausible connection between a rare human brain disease called Creutzfeldt-Jakob Disease (C-JD) and a disease that afflicts cows known as Bovine Spongiform Encephalopathy (BSE). American consumers were assured that "mad cow disease had never been detected in cattle in the U.S.". Government scientists worldwide made bold pronouncements concerning the safety of their nations' and the world's beef supply but they didn't have a clue about how terrible this situation could become. The absence of proof of risk doesn't mean there is no risk; the risk factors were dreadfully under-estimated.
BSE was first diagnosed in British cows in April of 1985. Government scientists claimed that there was no danger in eating British beef. After thousands of cattle began dying of BSE in 1988, the government finally ordered measures to curtail dangerous practices, such as feeding cows other ground-up cows to improve milk productivity, and using offal (waste parts) to make hot dogs and kidney pies. But all this came too late; some humans had already contracted the deadly mad cow disease.
The tenuous connection between Mad Cow Disease and the eating of English beef has been strengthened through research recently published by a group of London scientists. They examined the patterns of protein taken from the brains of cows that died from Mad Cow Disease and compared them with patterns of protein taken from brains of humans who died from vC-JD (British Mad Human Disease, a variant form of C-JD but it struck younger folks and it took them longer to die ) and found these proteins to be almost identical. John Colling"All lines of evidence converge on this conclusion...I think we should take it (vCJD) very seriously. We cannot predict how many future cases there may be".3
Folks contemplating kicking their beef-eating habits might appreciate knowing a bit of the setting and history of this ongoing scientific tragedy. The diverse threads of information coming from the media and official sources have become as tangled and misshapen as any twisted protein strand found in a demented brain.
While the wide variety of brain diseases in the world have their own distinctive symptoms and markers, mis-diagnosis occurs in as many as twenty percent of disorders like Alzheimers and Creutzfeldt-Jakob Disease . The only sure diagnosis is through the examination of the brain after death and then comparing tissue samples with identified samples of known disease. Transmissible Spongiform Encephalopathy (TSE) is identified by the characteristic sponge or Swiss cheese appearance of the brain tissue and by the plaques of mutated protein that form in the brain tissue and destroy synapses and neurotransmitter functions.
Mad Cow Disease, Creutzfeldt-Jakob Disease, Scrapie and Kuru are all Transmissible Spongiform Encephalopathies; none had been studied intently until early in the1960's when they were found to be transmissible. The most common form of domestic animal TSE is Scrapie, a neurological disease of older sheep and goats that has been around for over two hundred years. Afflicted animals become irritable, lose vision, rub themselves raw (hence Scrapie), and die.
Creutzfeldt-Jakob Disease (C-JD) and Kuru are the human TSE diseases. They afflict about one in one million people each year and are characterized by bizarre behavior, dementia, memory loss, stiffening of the muscles and difficulty walking; they are always fatal.
Kuru was first studied by Dr. Carleton Gajdusek when he visited the Fore Peoples of Papua, New Guinea during the late 1950's. The Fore were suffering from a population density that put a strain on limited resources. They practiced female infanticide and cannibalism and were in a constant state of warfare with their neighbors over land and pigs. Heterosexual relations were severely limited; the men spent most of their time preparing for war and engaging in homosexual relations with the young boys of the tribe, all part of an elaborate bonding needed to ensure macho warriors and dependable compatriots; solidarity was achieved through the sharing of semen.
The females were often abused and were thought to steal the men's strength and resolve in battle as well as their vital semen. Malnourishment of females and young children was normal so they supplemented their diet by eating anything that "crawled or crept". Midwives ate placentas of the new born and women dug up the partly decomposed bodies of relatives and ate and shared with young children the putrid flesh, brains and the accumulations of maggots, not as a religious ceremony but an attempt to fend off malnutrition.
Gajdusek observed that some of the Fore women and a few children died from symptoms indicating a neurological disorder: dementia, frenzied behavior, shuddering, loss of balance and eventual agonizing death. He studied the tribal dynamics and hypothesized that Kuru, which means "shaking disease" in Fore dialect, came from their habit of ceremoniously eating the brains of dead relatives.
He brought some diseased brain tissue back to the USA and soon discovered that when pureed Kuru tissue was injected into lab animals, they too developed the Kuru symptoms. When the diseased lab animals' brains were injected into other lab animals, they died the same excruciating deaths. This meant that the condition could be transmitted from organism to organism and was therefore transmissible, hence Transmissible Spongiform Encephalopathy (TSE). Scrapie and C-JD were also studied and later proven to be transmissible. Dr. Gajdusek received the Nobel Prize in 1976 for this research.
