Infectious Prions in the Saliva and Blood of Deer with CWD

[Murgen]

Reader, would these be "good' prions they shed, or the mis-shapen variety?

 

[rkaiser]

At least your article admits that this TSE can not be passed on to humans reader. Unlike the phony British stories of BSE magically causing vCJD in humans.

Back to your comments about scientific proof reader. I have never said that prions - or under the right conditions - misfolded prions cannot appear in blood, urine, saliva or even meat. What I have said is that these misfolded prions do not cause the unfortunate diner (or licker) to develop his own case misfolded prion situation. That is the magical theory that you and Terry profess as gospel.

The "so called" new studies on CWD still show nothing more than all of the old studies on BSE. Sure you can drench a cow with homoginate and find the misfolded prions in his gut. Does that prove transmission --- not a chance. What it proves is that if I ate a marble and puked it up - and you put that marble in murgens breakfast - and he ate it, murgen would have a marble in his stomach. Same with the CWD story. Take the saliva from one deer and put it in the other deer's gut and you will also find the illusive marble.

So what if the second animal becomes a CWD victim. You have still proven nothing more than possibly metals from the first unfortunate animal transmitted to the second and caused the misfolding of the second animals healthy prions.

As Econo has said already - who cares for now. You R2, and Terry, can continue to show your arrogance on the subject til the cows no longer come home. I support testing. I support removal of SRM's, and no I do not want to eat cow brains full of misfolded prions. bsetester left off the last part of my answer to his question to get himself out of a jam.
Remember my name R2 when the truth is told years from now. When the economics of BSE has finally run it's course and there is no meat left on those bones to fight over. Testing will speed this process up. As I have said before - Japan's full testing protocol is slowing disproving the misfolded prion transmission theory and more testing in North America will also. Unlike the professed wisdom of our Canadian Cattlemen's association that says BSE will be eradicated ---- more cases will be found. More youthful cases. And misfolded prions will be found in healthy functioning cattle once bsetester's test is accepted and Cargill and Tyson see some profit potential in testing.

Have a lovely day R2 and keep up the good fight (as you believe).

 

[Kathy]

Human absorption and retention of polonium-210 from caribou meat.

Thomas PA, Fisenne I, Chorney D, Baweja AS, Tracy BL.
Toxicology Centre, University of Saskatchewan, Saskatoon, Canada.

The gastrointestinal (GI) absorption factors and the biological retention times for polonium were determined for a group of 14 volunteers--seven men and seven women--from Saskatoon, Saskatchewan, Canada. Each volunteer consumed 2.0 kg of caribou meat containing known amounts of naturally occurring 210Po. Urine and faecal samples were collected for up to 65 days after meat consumption and analysed for 210Po. The average GI absorption factor for the 14 volunteers was 56 +/- 4% (range = 31-71%), not significantly different from the ICRP value of 50%. About 3% of absorbed polonium underwent prompt excretion by the urinary pathway. The remainder was retained by the body with a half-time >100 days, compared to the ICRP value of 50 days. The effect of these findings increases the dose estimate for ingestion of 210Po in food by a factor of 1.5 to 3.5. Thus, background doses to people consuming caribou and reindeer may be higher than previously thought.

PMID: 11843339

Have these people been "infected" with polonium? Did the "infectious" polonium get excreted in the urine? Do you think you'd find it in the lymphatic system? saliva? semen?


Does a soldier returning from Iraq, Afganistan or other DU contaminated regions (perhaps even weapons testing ranges in the USA), "infect" his wife with DU with his semen? Does he "infect" his unborn deformed child?

Mutat Res. 2004 Apr 14;548(1-2):75-84.
Methylation changes in muscle and liver tissues of male and female mice exposed to acute and chronic low-dose X-ray-irradiation.Kovalchuk O, Burke P, Besplug J, Slovack M, Filkowski J, Pogribny I.
Department of Biological Sciences, University of Lethbridge, 4401 University Drive, Lethbridge, Alta., Canada T1K 3M4. [email protected].

The biological and genetic effects of chronic low-dose radiation (LDR) exposure and its relationship to carcinogenesis have received a lot of attention in the recent years. For example, radiation-induced genome instability, which is thought to be a precursor of tumorogenesis, was shown to have a transgenerational nature. This indicates a possible involvement of epigenetic mechanisms in LDR-induced genome instability. Genomic DNA methylation is one of the most important epigenetic mechanisms. Existing data on radiation effects on DNA methylation patterns is limited, and no one has specifically studied the effects of the LDR. We report the first study of the effects of whole-body LDR exposure on global genome methylation in muscle and liver tissues of male and female mice. In parallel, we evaluated changes in promoter methylation and expression of the tumor suppressor gene p16(INKa) and DNA repair gene O(6)-methylguanine-DNA methyltransferase (MGMT). We observed different patterns of radiation-induced global genome DNA methylation in the liver and muscle of exposed males and females. We also found sex and tissue-specific differences in p16(INKa) promoter methylation upon LDR exposure. In male liver tissue, p16(INKa) promoter methylation was more pronounced than in female tissue. In contrast, no significant radiation-induced changes in p16(INKa) promoter methylation were noted in the muscle tissue of exposed males and females. Radiation also did not significantly affect methylation status of MGMT promoter. We also observed substantial sex differences in acute and chronic radiation-induced expression of p16(INKa) and MGMT genes. Another important outcome of our study was the fact that chronic low-dose radiation exposure proved to be a more potent inducer of epigenetic effects than the acute exposure. This supports previous findings that chronic exposure leads to greater genome destabilization than acute exposure.

