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Medical Forum / General / General / January 2004discussing Prion disease, BSE & phosmet use in Canada
Bob Bruner wrote below but unable to get google to format the reply: On 7 Jan 2004 23:38:21 -0800, a_plutonium@hotmail.com (Archimedes Plutonium) wrote: >This discussion arose under prion disease. And one of the sad remarks >that is obvious to most people is that ever since 1980, the science >community has done little to nothing to control this disease with the >rampant outbreak in England in the 1990s and the new prion diseases of >Mad Cow and vCJD in humans. Huh? Each time a transmissible prion disease has become evident, the transmission cycle has been broken. (Kuru, BSE, other CJD transfer such as on instruments). I don't know how you could expect much more. In the absence of transmission, these are extremely rare diseases. Until BSE/vCJD they did not even receive much attention, as not being very important. And the infectious agent wasn't even identified until in the 80s. bob Well I was thinking that the USA would be on its toes after the England loss of 1990s. To think that the USA would still be using brain and spinal cord and portion of the intestine in human consumption after having gone through the England crisis. And to think that a full ten years after the England crisis that here in the USA we would have such a shoddy tracking system should BSE outbreak. I do not think I am the only one alarmed as to the lay-backishness of the USA should a BSE outbreak occur. From the news lately it seems as though the USA was so lay-backish that they expected to never be an outbreak in the USA. And the fact that the animals in question are destroyed and not allowed to be researched. So as not being researched and thus not able to answer any questions. And the fact that a good alternative theory that Phosmet and metal-ions is the source of cause of this disease, yet no-one in Canada or the USA is looking into phosmet. All in all, I would say the treatment of the BSE in the USA in the past months and past 10 years after England crisis, that the USA treatment and readiness was a remarkably fumbled and shoddy dealing. We should have outlawed brain, spinal column, intestine portion in the 1990s. We should have outlawed all meatfeed and should have had a traceable system in place as a result of England. It appears as though the government agencies were banking on the idea that the USA will never have a BSE outbreak which was not the sensible plan to take. And worst of all, it seems as though no-one is calling for a check into whether Phosmet or pesticides or herbicides is the cause of this disease. Perhaps whenever someone wants to look to see if Phosmet is the culprit that the research is halted and that Phosmet is allowed to be sprayed in ever higher quantities. I see no outbreaks of BSE in Germany or in France yet they have plenty of cattle, but do they use phosmet in Germany and France. They use plenty of phosmet in Canada where the flies, I hear, come in swarms. I do not see Ann Veneman (forgive the spelling) of the EPA or any ranking Bush admin official calling out " let us get some scientists and pinpoint the true cause of this prion disease" I don't see that going on. I see only damage control. No, Bob, I get the general feeling that this USA outbreak of BSE was handled very poorly considering we had 10 years of learning from England in advance to prepare. Archimedes Plutonium whole entire Universe is just one big atom where dots of the electron-dot-cloud are galaxies >Bob Bruner wrote below but unable to get google to format the reply: >On 7 Jan 2004 23:38:21 -0800, a_plutonium@hotmail.com (Archimedes [quoted text clipped - 29 lines] >though the USA was so lay-backish that they expected to never be an >outbreak in the USA. I would agree somewhat with that last point, but it is a political issue, not scientific. (I understand that Prusiner has been arguing for better controls for some time.) Nevertheless, the record is 2 (known) cases of BSE in North America (at least one of which was born prior to the feed change -- not sure about the other), and no vCJD. Now, one can wonder about underreporting, but still there has been no evidence of any significant problem. Your original point above was trying to question the scientists. No, not at all. Maybe the beef lobby. (And now the beef lobby has changed its tune.) bob (snip) > I would agree somewhat with that last point, but it is a political > issue, not scientific. (I understand that Prusiner has been arguing [quoted text clipped - 11 lines] > > bob Hi Bob, I wonder if anyone has attempted to map globally every incident of Prion disease, where every case whether sheep, cow, human, ferret, etc etc has ever been reported? And I wonder if anyone also