While much is known about TSE, Gajdusek and his colleagues at the National Institute of Health were never able to isolate or identify an infectious agent in TSE. There were no tests to identify TSE in living tissue and only two ways to determine infectivity. A dead brain can be examined for sponge-like holes and plaques; or a broth of suspect brain tissue can be injected into a susceptible lab animal, which will become mad in 300 to 600 days if the mixture was infective.
At first, scientists working on TSE research suspected that the infective agent was a "slow virus". To determine the nature of this "slow virus", tissue containing TSE was injected into countless lab animals. Just one ongoing experiment could kill thousands including cows, mice, hamsters and monkeys. They were searching for a possible bio-warfare agent.
In 1969 World Health Organization reported their progress: "from painstaking work with visna and Scrapie, degenerative diseases of the central nervous system, and Kuru, a degenerative disease of the central nervous system of man... distinguished by the languishing character of the infection process they initiate. The incubation period in the host may be months or years, and the disease itself may progress laggardly towards an irreversible deterioration of the victim. Cells infected with 'slow' viruses are in general neither impaired nor stimulated to proliferate. Their functions are impaired but the nature of the dysfunction has not yet been clarified...The resistance of the Scrapie agent to heat, ether, formalin, and other enzymatic and chemical agents, as well as its very small particle size, poses the question whether it is a conventional virus, an incomplete virus, or some other agent. . . "
The Department of Defense also began trying to develop "a new infective microorganism which could differ in certain important aspects from any known disease-causing organism." In 1970 the Army awarded a ten million dollar grant toward the goal of developing a "super germ" that would inhibit or destroy the immune system.4
Political and economic interests have limited the debate on contentious issues exploring the genesis of the BSE agent by denying or misrepresenting the views of contrary scientists. At stake are the intensive farming methods that have become so common during the last three decades. Increased profits come from packing as many animals as possible into as small a space as possible, exploiting them to the maximum.
Their diet is the most unnatural aspect of the process. Cost effectiveness demands that every shred of every animal be used. A third to a half is saved for human consumption; most of the leftovers are rendered into high protein food for other animals. There1s not much time for grazing or scratching in the world of pens and cages and this foodstuff supplies much of the necessary protein needed for eggs, marbled beef and rich butter fat. We will soon understand the ramifications of forcing animals that we eat to become cannibals.
Foresight should have warned us that this was not healthy. But in the modern world we've created, where science and technology have conjured up a seemingly bounteous existence, we have come to rely on scientists for truth. We're all in danger of ingesting a TSE contaminated meal at any time yet our government and its scientists continue protecting moneyed and powerful interests over those of the consumer. As Michael Greger, a BSE researcher and scholar, writes: ". . .I think this crisis shows to what length governments will go to prevent financial harm to powerful lobbies in general, and in doing so risk immeasurable harm to those they claim to represent".
The Veterinary Committee of the European Union was told in 1990 to "take a cold attitude towards BSE so as not to provoke unfavorable reactions from the market. . .no more talk of BSE. . .we are going to ask the United Kingdom,through official channels, to stop publishing the research results. . .this BSE affair must be minimized through disinformation. Better to say the press has a tendency to exaggerate." 5
When Oprah declared she wouldn't eat another burger after learning on her show that cows eat cows, the Texas Agricultural Commissioner stated: "We're not going to sit back and let trash TV trash a vital industry . . ." He wanted to bring a lawsuit against one of the guests on the show under the state law that bans insulting perishable foods.
The USDA is doing everything in its power to suppress any notion that BSE exists in the USA. The wholesale price of beef has been plummeting for the last two years; consumers are frightened of beef for other valid reasons but the realization that it causes premature madness could result in a panic. Disregarding the vast accumulation of evidence, our current clumsy and ineffective research program is not objectively examining whether there is a form of mad cow disease in our food supply. The meat and dairy lobby controls the current government research and they have decided that a search is "not appropriate at this time".
Nor will they even consider banning the unnatural cannibalistic eating patterns they've imposed on former grass eaters; this habit is now intensifying with the introduction of bovine growth hormone. All it takes is a single teaspoon of infective mad cow meat or bone meal to begin the disease process but all feed manufactures still use meat and bone meal in high protein food. The FDA proposed the banning of at least the brains from the rendered feed mix but this was opposed by the American Meat Institute: "no good is accomplished by prejudicing segments of society against the meat industry".