PMID: 15063138

There is a huge difference between internal and external exposure to radiation. This Canadian study, above, shows that there is "greater genome destabilization" with the chronic low level exposure than acute radiation exposure. What this means is that radiation, even at low levels over a long period of time will cause damage to our chromosomes and DNA. These traits are then inherited by our children. The damage is irreversible.

But perhaps we should ask the Atomic Energy Commission(s) to investigate this further, they will surely tell us everything is just fine, don't worry - be happy.

Until the radio-active metals/prion hypothesis is disproven, it is just as plausible as the "infectious prion" hypothesis.

 

[flounder]

Human absorption and retention of polonium-210 from caribou meat.

Thomas PA, Fisenne I, Chorney D, Baweja AS, Tracy BL.
Toxicology Centre, University of Saskatchewan, Saskatoon, Canada.

The gastrointestinal (GI) absorption factors and the biological retention times for polonium were determined for a group of 14 volunteers--seven men and seven women--from Saskatoon, Saskatchewan, Canada. Each volunteer consumed 2.0 kg of caribou meat containing known amounts of naturally occurring 210Po. Urine and faecal samples were collected for up to 65 days after meat consumption and analysed for 210Po. The average GI absorption factor for the 14 volunteers was 56 +/- 4% (range = 31-71%), not significantly different from the ICRP value of 50%. About 3% of absorbed polonium underwent prompt excretion by the urinary pathway. The remainder was retained by the body with a half-time >100 days, compared to the ICRP value of 50 days. The effect of these findings increases the dose estimate for ingestion of 210Po in food by a factor of 1.5 to 3.5. Thus, background doses to people consuming caribou and reindeer may be higher than previously thought.

PMID: 11843339

Have these people been "infected" with polonium? Did the "infectious" polonium get excreted in the urine? Do you think you'd find it in the lymphatic system? saliva? semen?


Does a soldier returning from Iraq, Afganistan or other DU contaminated regions (perhaps even weapons testing ranges in the USA), "infect" his wife with DU with his semen? Does he "infect" his unborn deformed child?

Mutat Res. 2004 Apr 14;548(1-2):75-84.
Methylation changes in muscle and liver tissues of male and female mice exposed to acute and chronic low-dose X-ray-irradiation.Kovalchuk O, Burke P, Besplug J, Slovack M, Filkowski J, Pogribny I.
Department of Biological Sciences, University of Lethbridge, 4401 University Drive, Lethbridge, Alta., Canada T1K 3M4. [email protected].

The biological and genetic effects of chronic low-dose radiation (LDR) exposure and its relationship to carcinogenesis have received a lot of attention in the recent years. For example, radiation-induced genome instability, which is thought to be a precursor of tumorogenesis, was shown to have a transgenerational nature. This indicates a possible involvement of epigenetic mechanisms in LDR-induced genome instability. Genomic DNA methylation is one of the most important epigenetic mechanisms. Existing data on radiation effects on DNA methylation patterns is limited, and no one has specifically studied the effects of the LDR. We report the first study of the effects of whole-body LDR exposure on global genome methylation in muscle and liver tissues of male and female mice. In parallel, we evaluated changes in promoter methylation and expression of the tumor suppressor gene p16(INKa) and DNA repair gene O(6)-methylguanine-DNA methyltransferase (MGMT). We observed different patterns of radiation-induced global genome DNA methylation in the liver and muscle of exposed males and females. We also found sex and tissue-specific differences in p16(INKa) promoter methylation upon LDR exposure. In male liver tissue, p16(INKa) promoter methylation was more pronounced than in female tissue. In contrast, no significant radiation-induced changes in p16(INKa) promoter methylation were noted in the muscle tissue of exposed males and females. Radiation also did not significantly affect methylation status of MGMT promoter. We also observed substantial sex differences in acute and chronic radiation-induced expression of p16(INKa) and MGMT genes. Another important outcome of our study was the fact that chronic low-dose radiation exposure proved to be a more potent inducer of epigenetic effects than the acute exposure. This supports previous findings that chronic exposure leads to greater genome destabilization than acute exposure.

PMID: 15063138

There is a huge difference between internal and external exposure to radiation. This Canadian study, above, shows that there is "greater genome destabilization" with the chronic low level exposure than acute radiation exposure. What this means is that radiation, even at low levels over a long period of time will cause damage to our chromosomes and DNA. These traits are then inherited by our children. The damage is irreversible.

But perhaps we should ask the Atomic Energy Commission(s) to investigate this further, they will surely tell us everything is just fine, don't worry - be happy.