has attempted to track and record globally the use of phosmet and phosmet-related pesticides. What I am thinking is that if such a global report had been kept for the past 50 years that the maps would coincide with prion outbreak and phosmet usage. I am not skilled enough Bob, to be able to disassemble the phosmet molecule and be able to pinpoint where that molecule is able to associate or dis-associate in a bonding with Metallic-Ions and thus create a chemical environment in the brain where prion molecules start to proliferate the bad-prion-form. Bob, I do not know enough about the chemical structure of phosmet that would allow it to cause deformity of prion proteins in the brain. Perhaps it is the proclivity of phosmet to union with the manufacturing site of normal prion proteins and that when phosmet gets into a human brain, that it has this proclivity to cling to the prion manufacturing site within the brain. And by clinging to the site causes the site to spew out not well formed good prion proteins but deformed prion proteins. Question: Bob, has there ever been a case of prion disease where the victim is inflicted not with just one malformed prion but with 2 or more malformed prions. If so, then phosmet as the cause would answer that because the cookie cutter manufacturing site of good prion proteins interrupted by phosmet would begin to *vary* its deformity the longer it is in action, just like a machine tool part wears out and this wearing out will be seen in the final product. If Prusiner model was correct then there would be only one malformed prion but with a Chemical cause, the deformity varies with time as the cookie cutter is wearing down or wearing out. Archimedes Plutonium whole entire Universe is just one big atom where dots of the electron-dot-cloud are galaxies >Question: Bob, has there ever been a case of prion disease where the >victim is inflicted not with just one malformed prion but with 2 or >more malformed prions. I would be surprised if that has ever been noticed -- as much as anything because it would probably be hard to tell (at least until rather recently). And given the rarity of natural prion diseases, it would be unlikely that anyone had >1. If one wanted to study it intentionally, one could use lab rodents and lab strains of prions -- and see what happens. I have no idea whether any such work has been done. Of some possible interest... people who are heterozygous for two forms of the normal prion protein seem relatively resistant to getting "disease". No one knows what this means, but one possibility is that having two different forms available interferes with formation of a "homopolymer". I wouldn't put much weight in that. bob > >Question: Bob, has there ever been a case of prion disease where the > >victim is inflicted not with just one malformed prion but with 2 or [quoted text clipped - 16 lines] > > bob ##### Hi, Bob, anyone else, too....."Natural" prion diseases are NOT uncommon. About MANGANESE: leaving the organophosphate types of "triggers" for now, (obviously, they exist). The Manganese: Human diseases: not necessarily CJD or vCJD: There are a number of valances to Manganese. Is there a particularly healthful bioavailable valance for making properly functional cellular prions? Then, as well, the Manganese ferromagnetic variation was mentioned in only one abstract I scanned. It's pretty obvious that the sources would be common industrial pollution. Would the human metabolism differentiate between magnetic and non-magnetic?. Checking the fibrillary deposits of various kinds of "inclusion bodies" for the specifics of the Manganerse for not only Alzheimer's & Parkinson's but Multiple Sclerosis type diseases must have been done at some time over the last several years????? Yes????? Hopefully, Del ######## >> I would be surprised if that has ever been noticed -- as much as >> anything because it would probably be hard to tell (at least until >> rather recently). And given the rarity of natural prion diseases, it >> would be unlikely that anyone had >1. >> bob >##### Hi, Bob, anyone else, too....."Natural" prion diseases are NOT >uncommon. I was referring to humans, where the frequency is often given as about 1 in a million, per year. That is usually considered uncommon. >About MANGANESE: leaving the organophosphate types of "triggers" for >now, (obviously, they exist). No, it is not obvious. They are toxic, but so far as I know there is no evidence that they cause/affect prion disease. If you know of something, please give some info and a reference. That they cause similar symptoms is beside the point; things that kill nervous cells will tend to have similar effects. (I just noted in one recent post a 2002 paper that showed no effect of phosmet on prions. The paper seemed rather weak, but the context