Pesticides and the Link to Mad Cow Disease
What if the prevailing perceptions of the cause of mad cow disease, or bovine spongiform encephalopathy (BSE), were all wrong? Where prevailing opinion favors an infectious-agent model for BSE, maverick researchers, including figures no less noteworthy than Cambridge University prion biochemist David R. Brown, look further for the truth.
Conventional Explanations for BSEIn 1986, an unknown infectious agent migrated from sheep to cows in Britain, gaining strength and virulence in its cross-species jump. Following this, the BSE-causing agent spread further by the entry of infected materials (meat and bone meal) into the feed supply. More recently, the 1997 discovery of prions, and their implication as this hitherto unknown pathological agent, added a new aspect to the old story.
Abnormally shaped mutant proteins, known as prions, cause several diseases, including Kuru, Scrapie, Chronic Wasting Disease, and Bovine Spongiform Encephalopathy. Chemically the same as normal proteins, they transform normal proteins into misfolded, brain-wasting agents, which cause cells to develop sponge-like holes, called vacuoles. The destruction of brain cells produces neurological damage and death.
Concerns with Conventional ExplanationsBut are prions actually themselves infectious agents? While it is known that feeding on already infected matter will spread the disease (for which reason, feeding cattle on beef byproducts was banned in the United States in 1997), is this truly the only means of infection? Such an assertion would beg many questions, such as the following: Why has the outbreak of mad cow in British beef so far outnumbered the total in the rest of the world? Why was BSE discovered on organic farms in cows brought in from the outside, but not on those raised from birth on the organic farms, even though organic farming rules at the time permitted limited feeding on meat and bone meal products? Why has the human form been found in long-term vegetarians? And why have infections followed a curious geographic pattern consistent with the usage of organophosphate pesticides?
The Role of Organophospate PesticidesThe alternative view on what spreads BSE and its human equivalent, variant Creutzfeldt-Jacob disease or vCJD, centers around factors in the environment to which one is exposed. It has been championed by British dairy-farmer-turned-scientist Mark Purdey, joined by other prominent scientific figures such as David Brown. Purdey was one of a handful of farmers to oppose the use of organophosphate pesticides when their use was mandated by the British government in 1984, in order to curb a warble fly epidemic. These insecticides, in an oil base, were being poured along the spines of cattle, where they absorbed into the cow’s body and turned it more or less permanently toxic to warble flies. Purdey felt concern about the high doses of this chemical, which had been developed as a neurotoxin by the Nazis, being applied so close to the spinal column. The first cases of neurological problems were reported in British cows in 1985. When BSE was discovered in other countries it was in places such as France’s Bretagne, where organophosphate pesticides were encouraged by the French government. As in Britain, BSE cases first occurred a few years after the pesticide program was initiated. In addition, BSE cases in Britain began to decline at the same time the warble fly eradication program ended.
The Role of Prions: Debate and a Cover-upWhen the first cases of BSE were reported, Purdey and his supporters felt that their concerns about organophosphates had been justified. However, the next direction conventional explanations took was towards the role of the prion itself as an infectious agent, a mysterious origin, rather than a solely immediate cause. The chief scientist leading the push to discredit Purdey’s explanation, Dr. David Ray, later was found to have been on the payroll of ICI, an insecticide manufacturer. Purdey retorted to this development with the theory of organophosphates as triggering the mutation of normal proteins (located just millimeters from the point of application) into the misfolded prions.
The Effects of Manganese ExposureCambridge’s David Brown, who specializes in prion research, also rejects the theory of the prion as being itself an infectious agent. Instead, he proposes that interaction with manganese can change the prion from a benign protein into its pathological, mutated form. The cell is particularly vulnerable when its levels of copper, a constituent of the normal protein, are low. Prion proteins will bond with copper with benign results, but forms the dangerous manganese bonds as a replacement if copper levels are insufficient while manganese is plentiful. Brown has shown that he can cause the prion to enter its misfolded state by manipulating its supplies of manganese and copper, with no contact with any infectious material being involved.
The Organophosphate-Manganese Theory
In brief, the proposed environmental-based BSE theory is as follows:
1. High doses of organophosphates in pesticides poisoned nearby proteins and decreased the amount of copper in these cells.
2. The feed given to the animals contained high levels of manganese, some of which was of poultry origin. (Animal-feed grade poultry typically ends up mixed with a fair bit of chicken manure. Chickens have been fed high quantities of manganese to strengthen egg shells. And chickens notoriously excrete most of the supplements fed to them – including manganese.)
3. Copper deficiencies and the abundance of manganese combined to alter normal, healthy proteins to the abnormal prions, producing the BSE disease.
A considerable amount of supplemental real-world data have been obtained to add to the labwork supporting the manganese hypothesis. 80% of Britain’s cases of human vCJD have been observed in rural areas, even though about 80% of all Britons live in urban areas. This statistic is a result of organophosphate pesticides having been used on crops, and subsequent exposure occurring in farming communities. For example, in a particular cluster in Kent, organophosphate pesticides were being used on hops, at 100 times the average levels for other crops. In places were prion diseases have been seen but organophosphates have seen little use, high levels of manganese have been found, coupled with low copper. For example, Chronic Wasting Disease is a major issue in Colorado, among deer and elk are sometimes forced by overpopulation to graze on pine needles. These pine needles were found to contain extremely high manganese levels, which were theorized to be caused by acid rain from smelters located upwind. In Iceland, Scrapie, the prion disease found in sheep, is associated with high manganese and low copper soil content. And in Slovakia, two clusters of vCJD are located near ferromanganese factories, and glassworks, which are heavy users of manganese. Finally, there is an occupational disease of a bygone era known as “Manganese Madness,” where miners exposed to massive doses of manganese have exhibited a condition very similar to spongiform encephalopathy.
Industrial Resistance to Progress in SafetyWith all the evidence to support organophosphates as the triggering factor in BSE and vCJD, why is there such a lack of public awareness? Perhaps it has to do with the fact that organophosphates see heavy use today in the agricultural industry. As people realized the toxic effects of organochlorine-based pesticides, a shift was made to organophosphates, which are present in most of the insects and herbicides produced by the agrochemical industry today. These agents are the foundation of modern, non-organic farming, in which certain crops, such as strawberries, routinely receive generous doses of up to twenty different pesticides during the course of the growing season. In fact, most non-organic produce bears measurable traces of organophosphates – which, as we have seen, were originally developed as a wartime neurotoxin! Genetically modified crops are also dependent on heavy usage of organophosphorus herbicides.
Implications for the FutureClearly, if the environmental model for BSE were to achieve widespread acceptance, certain important changes in farming would need to be made. Obvious would be the prohibition of organophosphate use on livestock, and thought would need to be given to the various relative levels of mineral supplements provided to them. However, on a more sweeping scale, the pesticide underpinnings of the modern world’s chemical-dependent farming system would have some serious consideration due, with the attendant economic and cultural impact. But without, it is to be hoped, the BSE.
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