Until the radio-active metals/prion hypothesis is disproven, it is just as plausible as the "infectious prion" hypothesis.

no its not, transmission studies have proven this.

you can glow all you want kathy, but it has nothing to do with the cause of transmissible spongiform encephalopathy. nothing you have posted shows this. so try again. BY they way, why the change, your were pushing the OP theory, now your on the nuke wagon again. make you mind up... tss

 

[Murgen]

perhaps even weapons testing ranges in the USA), "infect" his wife with DU with his semen

Are TSE's passed this way? Do we know yet?

 

[bse-tester]

Kathy wrote:

Until the radio-active metals/prion hypothesis is disproven, it is just as plausible as the "infectious prion" hypothesis.

If it was, then 185,000 cases of BSE in the England alone would mean that country would certainly glow in the dark if your hypothesis was fact and hypothesis.

Prion transmission studies have been proven and perhaps metal contamination will come into general acceptance.

You do however make it sound as if the entire planet is glowing with the remnants of nuke fallout or the remains of spent DU used in combat zones. Believe me, I have been in combat zones and there are not as much DU being used as you may think. But to suggest that all cases of BSE, vCJD, CWD CJD or whatever other TSE is caused by nothing other than metal contamination is bordering on a single-minded point of view that in the world of science, is regarded as being not only foolish, but often dangerous. Now before you get all flustered and upset Kathy, I am not against the hypothesis of metal contaminants having a role, (you know that) but I am absolutely against discounting the known transfer methods and what is already known in lieu of only metal contamination.

 

[Kathy]

Don't you just love how flounder trys to make it look like I change my hypothesis, and that somehow this makes me desperate. You have more twists than a pretzel, tss.

Terry stated:

no its not, transmission studies have proven this.

and where is this proof?

you can glow all you want kathy, but it has nothing to do with the cause of transmissible spongiform encephalopathy. nothing you have posted shows this. so try again. BY they way, why the change, your were pushing the OP theory, now your on the nuke wagon again. make you mind up... tss

The fact is that disease processes are usually "MULTI-FACTORAL".

A new study I just received reviews this multi-factoral cause/effect paradigm.

Genes and the Environment in Neurodegeneration

Fabio Coppede` Æ Michelangelo Mancuso Æ, Gabriele Siciliano Æ Lucia Migliore Æ Luigi Murri

Neurodegenerative diseases are a heterogeneous group of pathologies which includes complex multifactorial diseases, monogenic disorders and disorders for which inherited, sporadic and transmissible forms are known. Factors associated with predisposition and vulnerability to neurodegenerative disorders may be described usefully within the context of gene–environment interplay. There are many identified genetic
determinants for neurodegeneration, and it is possible to duplicate many elements of recognized human neurodegenerative disorders in animal models of the disease. However, there are similarly several identifiable environmental influences on outcomes of the genetic defects; and the course of a progressive neurodegenerative disorder can be greatly modified by environmental elements. In this review we highlight some of the major neurodegenerative disorders (Alzheimer's disease, Parkinson's disease, Amyotrophic lateral sclerosis, Huntington's disease, and prion diseases.) and discuss possible links of gene–environment interplay including, where implicated, mitochondrial genes.

(from the above study):

Among environmental factors metals have been extensively studied for their possible contribution to neurodegeneration; the brain is, among human organs, the most capable to concentrate metals, so that either human ingestion of metals present in drinking water or accumulated in animal meat, or environmental and occupational exposure to metals may result in their accumulation in the brain. After accumulation metals can react with proteins, leading to protein damage or aggregation, ultimately leading to neurodegeneration. Moreover metals can contribute to an increased oxidative stress, thus predisposing to neurodegeneration.

I don't feel discredited by you flounder when you say I push the OP connection and now I'm on the radiological connection. Sorry to disappoint you.

Accumulation of Uranium from DU in the Peyer's Patches may not mean anything to you, but I believe there will be more to come on this subject.

 

[rkaiser]

No biggy Kathy - the blinder-ed minds of Terry, R2, and to a certain extent bsetester cannot see the common picture of natural healthy imbalance that metal contamination paints.

 

[Kathy]

There is a great deal of study taking place on the damaging GENETIC effects of low dose radiation.

The fetus and young children are the most susceptible to this damage.

In utero the damaging effects of radiation and/ or metal or chemical exposures is showing that DNA can be altered. The timing of exposure is CRITICAL!

Exposure times will result in varying damage to DNA. This damage can result in a child that doesn't produce the appropriate enzymes or metalloproteins, for example, which are required to detoxify the body of metals. Autism is a fine example of this.

I noticed yesterday that the University of Saskatchewan is boosting some of their new work on a DNA vaccine. Really, or is this new type of "vaccine" actually adding a DNA (circular fragment) to the body to force it to produce/stimulate lacking protein production (like enzymes and metalloproteins).

On first glance, it looks like damage to DNA, (by whatever cause), and a deficiency in production - or lack of stimulation of production of various enzymes/metalloproteins etc. is what is being manipulated here.

This is turning a "vaccine" into something else. It is an iatrogenic injection of a circular DNA fragment which will stimulate production of these missing proteins, not antibodies.

