page 6

The Origins of BSE - Page 6

2. Foreign metal manganese contamination and its substitution at PrP’s vacant Cu domain

The high levels of Mn recorded in sporadic, familial and nvTSE cluster environments have been published previously (4)(5). Environmental sources of Mn have stemmed from airborne emissions out of volcanoes, steel, ceramic, brick. dye, glass, munitions, battery factories, lead-free petrol refineries, autocar exhaust emissions, aeroplane take-off flight paths, spraying of liquid Mn based fertilisers and fungicides, etc. Airborne Mn can enter the CNS via the nasal-olfactory route of inhalation (88) - the route of Mn absorption which presents the greatest risk in respect of initiating TSE.

It has been proposed that the addition of Mn oxide into artificial calf milk powders at levels up to 1000 times those found naturally in cows milk (5), coupled with the inclusion of Mn oxide in a range of free access dairy livestock mineral supplements and concentrated feeding stuffs (89), underlies a major source of potential Mn overloading of the CNS in the intensively farmed BSE endemic countries.

Exposure to high levels of dietary Mn in the early/embryonic life of the calf exacerbates the problem of Mn toxicity; since the homeostatic regulation of metal uptake into the brain at the blood brain/CSF barriers is underdeveloped in the immature mammal (90).

Very low incidence of BSE in beef suckler herds (1) and total absence of BSE in 100% of cattle raised on fully converted organic farms (87) can both be explained by the fact that these farms employed real cow’s milk rather than the Mn fortified artificial milk replacer powder for rearing their calves. Nor did these types of farm feed high inputs of Mn supplemented concentrate feeds, as was customary in the conventional intensively farmed dairy herds that demonstrated a high incidence rate of BSE.

A substantial increase in the use of Mn based fertiliser and fungicide sprays (4) on the high grade lowland farmland in the UK during the 1980s has also caused an increase in atmospheric and in-feed Mn exposure of the bovine during the BSE period.

Mn may have also entered the bovine food chain due to its significant presence as an impurity in some forms of phosphate fertiliser (91) and where Mn rich chicken manure has been utilised as a fertiliser or as a protein booster/binding ingredient in concentrated feeds (4).

An interesting correlation exists between the areas of Mn deficiency in soils (92) and the distribution of vCJD cases in the UK (93) See map 1 and 2 (below)

Perhaps this correlation can be explained by the fact that the customary spraying of Mn deficient farmland with liquid Mn fertiliser - up to four times per growing season - subjected human populations residing in villages/towns within these areas to significant toxic levels of airborne Mn particulates. Given the high percentage of vCJD cases erupting in rural/small town populations, this route of Mn contamination seems feasible.

Interestingly, the high dietary intakes of Mn concentrated pine needles (4)(5) and ‘addictive’ brands of Mn enriched mineral supplements amongst the deer and elk herds of Wisconsin/Colorado may also partly explain the aetiology of CWD in these well renowned low copper districts (4). Hunters are currently putting down addictive brands of Mn rich mineral lick for ‘hooking’ deer to their shooting territories as well as for reasons of promoting their antler growth.

It is interesting that all captive and free ranging species that have succumbed to TSE to date – cattle, cats, zoo animals, mink, deer, goats, humans – involve species that are routinely fortified with Mn additives in their replacement milk powders, etc, and mineral supplements (4)(5). Furthermore, Mn is largely absorbed through the duodenum; explaining the more efficient absorption rate of 10-18% of available dietary Mn in ruminants in relation to the less efficient absorption rate of 2-5% of available Mn in the diet of monogastrics (89). Perhaps this significant differential in the rates of Mn absorption between ruminants and monogastrics explains why ruminants demonstrate a high susceptibility to TSEs, whilst monogastrics, such as poultry, dogs, pigs, etc, have remained virtually TSE-free.

3. High intensities of eco-oxidants in the rural environments where BSE/vCJD occurs

The association between TSE cluster zones and environments demonstrating high intensities of UV, ozone and other oxidants has already been extensively discussed (5). The high altitude, snow covered, coniferous, mountain or coastal locations that commonly characterises the cluster zones of traditional TSE (4)(5) are well recognised for their above average intensities of UV and ozone (94).

Interestingly a greater majority of both sporadic CJD (95) and nvCJD cases have surfaced in individuals living in rural villages or coastal locations during their period of clinical onset (5) (See map 1 & 2) Both domestic livestock and rural human populations are exposed to the highest levels of eco-oxidants in relation to populations residing in large towns; since levels of UV are considerably lower in urban environments because the canopy of airborne smog particulates overlying towns serves to absorb and deflect incoming UV rays (96). Furthermore, ozone tends to form in rural and high ground areas due to migration of exhaust gases out of the towns into the high UV areas – thus bringing together the entire set of prerequisites required for ozone oxidant formation in these areas (97)(94). Has the increased cocktail of oxidants that is contaminating the modern world (increased UV in the northern hemispheres due to stratospheric ozone thinning, etc), assisted in the emergence of the more aggressive new strain TSEs over the last years?

An increased intensity of oxidizing agents in the environment of the cow would ensure an ‘in situ’ oxidative transformation of Mn2+ prions into Mn3+ prions in tissues, like the retina, that are in the front line of defence against incoming eco-oxidative assault by UV, ozone, etc. These so called ‘prion production plants’ See diagram 4 (below),

churn out a steady supply of Mn 3+ prions into the CNS, where the newly formed Mn 3+ component is rendered ‘susceptible’ to infrasonic shock induced metamorphosis at a later date; whereupon paramagnetic Mn 3+ prions are transformed into the fully fledged, ferrimagnetic pathogenic prions.


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