suggests there is no evidence to the contrary.) >The Manganese: Human diseases: not >necessarily CJD or vCJD: There are a number of valances to Manganese. >Is there a particularly healthful bioavailable valance for making >properly functional cellular prions? no known relevance, AFAIK. If you know of something, please give some info and a reference. bob > > >> [quoted text clipped - 33 lines] > > bob ##### AFAIK too, there's a lot of real tight info necess. Excess Manganese coupled with shortage of copper would probably be a prerequisite for Phosmet or other toxicity to trigger any accellerated reaction, but that is only "probably". It might have directed research a bit more re: the pollution or other factors if those 450 calves were tested. (Though I suspected they wouldn't) Still searching Del Crow ##### (snipped) > ##### AFAIK too, there's a lot of real tight info necess. Excess > Manganese coupled with shortage of copper would probably be a [quoted text clipped - 3 lines] > tested. (Though I suspected they wouldn't) Still searching > Del Crow ##### Seems as though copper plays a central role in prion disease. Whenever any metals arise in connection to prion disease, copper seems always in that list. It has been said in biology that copper is an essential component of life. But I never learned or understood why it is essential. And then I would want to know whether this essentialness is connected to the action or performance or job of the prion protein molecule. Question: is the essentialness of copper for life on Earth confined to the brain anatomy? Or is the essentialness for all multicellar organisms a generalized essentialness or is it a specific essentialness such as the brain region. Archimedes Plutonium whole entire Universe is just one big atom where dots of the electron-dot-cloud are galaxies Copper is a key component of many, if not all, redox enzymes in biological systems. It is also the key component of haemocyanin. However, copper is only present in small amounts in organisms and large amounts can be toxic.  SignatureMark Petten MSc Student Acadia University Department of Biology "Research is the process of going up alleys to see if they're blind" -Bates' Law of Research > (snipped) > > [quoted text clipped - 23 lines] > whole entire Universe is just one big atom where dots > of the electron-dot-cloud are galaxies > Copper is a key component of many, if not all, redox enzymes in biological > systems. It is also the key component of haemocyanin. However, copper is > only present in small amounts in organisms and large amounts can be toxic. Yes, someone else emailed me saying that copper is necessary for "collagen connective tissue formation" I think it would be fair to say that the general purpose of good prion proteins is that of connective tissue. And fair to say that the proteins involved in Alzheimers is that of a purpose of connective tissue. Not sure whether that applies to Parkinsons. What I sense from this is that the diseases of Alzheimers and Prion are linked in that their gone awry proteins were used for the purpose of connective tissue, and that the copper environment had been disturbed to the point where the disease arose. Whether the disease of prion or Alzheimers is a copper excess or deficiency is unclear to me. Although I would guess from the discussion on the pesticide phosmet that it is a deficiency of copper. Archimedes Plutonium whole entire Universe is just one big atom where dots of the electron-dot-cloud are galaxies > Copper is a key component of many, if not all, redox enzymes in biological > systems. It is also the key component of haemocyanin. However, copper is [quoted text clipped - 31 lines] > > whole entire Universe is just one big atom where dots > > of the electron-dot-cloud are galaxies #### Not just brain, whole body, every cell, hundreds to thousands of mitochondria per cell require trace minerals to function. Some substitutions are commonally made Faulty prions, mainly carrying (I am adding this word in here)"magnetized" Manganese on the amino acid Tyrosine where 4 molecules of copper should be becomes a "wrong" breakpoint creating a bottlenneck of processes. Manganese has the interesring ability of being able to oxidize several times > #### Not just brain, whole body, every cell, hundreds to thousands of > mitochondria per cell require trace minerals to function. Some [quoted text clipped - 3 lines] > breakpoint creating a bottlenneck of processes. Manganese has the > interesring ability of being able to oxidize several times I have told Bob that yeast studies are irrelevant to Prion disease because yeast does not carry the diseases of prion. But perhaps yeast studies can now be useful. Experiments: I believe no-one has experimented with yeast where they inject magnetic manganese ions and