Therefore, bse-tester, to answer your questions - yes there is massive contamination of the environment in areas that utilize alot of radio-active materials. Disease processes or genetic mutations will depend on the time of release/exposure, the isotope exposed to, and the stage of fetal development when exposed, etc.

It is well understood that an adult will usually respond quite differently to an exposure, than a fetus or child. Scientific work on genetic, or epigenetic, DNA damage is just amazing stuff. The consequences of our contamination of the environment are beginning to show in massive increases in diseases like cancer.

I don't discount that feed transmitted metals and chemicals. I am simply very upset that a protein is labelled as infectious, while researchers ignore the metal contamination of the protein as a potential cause of its malformation.

Damage to DNA (either eggs, sperm, or fetal) is very evident with the use of depleted uranium, yet the US government, and to a lesser degree the UK government, completely ignore this and leave their soldiers and their families "Drifting in the Wind".

The fact that so many soldiers now have children with disabilities/deformities, puts these families in a tight spot. If they leave the army (US, UK) who will take care of the medical needs of their children? Thank God in Canada we have a better health system.

 

[flounder]

There is a great deal of study taking place on the damaging GENETIC effects of low dose radiation.

The fetus and young children are the most susceptible to this damage.

In utero the damaging effects of radiation and/ or metal or chemical exposures is showing that DNA can be altered. The timing of exposure is CRITICAL!

Exposure times will result in varying damage to DNA. This damage can result in a child that doesn't produce the appropriate enzymes or metalloproteins, for example, which are required to detoxify the body of metals. Autism is a fine example of this.

I noticed yesterday that the University of Saskatchewan is boosting some of their new work on a DNA vaccine. Really, or is this new type of "vaccine" actually adding a DNA (circular fragment) to the body to force it to produce/stimulate lacking protein production (like enzymes and metalloproteins).

On first glance, it looks like damage to DNA, (by whatever cause), and a deficiency in production - or lack of stimulation of production of various enzymes/metalloproteins etc. is what is being manipulated here.

This is turning a "vaccine" into something else. It is an iatrogenic injection of a circular DNA fragment which will stimulate production of these missing proteins, not antibodies.

Therefore, bse-tester, to answer your questions - yes there is massive contamination of the environment in areas that utilize alot of radio-active materials. Disease processes or genetic mutations will depend on the time of release/exposure, the isotope exposed to, and the stage of fetal development when exposed, etc.

It is well understood that an adult will usually respond quite differently to an exposure, than a fetus or child. Scientific work on genetic, or epigenetic, DNA damage is just amazing stuff. The consequences of our contamination of the environment are beginning to show in massive increases in diseases like cancer.

I don't discount that feed transmitted metals and chemicals. I am simply very upset that a protein is labelled as infectious, while researchers ignore the metal contamination of the protein as a potential cause of its malformation.

Damage to DNA (either eggs, sperm, or fetal) is very evident with the use of depleted uranium, yet the US government, and to a lesser degree the UK government, completely ignore this and leave their soldiers and their families "Drifting in the Wind".

The fact that so many soldiers now have children with disabilities/deformities, puts these families in a tight spot. If they leave the army (US, UK) who will take care of the medical needs of their children? Thank God in Canada we have a better health system.

no worry kathy, just go get you a radioactive suit like bart, then you will have nothing to worry about :lol: :lol: :lol:



http://www.simpsonscollectors.com/wospdb/figure.asp?fig=f0022&bimg=true




WILL NOT change the facts of Transmissible Spongiform Encephalopathies, the fact that radioactive isotopes have absolutely nothing to do with the cause of TSE. you have failed time and time again to produce any evidence of this. on the other hand, TSEs are infectious, they are transmissible, thus, there is your proof otherwise. but keep on passing this gargabe of yours, well call junk science. heck, even your favorite doctor and metal guru Dr. David Brown does not believe that metals cause TSE, or OPs. nope, you can post all this garbage you want about ops this and metals that (if you can ever make your mind up which band wagon you wish to be on), but they do not and never have caused any TSE i.e. mad cow disease, 'sound science' has proven this. i.e. transmission studies, where nukes and ops had nothing to do with them. BUT you keep on posting this junk science, just shows how ignorant you are of the topic, maybe you and old rkaiser can both suit up together and glow at the same time and have a radioactive isotopes party or something, but it has absolutely nothing to do with this topic of CWD and transmission by blood and saliva of this thread. ...TSS

 

[bse-tester]

Kathy wrote:

I don't discount that feed transmitted metals and chemicals. I am simply very upset that a protein is labelled as infectious, while researchers ignore the metal contamination of the protein as a potential cause of its malformation.

Randy wrote:

No biggy Kathy - the blinder-ed minds of Terry, R2, and to a certain extent bsetester cannot see the common picture of natural healthy imbalance that metal contamination paints.

The one thing that Kathy does know regarding my position on metal contaminants is that I am on record as saying that there is evidence to support the hypothesis surrounding the question of the manner in which certain metals, (Copper) affects normal PrP and brain function.

