| Hog Watch Manitoba News February 2004 |
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USDA
Misleading American Public about Beef Safety When will we learn the danger of contaminating the food chain? Do we never learn? Ages ago, Rachel Carson warned us in her book Silent Spring of the effects of pesticides such as DDT in the food chain. We banned DDT only after witnessing disastrous declines in birds of prey such as eagles. Like the eagle, we are at the top of the food chain and therefore subject to accumulate fat-soluble toxins and carcinogens found in the food we eat ("Carcinogens found in farm-raised Atlantic salmon raise health alarms," Journal, Jan 9). It's not surprising that DDT, PCBs, dieldrin, and organochlorine pollutants are found in both wild and farmed fish. These manmade chemicals persist in the environment for decades. The toxins we have released are absorbed by the phyto- and zoo-plankton that form the base of the marine food chain. These organisms are eaten by shellfish and fish fry, which in turn form the food base for larger fish such as salmon. Each step of the food chain can result in a tenfold concentration of fat-soluble pollutants. It's not surprising either that farmed fish contain significantly more of these toxins than their wild counterparts. Whereas the wild salmon eat a varied diet and feed further from the sources of pollutants, the farmed fish are fed pellets made of ground up fish, placing them at a higher level in the food chain. Essentially all the toxins found in the 2.4 kg of pellets consumed to produce one kilogram of farmed salmon will appear in the product we consume. Eighty per cent of the salmon consumed in North America comes from salmon farms. Fish wastes and uneaten feed smother the sea floor beneath these farms, generating bacteria that consume oxygen vital to shellfish. It's estimated that one million live farmed Atlantic salmon have escaped in the Pacific Northwest. Fish ecologists fear that hybrids of these farmed fish with wild salmon could lead to the disappearance of wild salmon. Studies are going on into the production of genetically modified Atlantic salmon so as to shave a year off the time it takes to raise a market-size farmed fish. The escape of these GM fish could be disastrous for wild fish populations. Even if farmed salmon did not have significantly higher levels of toxins than their wild salmon, the environmental damage inflicted by fish farms is sufficient to choose not to buy farmed salmon. Cecily Mills, Edmonton Insecticide
Causes Mad Cow Disease Reprinted from HYPERLINK "http://eionews.com/" eionews.com, email - HYPERLINK "mailto:news@eionews.com" news@eionews.com 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, 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 agentis 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 olumn, 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 iseases, 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 daughterwere 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. Do Not Use Systemic Organophosphate Insecticides Useful Links DR. MERCOLA'S COMMENT: Fascinating information about the truly horrible things that pesticides can do and the ravesty of Mad Cow Disease. Related Articles:
BSE
Testing Vital and Affordable SASKATOON, Sask.—“Testing for BSE would add less than a penny to the cost of a hamburger. BSE testing is completely affordable and is vital if we are to restore consumer confidence, re-open markets, and end the instability and uncertainty that grips Canadian cattle farmers,” said NFU President Stewart Wells.
France and many other European Union countries test all cattle over 30 months of age for BSE. The NFU has obtained cost estimates from a number of U.S. and European sources. BSE test costs range from about 5 cents to 9 cents [Canadian $] per pound of dressed meat, or about $30 to $55 per animal.
In an August 2003 letter to Prime Minister Jean Chretien, the NFU recommended that Canada learn from the experience of European nations and implement testing regimens similar to those countries—test all cattle over 30 months of age for BSE.
Cattle over 30 months of age represent less than 20% of cattle slaughtered each year in Canada and North America. “Paying even 9 cents per pound on 20% of our cattle works out to just 2 cents per pound overall— less than one penny per burger!” said Wells. He continued: “It is inconceivable that we would try to save that penny and put at risk the health of Canadians and the future of our family farms.” Wells noted that French farmers, retailers, and consumers seem to be very happy with the mandatory testing in the EU. “Canadian consumers would be happy to spend an extra penny on a hamburger if that penny bought them peace of mind,” said Wells.
Wells concluded: "Markets and consumers hate uncertainty. Let's take the uncertainty out of the BSE situation and test all cattle over 30 months." For More Information: Stewart Wells, NFU President: (306) 773-6852 or 741-7694 Ranald MacFarlane, N.B. and P.E.I. Coordinator: (902) 887-2917 Don Mills, Ontario Coordinator: (519) 225-2163 Jan Slomp, Alberta Coordinator: (403) 843-2068 Darrin Qualman, Executive Secretary: (306) 652-9465
We
need to create an independent food safety agency whose sole responsibility
is to protect the public health. The Cow Jumped Over the U.S.D.A. For her, it's a familiar message. Before joining the department, Ms. Harrison was director of public relations for the National Cattlemen's Beef Association, the beef industry's largest trade group, where she battled government food safety efforts, criticized Oprah Winfrey for raising health questions about American hamburgers, and sent out press releases with titles like "Mad Cow Disease Not a Problem in the U.S." Ms. Harrison may well be a decent and sincere person who feels she has the public's best interest at heart. Nonetheless, her effortless transition from the cattlemen's lobby to the Agriculture Department is a fine symbol of all that is wrong with America's food safety system. Right now you'd have a hard time finding a federal agency more completely dominated by the industry it was created to regulate. Dale Moore, Ms. Veneman's chief of staff, was previously the chief lobbyist for the cattlemen's association. Other veterans of that group have high-ranking jobs at the department, as do former meat-packing executives and a former president of the National Pork Producers Council. The Agriculture Department has a dual, often contradictory mandate: to promote the sale of meat on behalf of American producers and to guarantee that American meat is safe on behalf of consumers. For too long the emphasis has been on commerce, at the expense of safety. The safeguards against mad cow that Ms. Veneman announced on Tuesday - including the elimination of "downer cattle" (cows that cannot walk) from the food chain, the removal of high-risk material like spinal cords from meat processing, the promise to introduce a system to trace cattle back to the ranch - have long