With a hundred million cattle, the USA has the highest per capita beef consumption in the world. What is not generally known and which the US Department of Agriculture denies is that we have a form of Transmissible Spongiform Encephalopathy in our herds. It is known as "Downer Cow Syndrome" and causes over 300,000 cattle deaths every year. When these cows are put under stress they stagger around, bellowing, and then fall down and are unable to get back up. If these "downers" are kept alive long enough (some are literally dragged to the market), they can be ground up and fed to you, and the bones, lips, head,etc. boiled into a gelatin which soon may become the marshmallow topping and the ice cream for your favorite sundae. 6
If unsafe for human consumption, the sorry creature is melted down and used as pet food and animal feed. Did you even know that the diet of dairy cows consists of other ground up animals - not just cows but sheep, goats, chickens, and whatever other dead meat they can scrape off the slaughterhouse floor? When cows fed this diet, including the downers, are no longer productive, they are then ground into hamburgers, 2.6 billion lbs. yearly. Does this seem safe?
The "slow virus" was never found. That theory has recently been supplanted by the prion (pree-on) hypothesis. Prions (Proteinaceous Infectious Particles) were named by Dr. Stanley Prusiner before he even discovered them because "Prion is a terrific word. It1s snappy. . .It isn't easy to come up with a good word in biology. One hell of a lot of bad words people introduce get thrown away."7
Prusiner's research and public relations campaign has convinced many scientists that prions and prions alone are the infectious agents that cause Transmissible Spongiform Encephalopathy. These mutant or rogue proteins are found in most autopsies of Transmissible Spongiform Encephalopathy brain tissue and form the plaques that cause neural disruption. The prions seem to transform the healthy protein into harmful plaques and tangles. How this occurs is not quite clear. To accept Prusiner's theory is to accept changes in the basic concepts of biology.
He and his supporters have garnered millions of dollars in research grants and are said to be doing brilliant work. He wins award after award, but reasonable doubt still exists. How do prions replicate without DNA or RNA? How can he account for the various strains of TSE? Where is the one to one relationship between prions and TSE infection that he promised? One critic commented that "some parts of the prion hypothesis are getting into medieval thought processes".8
Frank O. Bastian, director of neuropathology at the University of South Alabama, is also skeptical of the prion theory. "The prion was bull-dozed in the press and scientific community. The prion is a red herring."9 He maintains that the TSE infective agent is a spiroplasma. "Spiroplasmas are similar to mycoplasmas in that they do not have a cell wall and have among the smallest genomes of any living organisms. Spiroplasmas, which were only discovered in 1976, are present in the hemolymph of almost all insects. There are probably several million strains of spiroplasmas."
Dr. Bastian has been scrutinizing and writing about spiroplasmas since 1976 when he first observed the minute organisms in the brain tissue of a C-JD cadaver. "I saw a spiral structure foreign to the tissue. It had features of the newly reported spiroplasmas".
As the editor of the only reference book on C-JD, he considers himself an authority on the subject, but his opinion is seldom asked on the BSE crisis, nor are his views given much credence. "A shortcoming in the prion theory is that C-JD and Scrapie can be transmitted without prions. Brain material from which the prion has been removed with antibodies can still infect animals." He insists that the prion is nothing more than reconfigured protein, created by the host as a defense against the machinations of the invading spiroplasma.
The spiroplasmas replicate in the spleen and the lymph nodes; then they migrate toward the brain. They1re able to bind protein in a way that confuses the immune system into believing they they1re part of the host. "Spiroplasmas are similar to mycoplasmas, (small bacteria-like organisms) and it is a well known phenomenon that mycoplasmas are able to blend with cell membranes. What happens, possibly, is that spiroplasmas essentially fuse with host. . .blending with the background, so you would not see it unless you had a marker to label it. Developing such a marker has been difficult because spiroplasmas are difficult to cultivate. No more than half of the known strains are culturable."10
There's a simple elegance to this direct and understandable hypotheses, but the prion theory has become accepted by scientists; spiroplasmas are seldom if ever mentioned as the possible cause of these diseases even though Bastian indicates that it would be a relatively simple task to prove his suppositions. "Definitive evidence of this link would be to demonstrate that spiroplasma DNA occurs in the brain tissue of people with C-JD and related illnesses, but not in brain tissue from controls. This could be done by using polymerase chain reaction assays to detect nucleotide sequences in genes unique to spiroplasmas and common to all types of spiroplasmas. I have 15 types of spiroplasmas in my laboratory and am in the process of looking for nucleotide sequences common to all of them." This research is the only hope we have for developing a test that can determine how serious Mad Cow Disease has become and where it has spread. Resistance to Bastian1s ideas means resistance to such a test. Is the National Institute of Health afraid of what we might find? In March of this year, just as the furor over mad cow disease began to peak, Dr. Gujdusek was arrested at gun point in his driveway by six FBI agents. He was charged with two counts of child abuse and two counts of having oral sex with a juvenile. He was released on $350,000 bond and placed on administrative leave by the National Institute of Health. The journals he kept on the sexual practices of the New Guinea males had been given to the US Senate. Why or by whom is not clear. The Senate asked the FBI to investigate. Gujdusek brought 56 Papaun children to the US for education. One of these kids has admitted that he had sex with Gujdusek.11
These journals have been around for 30 years. Why the big uproar just now? Gajdusek knows more about these diseases that anyone but has been effectively silenced since his arrest. It would be helpful to question him.