There is also strong evidence of how normal PrP, once affected by copper in particular, tends to react and, by way of example, has a profound effect on how the electrical pathway that neurons travel on within the brains neural network. These malformed prions quite literally do not allow the electrical impulse to make it from point "A" to point "B" and therefore, the signal that may cause one to move that finger, or turn that head never reaches its destination to trigger the movement. Hence, we see clinical symptoms. The causative effect of neural "signal loss" is commonly misdiagnosed and up until fairly recently, the idea, or hypothesis of metallic interference, or direct contamination of the neural network caused by either an abundance of or a severe lack of copper has been gaining ground.

Kathy, and you Randy, have to know that I do not discount the role that metals play within our bodies. Having said that, I am always cautious when it comes to throwing out "one" hypothesis and favoring another especially when the "one" has been already proven and the latest hypothesis, although showing extremely interesting potential, has still yet to be catogorically proven. I hope that puts the question to bed as to whether or not I support the hypothesis surrounding metal contamination? I am a supporter of the idea but still need more information from known and accepted scientific studies. Yes, I have read some and yes, they were most interesting. Ron.

 

[rkaiser]

And that is why I separated you from Terry and R2. I don't read every thread on this site and have not read anything like this one you just posted.

Still cannot see how you see solid proof in the infectious theory but impressed with your vote of support for something that may actually solve the TSE puzzle rather than maybe slow a possible spread by way of a theory on feed transmission of the misfolded prion protein.

 

[bse-tester]

I have asked Kathy to give me a simple definition of the word "Infectious." She chose not to. Would you?? Just a question as to what your definition is of the word and its basic meaning.

Thesaurus states it could be:

Communicable (Adj.)
Transmittable
Contagious
Transferable
Catching (Catchable)

We know that PrPsc is most certainly Transmittable - hence its association with the term "Transmissable Spongiform Encephalopathy."

We also know that it is most certainly contagious.

To this end, I would strongly suggest that the term "Infectious" is not only descriptive of the PrPsc but also most applicable. Having said that, I do also believe that there may well be some substance to the metal imbalance hypothesis. The case being made each day for the metal theriors should not, in any way, take way from the known facts surrounding the infectiousness of PrPsc. THere seems to be an underlying argument being pout forward to remove the definitive term "infectious" from any literature describing PrPsc. That, in my opinion, would be wrong becasue by virtue of it being contagious, transmittable/transmissible and most certainly transferable, it falls under the definition of being an infectious disease. It is also one that once it enters the body, it will most certainly replicate itself until clinical signs of its presence begin to manifest and become outwardly noticeable.

 

[rkaiser]

bsetester -

THere seems to be an underlying argument being pout forward to remove the definitive term "infectious" from any literature describing PrPsc.

You mean there are more people out there, other than Kathy and I and a few other on this site that don't believe that the misfolded prion is infectious?

Everything that has happened to date with TSE's (maybe they should change the name and drop the T) can be explained with the metal imbalance theory. A lot of things cannot be explained by simply talking about TSE's being infective.

Clusters like the kuru situation, the large number of BSE in Britain, and even the atypical BSE animals, that seems to have the Americans thinking they are off the hook economically, can all be explained by the metal contamination theory. Does infection solve these mysteries. Not a chance. In fact every cluster gives us a mysterious infectious answer that cannot be proven. Can anyone prove that any one of the vCJD cases in Britain was unquestionably caused by cattle. NO. Did the kuru die because they eat human brains - Maybe - but still no unquestionable proof. And what the hell is going on with this atypical stuff?

You have to admit that the metal theory even fits the situation in Britain and Mark Purdey's agreement that feed may have transmitted metals to unfortunate diners and thus their BSE condition.

Every one of the hundreds of studies that Terry refers to can be explained by the metal contamination theory. What's wrong with that bsetester? What's wrong with that?

 

[flounder]

bsetester -

THere seems to be an underlying argument being pout forward to remove the definitive term "infectious" from any literature describing PrPsc.

You mean there are more people out there, other than Kathy and I and a few other on this site that don't believe that the misfolded prion is infectious?

Everything that has happened to date with TSE's (maybe they should change the name and drop the T) can be explained with the metal imbalance theory. A lot of things cannot be explained by simply talking about TSE's being infective.

Clusters like the kuru situation, the large number of BSE in Britain, and even the atypical BSE animals, that seems to have the Americans thinking they are off the hook economically, can all be explained by the metal contamination theory. Does infection solve these mysteries. Not a chance. In fact every cluster gives us a mysterious infectious answer that cannot be proven. Can anyone prove that any one of the vCJD cases in Britain was unquestionably caused by cattle. NO. Did the kuru die because they eat human brains - Maybe - but still no unquestionable proof. And what the hell is going on with this atypical stuff?

You have to admit that the metal theory even fits the situation in Britain and Mark Purdey's agreement that feed may have transmitted metals to unfortunate diners and thus their BSE condition.

Every one of the hundreds of studies that Terry refers to can be explained by the metal contamination theory. What's wrong with that bsetester? What's wrong with that?

it's just not true from any scientific finding, that's what's wrong with it. ...TSS

 

[bse-tester]

Randy wrote:

Clusters like the kuru situation, the large number of BSE in Britain, and even the atypical BSE animals, that seems to have the Americans thinking they are off the hook economically, can all be explained by the metal contamination theory.