measure the affects thereof. It is quite possible to turn perhaps yeast into dangerous disease infecting yeast by the infusion of magnetic manganese ions. And in those cases in past history that were given a description of "spontaneous prion disease" were perhaps not really spontaneous but cases in which an individual ate both yeast plus magnetic manganese ions and the combination of the two into the body began the prion disease. Question to DelCrow: How does the ion of magnetic manganese hold up as far as stability is concerned? Because we know that prion diseases is very persistent and needs high temperatures of burning carcass to extinguish the disease. So, does high temperature burning destroy the Magnetic Manganese?? How stable and persistent is Magnetic Manganese in the environment?? Archimedes Plutonium whole entire Universe is just one big atom where dots of the electron-dot-cloud are galaxies > > > >> [quoted text clipped - 41 lines] > tested. (Though I suspected they wouldn't) Still searching > Del Crow ##### #####Sorry, I think I missed the hidden question. I won't give referencxes, but it should be quick enough to pull a few of these prion diseases off the web. Amyotropic Lateral Sclerosis, Alzheimer's Disease, Parkinson's, Multiple Sclerosis, Myesthenia Gravis, Inclusion Body Myositis, etc. Del #### > > > > >> [quoted text clipped - 47 lines] > Disease, Parkinson's, Multiple Sclerosis, Myesthenia Gravis, Inclusion > Body Myositis, etc. Del #### #### Re: the several "valences" of Manganese. Some, Manganese if not all will become magnetized and lost in common idustrial uses, ie anything resembling welding. Most Mg fume is removed from major venting stacks by electrical "scrubbing". What leaves has large possibility of having become "magnetized" in the "cleansing" process. The airborne ions can go quite a way and are most easily absorbed by humans and animals at this stage (not to ignore soil pollution and plant uptake entirely but...) magnetic Manganese gets into the animal and human metabolism where it supplants some copper (which "might" be in short supply.."might not", too) but the codon (which "might" or "might not" be genetically pre-adjusted to using some Manganese instead of copper) sends out the magnetized Manganese instead of copper on those Tyrosine aminos.....creating a breakpoint, which it might have dealt with, "probably", anyway. But when the cell tries to neutralize this magnetized Manganese, throwing Superoxide Dismutase with other ions of other metals onto it the Manganese can oxidize several times, and these other complicated molecules stick to it, making quite large "inclusion bodies". But, still, only "chemically" neutralized, the magnetic Manganese is prone to grab iron molecules....or maybe only inhibit movement of iron within the mitochondria. The mitochondria therupon tends to suffocate for lack of oxygen transfer (iron movement is necessary). The cell tries to isolate the problemmatic Manganese in vacuoles away from its power sources (mitochondria). Inclusion bodies, fibrillary tangles, energy loss, nerve and muscle wasting, downer cows and downer people occur. Please give me heck over this flight of fancy, I really hate to waste your time. Del Crow ####### > >Question: Bob, has there ever been a case of prion disease where the > >victim is inflicted not with just one malformed prion but with 2 or [quoted text clipped - 16 lines] > > bob ####### I would put a bit more weight in it, Bob. Apparently quite a few of the noticeable human prion malfunctions or adjustments (I'm shifting terminology a bit) are on codon 102 (?) and 129 (?) it seems codons,(which make the prions) possibly most of them, are not only "on" and "off" but are variable, maybe even adjustable.(Wilf Jefferies bioscience lab at UBC). It would be nice to know more about specific functions, though..and be able to make some "natural" adjustments without MD Mis-Diagnosis or Metabolic-Damage which, incidentally can be "triggering" "Inclusion Body" diseases in humans. I don't even pretend to be any kind of endocrinologist or bioscientist. Feel free to correct me where I err. Del Crow ###### >> Of some possible interest... people who are heterozygous for two forms >> of the normal prion protein seem relatively resistant to getting [quoted text clipped - 5 lines] >####### >I would put a bit more weight in it, Bob. When I said not to put much weight in it, I was referring to my attempt to offer an explanation for it. The basic facts seem quite good, so yes the phenomenon (heterozygotes are relatively resistant) is undoubtedly real. But the reason for it is not known -- and will probably not be until there is a better understanding of the disease process. There is nothing inherent in the prion model about causing disease, and how it does so is quite