been demanded by consumer groups. Their belated introduction seems to have been largely motivated by the desire to have foreign countries lift restrictions on American beef imports. Worse, on Wednesday Ms. Veneman ruled out the most important step to protect Americans from mad cow disease: a large-scale program to test the nation's cattle for bovine spongiform encephalopathy. The beef industry has fought for nearly two decades against government testing for any dangerous pathogens, and it isn't hard to guess why: when there is no true grasp of how far and wide a food-borne pathogen has spread, there's no obligation to bear the cost of dealing with it. The United States Department of Agriculture is by no means the first such body to be captured by industry groups. In Europe and Japan the spread of disease was facilitated by the repeated failure of government ministries to act on behalf of consumers. In Britain, where mad cow disease was discovered, the ministry of agriculture misled the public about the risks of the disease from the very beginning. In December 1986, the first government memo on the new pathogen warned that it might have "severe repercussions to the export trade and possibly also for humans" and thus all news of it was to be kept "confidential." Ten years later, when Britons began to fall sick with a new variant of Creutzfeldt-Jakob syndrome, thought to be the human form of mad cow, Agriculture Minister Douglas Hogg assured them that "British beef is wholly safe." It was something of a shock, three months later, when the health minister, Stephen Dorrell, told Parliament that mad cow disease might indeed be able to cross the species barrier and sicken human beings. In the wake of that scandal, France, Spain, Italy, Germany and Japan banned imports of British beef - yet they denied for years there was any risk of mad cow disease among their own cattle. Those denials proved false, once widespread testing for the disease was introduced. An investigation by the French Senate in 2001 found that the Agriculture Ministry minimized the threat of mad cow and "constantly sought to prevent or delay the introduction of precautionary measures" that "might have had an adverse effect on the competitiveness of the agri-foodstuffs industry." In Tokyo, a similar mad cow investigation in 2002 accused the Japanese Agriculture Ministry of "serious maladministration" and concluded that it had "always considered the immediate interests of producers in its policy judgments." Instead of learning from the mistakes of other countries, America now seems to be repeating them. In the past week much has been made of the "firewall" now protecting American cattle from infection with mad cow disease - the ban on feeding rendered cattle meat or beef byproducts to cattle that was imposed by the Food and Drug Administration in 1997. That ban has been cited again and again by Agriculture Department and industry spokesmen as some sort of guarantee that mad cow has not taken hold in the United States. Unfortunately, this firewall may have gaps big enough to let a herd of steer wander through it. First, the current ban still allows the feeding of cattle blood to young calves - a practice that Stanley Prusiner, who won the Nobel Prize in medicine for his work on the proteins that cause mad cow disease, calls "a really stupid idea." More important, the ban on feed has hardly been enforced. A 2001 study by the Government Accounting Office found that one-fifth of American feed and rendering companies that handle prohibited material had no systems in place to prevent the contamination of cattle feed. According to the report, more than a quarter of feed manufacturers in Colorado, one of the top beef-producing states, were not even aware of the F.D.A. measures to prevent mad cow disease, four years after their introduction. A follow-up study by the accounting office in 2002 said that the F.D.A.'s "inspection database is so severely flawed" that "it should not be used to assess compliance" with the feed ban. Indeed, 14 years after Britain announced its ban on feeding cattle proteins to cattle, the Food and Drug Administration still did not have a complete listing of the American companies rendering cattle and manufacturing cattle feed. The Washington State Holstein at the center of the current mad cow crisis may have been born in Canada, but even that possibility offers little assurance about the state of mad cow disease in the United States. Last year 1.7 million live cattle were imported from Canada - and almost a million more came from Mexico, a country whose agricultural ministry has been even slower than its American counterpart to impose strict safeguards against mad cow disease. Last year the Agriculture Department tested only 20,000 cattle for bovine spongiform encephalopathy, out of the roughly 35 million slaughtered. Belgium, with a cattle population a small fraction of ours, tested about 20 times that number for the disease. Japan tests every cow and steer that people are going to eat. Instead of testing American cattle, the government has heavily relied on work by the Harvard Center for Risk Analysis to determine how much of a threat mad cow disease poses to the United States. For the past week the Agriculture Department has emphasized the reassuring findings of these Harvard studies, but a closer examination of them is not comforting. Although thorough and well intended, they are based on computer models of how mad cow disease might spread. Their accuracy is dependent on their underlying assumptions. "Our model is not amenable to formal validation," says the Harvard group in its main report, "because there are no controlled experiments in which the introduction and consequences of B.S.E. introduction to a country has been monitored and measured." Unfortunately, "formal validation" is exactly what we need. And the only way to get it is to begin widespread testing of American cattle for mad cow disease - with particular focus on dairy cattle, the animals at highest risk for the disease and whose meat provides most of the nation's fast food hamburgers. In addition, we need to give the federal government mandatory recall powers, so that any contaminated or suspect meat can be swiftly removed from the market. As of now all meat recalls are voluntary and remarkably ineffective at getting bad meat off supermarket shelves. And most of all, we need to create an independent food safety agency whose sole responsibility is to protect the public health. Let the Agriculture Department continue to promote American meat worldwide - but empower a new agency to ensure that meat is safe to eat. Yes, the threat to human health posed by mad cow remains uncertain. But testing American cattle for dangerous pathogens will increase the cost of beef by just pennies per pound. Failing to do so could impose a far higher price, both in dollars and in human suffering. Eric Schlosser is author of "Fast Food Nation" and "Reefer Madness."
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