I believe he made two serious mistakes in his work with Kuru. The first was his misunderstanding of the way that Kuru was transmitted. His assumption that Papuans were circulating the disease among themselves through ceremonial cannibalism was only partially correct. Another vital factor must have been their habit of consuming vast amounts of maggots and mites attached to the decayed flesh. Hundreds of common arthropods reside on dead bodies, the most common being a wide variety of maggots and mites. Researchers have transmitted Scrapie to mice by inoculating them with material from hay mites gathered from Scrapie infected farms. Bastian found this information "very exciting data." He insists that spiroplasmas are found in all arthropods. If this is true then our bodies must have built a strong barrier between us and them or we'd all be goners by now. Until lately, these diseases were very rare, one in a million.
This brings me to Gajdusek's second mistake. He thoughtlessly brought Kuru brain tissue to US labs and began injecting it into countless numbers of lab animals. Usually the more hosts a pathogen passes through, the more virulent it becomes. Apparently the new and more communicable form of Kuru has escaped the confines of our national labs and is now in the food supply. Did some of the infected cows or other lab animals or their infected offspring end up in high protein supplements?
The involvement of National Institute of Health in spreading this sickness from a frenzied tribe in New Guinea to British cows and then back into British citizens must be examined. They would like you to believe that Scrapie infected sheep, ground up and fed to cows, caused the outbreak. They argue that the process used to extract protein from all the leftover meat scraps was modified in 1980. This allowed the disease to spread because the new methods didn't kill the infective agent in Scrapie.
This is plausible since the new process doesn't destroy the infective agent, but Mad Cow Disease isn't Scrapie, it's Kuru, a completely different strain of Transmissible Spongiform Encephalopathy . Gujdusek has admitted this much but no one seems to understand or care about the implications of such admissions.
How did Kuru get into cows if it wasn't put there by thousands of bio-warfare experiments carried out by the National Institute of Health? Mad Cow Disease is another startlingly clear reminder of what can happen when we allow scientists to secretly muck around with biologically hazardous substances.
- Michael Greger "The Public Health Implications of Mad Cow Disease"
- The Sacramento Bee, March 22, 1996
- The Times:Britain: Oct. 24,1996 by Nigel Hawkes
- Leonard G.Horowitz, "Emerging Viruses:AIDS and Ebola—Nature, Accident or Genocide", ppg. 15-19
- Fabienne Maleysson, Que Choisir, September 1994, pg. 308
- Michael Greger, "The Public Health Implications of Mad Cow Disease"
- Gary Tauber, "The Name of the Game Is Fame", Discover, December, 1986
- Rosie Mestel, "Putting Prions to the Test", Science, July 12, 1996
- Dr. Frank Bastian, personal correspondence, September 4, 1996
- Infectious Disease News, June, 1996
- Claire W. Gilbert, Ph.D., "Dr. Gujdusek and Mad Cows"
- Prusiner S.B, "The Prion Diseases" Scientific American Jan 1995
- Richard Lacy, "How Now Mad Cow", 1995
- Dr. Shaun Heaphy, "Prion Diseases"1996
- Michael Greger, "Mad Cow Disease-Much More Serious Than AIDS"
- James Wood, "Some Facts To Help Inform About BSE/CJD"
- Larry Mark, "Bovine Spongiform Encephalopathy" USDA
- Michael Greger,"The Public Health Implications of Mad Cow Disease"
- John Collinge M.D. "New Diagonstic Tests for Prion Diseases", New England Journal of Medicine Editoral, September 1996
- Karen Kreeger, "Researchers Homing in on Mechanisms of Encephalopathic Diseases", The Scientist, June 10, 1996