unclear. >Apparently quite a few of >the noticeable human prion malfunctions or adjustments (I'm shifting >terminology a bit) are on codon 102 (?) and 129 (?) it seems >codons,(which make the prions) possibly most of them, are not only >"on" and "off" but are variable, on/off has no meaning with respect to these codons. But different forms of the gene code for different amino acids at those positions. >maybe even adjustable. A somatic mutation in the prion gene could indeed make one more susceptible. But emphasize that is not an intrinsic part of the process. bob > >> Of some possible interest... people who are heterozygous for two forms > >> of the normal prion protein seem relatively resistant to getting [quoted text clipped - 30 lines] > > bob ###### I am pretty sure what's "intrinsic" is not necessarily more than a small part of the problem. Whether "organelles" are adjustable or not, there are, even now, lists of known and suspected triggers for human prion-related disorders. With 254 codons, I think you are pretty much right, being suspicious of the "off" or "on", but with only 20 amino acids, the sequencing seems to be pretty important....cellular supply and demand....shipment.....addressing.....carrying the right pizzoelectric messenger (snap fasteners come to mind). If you are saying "it ain't easy" even for a MD,PhD,professor or lab technician, well I bet you are right! Can you say that Manganese is NOT a major part of the prion problem we have? Can you say that there is NO PRION PROBLEM in humans? Can you say that there is NO LINK to pollution? If you do....oh, well, sorry to waste your time. Del Crow #######3 > >> Of some possible interest... people who are heterozygous for two forms > >> of the normal prion protein seem relatively resistant to getting [quoted text clipped - 30 lines] > > bob Bob, I wonder if you know the geometry of the phosmet molecule? I have a storm full of questions about that geometry. Whether it has an affinity for metal-ions? Whether it has a bonding affinity for the prion molecule or the prion manufacturing site (codons). If phosmet has a unique geometry that bonds with the manufacturing site of prion proteins then that interference is the cause of the prion disease. Just as sickle cell is caused by a ruination of the iron heme, then prion disease is seen as a ruination of the site wherein more prion molecules are formed, and once a phosmet molecule attaches to the manufacturing site of normal prions, like a cookie cutter it spews out malformed prion proteins. Likewise, Alzheimers is a ruination of a site in the brain caused by some foreign molecule that attaches or bonds to the site where normal proteins should be cookie cut but instead plaque proteins are cookie cut. Aluminum and aluminum compounds maybe the likely cause of Alzheimers, whereas phosmet is the likely cause of prion disease. As for Parkinson, it too probably originates from some chemical in the environment. I suspect that recorded history has never come across Parkinsons until the 20th century. It is most frequent in the farm communities and so the suspicion would veer towards some modern day farm chemical. The fact that all three above are brain diseases supports the claim they are all some environmental chemical caused disease which takes time to accumulate in animal bodies and which attack the brain because other parts of the body can get rid of except the brain. And because the brain is easier to spot as to something going wrong with an animal-- behaving strangely. Chemical origin would also answer the best as to why these diseases seem to be both hereditary and environmental in that they are not really hereditary but some genetics is more susceptible such that if one member of the family procures prion or Alzheimers, they have not removed the chemical that causes it from their daily living environment and as such the other members of the family also contract the disease. Phosmet is concentrated in farm communities and England uses alot of phosmet and so it is probably the cause of the England scrapie and BSE and why England has the highest rates of prion disease. Aluminum used so much in the 20th century for cooking and packaging-- those billions of aluminum cans, that one cannot resist the suspicion that the rise of frequency of Alzheimers and perhaps Parkinsons follows the rise of the use of aluminum. I believe even toothpaste has a aluminum compound. Bob, can you tell me whether the phosmet molecule geometry is conducive to bonding to prion protein molecules? Whether their surface geometry of phosmet is conducive to interacting with the surface geometry of prion proteins? Archimedes Plutonium whole entire Universe is just one big atom where dots of the electron-dot-cloud are galaxies |
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