First of Randy, you should study the "Kuru situation" as you call it. Kuru resulted from the cannibalistic practice of the hill tribes in Papua New Guinea which consisted of them eating the brains of the dean family members in a practice that they believed would keep their spirits alive within them once they ate the brain. Kuru, otherwise known as the "Smiling Disease," was, for the most part, a "situation" that was confined to Papua New Guinea. It was not a cluster that was the result of metal contamination at all. In fact, it was traced to have evolved from one "infected" person within the tribe and it spread rapidly with each death as all members of each family and extended families partook of the ritual eating of the deam person's brain and to some extent, muscle tissues. They did not worry about SRM removal.

As forthe large amount of BSE bovine deaths in the UK, the metal theories have been put forward but the jury is still out.

As for the proof you required regarding the causes of vCJD in the UK, the science jury has rendered its verdict and the British Government even came out in 2003 and stated very clearly that they were aware of the link between BSE infected meat and vCJD and that, by their own estimation, as many as 4300 or so potential cases would likely show up with the next decade or so. I guess if the British Government admits to the link between BSE infected meat products and vCJD then surely there has to be some credence to it Randy?

Read this and you decide.

Kuru Among the South Fore

Kuru is a neurodegenerative disorder that surfaced among the South Fore of New Guinea, and the dynamics of this disease have been explored by various scholars. Lindenbaum worked with the South Fore and studied the kuru disease. Zigas worked in New Guinea, and Gadjusek also traveled there in 1957 to study disease patterns in primitive and isolated populations (Gadjusek, 1996). Lindenbaum, Zigas, and Gadjusek were all crucial to explaining the marked, specific properties of kuru to the rest of the world.

The kuru epidemic reached its height in the 1960's (Lindenbaum, 1979). Between 1957 and 1968, over 1,100 of the South Fore died from kuru (Lindenbaum, 1979). The vast majority of victims among the South Fore were women. In fact, eight times more women than men contracted the disease (Lindenbaum, 1979). It later affected small children and the elderly at a high rate as well. This is to be expected, since women were the prime participants in mortuary cannibalism (Lindenbaum, 1979). It is currently believed that kuru was transmitted among the South Fore through participation in such cannibalism. Upon the death of an individual, the maternal kin were in charge of the dismemberment of the corpse (Lindenbaum, 1979). The women would remove the arms and feet, strip the limbs of muscle, remove the brains, and cut open the chest in order to remove internal organs (Lindenbaum, 1979). Lindenbaum (1979) states that kuru victims were highly regarded as sources of food, because the layer of fat on victims who died quickly resembled pork. Women also were known to feed morsels such as human brains and various parts of organs to their children and the elderly (Lindenbaum, 1979).

Misinterpretations of Kuru

Scholars who first studied the disease among the South Fore initially had two major misconceptions concerning the nature of the disease. They first incorrectly postulated that it was a genetic disorder. After this possibility was ruled out, scientists next asserted that kuru was the manifestation of a slow virus. Genetic disorders can be fully understood through application to population genetics. Mutations provide variation and fuel natural selection. A genetic disorder is one that is caused by a mutation that is passed on to subsequent offspring. Since kuru had a tendency to occur among family members (Lindenbaum, 1979), the original notion that it was a genetic disorder seems somewhat appropriate. This possibility was eventually ruled out, because kuru was too common and too fatal (Lindenbaum, 1979). A completely lethal genetic disorder would drastically reduce the fitness of a population. Sooner or later it would die out of the gene pool. This fact led scholars to seek additional possible explanations to describe the dynamics of the disease.

Studies on chimpanzees injected with brain material from a victim led scientists to believe the agent was a slow virus, because the chimps developed a very similar condition after a long incubation period (Gadjusek et al., 1966). Gadjusek was responsible for conducting these tests on chimps. He defined a slow virus as a viral disease with an abnormally long incubation period (Gadjusek et al., 1966). In humans, kuru had an incubation period with a minimum of two years and maximum of 23 years (Lindenbaum, 1979:26). Gadjusek's results also confirmed the infectious, transmittable nature of the prion. Mestel (1996:185) writes, "Since then, his [Gadjusek's] team has shown that CJD [Creutzfeldt-Jakob disease] and GGS [German-Straussler-Scheinker syndrome] are also infectious..." With kuru, there was no evidence of an immune response or an antibody. It will become evident later that both of these hypotheses were incorrect. For now, the specific symptoms of kuru are relevant in gaining a more complete understanding of the disease as a neurological disorder.

Symptoms of Kuru

Gadjusek studied kuru, and he found the condition of kuru victims to be an upsetting sight. He explains, "...to see them, however, regularly progress to neurological degeneration in three to six months (usually three) and to death is another matter and cannot be shrugged off" (Gadjusek, 1996:10). Gadjusek (1973) reported three main stages in the progression of symptoms. The first stage is called the ambulant stage, and it includes unsteadiness of stance, gait, voice, hands, and eyes; deterioration of speech; tremor; shivering; in- coordination in lower extremities that moves slowly upward; and dysarthria (slurring of speech) (Gadjusek, 1973). The second stage is also known as the sedentary stage, and Gadjusek (1973) defines it with the following symptoms: patient can no longer walk without support, more severe tremors and ataxia (loss of coordination of the muscles), shock-like muscle jerks, emotional lability, outbursts of laughter, depression, and mental slowing (it is important to note that muscle degeneration has not occurred in this stage, and tendon reflexes are usually still normal) (Gadjusek, 1973). The third stage is the terminal stage, which is marked by the patient's inability to sit up without support; more severe ataxia (loss of muscle coordination), tremor, and dysarthria (slurring of speech); urinary and faecal incontinence; difficulty swallowing (dysphagia); and deep ulcerations appear (Gadjusek, 1973). Cerebellar dysfunction is the cause of these conditions. Symptoms are generally common among prion diseases, as a comparison with Creutzfeldt-Jakob disease will demonstrate.

Comparison to CJD

Creutzfeldt-Jakob disease displays striking similarities to kuru in regards to symptoms displayed and organ damage (mostly to the brain). Comparisons and parallels are evident between these two prion diseases. By inspecting an in depth case study of CJD from Massachusetts General Hospital, it is possible to gain a more complete understanding of prion diseases.

At age 47, a woman feeling depression sought professional help at Massachusetts General Hospital (Scully et al., 1993). She became hypoactive, noticed impairment of her recent memory, and had urinary incontinence (Scully et al., 1993). Within a few months she became dizzy and had an unstable gait (Scully et al., 1993). At this point a computed tomographic scan (CAT scan) of the brain showed slight cerebral and central atrophy; delusion began to set in (Scully et al., 1993). According to Scully et al. (1993), by age 50 the patient's cranial-nerve functions were still normal, as well as motor power, sensation, and coordination. The next symptom to appear was the occurrence of inappropriate laughter, and her replies to questions became irrelevant and incorrect (Scully et al., 1993). Mild tremor was noted, although the cranial-nerve functions, strength, coordination, and sensation were still intact (Scully et al., 1993). At this time another CAT scan was performed, and the results were the same as the year before (Scully et al., 1993). Within a week after this scan, she was readmitted with shaking spells (Scully et al., 1993). There was a constant alteration between laughing and crying, but reflexes were still normal (Scully et al., 1993). By the age of 51 and a half years, her speech had deteriorated rapidly, and a new CAT scan showed marked cerebral and cerebellar atrophy (Scully et al., 1993). According to Scully et al. (1993), gradual deterioration continued up until her death four months prior to her fifty-fourth birthday.

Important similarities occur between Creutzfeldt-Jakob disease (CJD) and kuru. Both prion diseases cause tremor and inappropriate laughter. Depression was expressed early in CJD and in stage two of kuru. Unsteadiness in gait and sporadic muscle jerks were observed in both ailments. Dysarthria occurred in kuru during the initial stages of the diseases and in CJD more towards the end, and the exact same situation is seen with the condition of urinary incontinence as well.

The Prion Protein

The exact nature of kuru perplexed scholars for decades after the discovery of the ailment, until Prusiner identified and defined prion diseases in 1982 (Prusiner, 1995). Prusiner (1991) classified a prion as an infectious particle composed of a protein that causes neurodegenerative disorders. According to Cashman (1997), prions are infectious agents by biological and medical criteria. However, they are also fairly unique, and properties of prions differ from those of conventional microbes. All known prion diseases are fatal. Such diseases are often called spongiform encephalies, because they frequently cause the brain to become spongy and riddled with holes (Prusiner, 1995). Well known prion diseases include scrapie, bovine spongiform encephalopathy (mad cow disease or BSE), and Creutzfeldt-Jakob disease (CJD). Less well-known prion diseases include the following: transmissible mink encephalopathy, chronic wasting disease, feline spongiform encephalopathy, exotic ungulate encephalopathy, German-Straussler-Scheinker syndrome (GSS), and fatal familial insomnia (Krakauer et al., 1997). Of these infirmities, four affect humans: Creutzfeldt-Jakob disease, Gertsmann-Straussler-Scheinker syndrome, fatal familial insomnia, and kuru. The most common form of prion disease is scrapie, expressed in sheep and goats (Prusiner, 1995). According to Cohen et al. (1994), prions cause a variety of degenerative neurologic diseases that can be infectious, inherited, or sporadic in origin. The cause of the sporadic forms is unknown; inherited forms are caused by up to twenty different mutations of the human PrP gene; and the infectious forms are transmitted through contact with or consumption of previously infected tissues (Prusiner, 1997).

PrPC is the normal, cellular prion protein, and it is converted into PrPSc (Prusiner, 1997). Mutations in the 102nd codon of this gene have been linked to neurodegeneration, which is the main, encompassing attribute of the prion diseases. Prusiner (1995) identified 15 amino acids at one end of the PrP protein. Using this knowledge, molecular probes were constructed and used to study the sequences of the normal verses the mutated form of the gene (Prusiner, 1995). Specifically, Prusiner discovered that the amino acid leucine is substituted by the amino acid proline (Prusiner, 1995). An incident of this type is commonly known as a point mutation. In the case of prion proteins, this mutation encodes additional copies of an octapeptide repeat toward the 5' end (Krakauer et al., 1997). The normal protein consists of mainly alpha helices with a spiral backbone, but the new, mutated prion protein is predominately formed by beta strands with a fully extended backbone (Prusiner, 1995). This alteration in tertiary structure provides evidence for post-translational modification of the protein.

 

[rkaiser]

I have to apologize for confusing the kuru situation with an article I read a few years ago by Mark Purdey about Groote Eylandt. Part of the article posted below. Link if you like to the rest.

I guess you have me on this one bse tester - after all -

It is currently believed that kuru was transmitted among the South Fore through participation in such cannibalism.

Currently believed. Just like it is currently believed that people died from eating cattle in Britain and thousands more are yet to die. No way of proving it - but currently believed. Are you and R2 and Terry comfortable waiting for you day in the spotlight when the graves are being dug. Or would you rather focus on the cause of this terrible problem. No way muchacho - We're out to prove Randy Kaiser and Kathy wrong. :roll:

Fight hard for testing Ron - and battle the government for more control over SRM's Terry and R2 - but don't waste any more of your time trying to convince me that the misfolded prion has a magical way of moving through an animals body like nothing else in the history of animals on this earth.

None of the studies that any of you have posted has told me how this process works - other than some unknown factor - factor X - or simply magic. :roll:

I will ask again bsetester - What is wrong with the theory of metal contamination? Different than the theory of infection, but not really harmful to it. Does my disbelief in the physical transmission of the misfolded prion bother you that bad.

To the Ends of the Earth

To the Ends of the Earth - Mark Purdey
When we think of metal poisoning; lead, mercury and aluminium intoxication invariably springs to mind. But the insidious toxic properties of the metal manganese have almost been completely overlooked. Modern health authorities could learn a lesson from the alchemists of the Byzantine era who regarded manganese as the black magic metal; whereby the quantum capacity of manganese to absorb light and sound, can induce a lethal 'Jekyll and Hyde' style conversion of this metal from innocuous to toxic form.

Manganese exposure has been associated with the original cause of many neuro-degenerative diseases. As part of my quest to identify the original causes of BSE, I had travelled to Groote Eylandt - a one time enchanted tropical island in the Gulf of Carpentaria, NE Australia, where bush lands and forests of stringy backed eucalyptus, pandanus and cypress pine have supported ideal nomadic hunter /gatherer grounds for several Aboriginal clans.

The history of this remote island has witnessed a bizarre degree of 'heaven and hells'; Not only do the island's soils play host to the mother of all manganese concentrations, but its flamboyant rainforest ecosystems have supported some of the most pure bred Aboriginal clans alive in Australia today. But as I was soon to learn, the tropical charms of a Groote Eylandt of 'pick-your- own' coconuts and turquoise seas can be deceptive to the uninformed outsider.

I was interested in the emergence of a cluster of mystery progressive, fatal neuro-degenerative diseases (collectively known as Groote Syndrome ) that had erupted in this remote Aboriginal outback of the Northern Australian territories. According to the Elders, the problem first developed in the late 1960s after the mining corporation started open cast mining of manganese on the island in the early 1960s, whereupon a fine black manganese dioxide dust gradually cloaked the precise region of the island where Groote syndrome has now emerged; Angurugu village. But the mining corporation funded experts have, not surprisingly, spun a different story line on the origins of this disease.

After broadcasting of the BBC film "Mad Cows and an Englishman" on ABC Four Corners in Australia, I received a deluge of correspondence from people concerned about manganese contamination on Groote Eylandt. One of the most inspiring communications came from Susannah Churchill of Canberra, who, unlike your average academic, had actually lived with the Aboriginal folk herself whilst researching for her thesis. Her completed manuscript on Groote syndrome makes a refreshingly impartial read. It's a study that combines a lateral mix of cultural, genetic and geo-medical perspectives. I could also strongly relate to her suggestion that Groote syndrome was yet another satellite extension of the famous South Pacific clusters of "Guam Syndrome" - pockets of high manganese/high aluminium terrain where a variety of Alzheimer's/Motor Neurone/Parkinson's - like neuro-degenerative diseases had burst out at an incidence rate that was fifty times higher than the average international rate.

By amazing coincidence, the parents of my only Australian friend, Jo Wooding, turned out to have once lived in the same house in Canberra where Susannah used to live. So when Jo next visited her parents in Canberra, she was able to pick up a copy of the thesis and deliver it directly back to me on her return to London. After reading the document, I found myself compelled to visit Groote Eylandt.

One year later, I received a welcome donation of £500 from a Canadian reader of the Mid Atlantic Bio Dynamic Farming Association's website 'BD Now' who had been promoting my work. This enabled me to raise sufficient money to launch my long awaited eco-detective investigation into the origins of this mystery cluster.

 

[Kathy]

bse tester, Ron, stated:

I have asked Kathy to give me a simple definition of the word "Infectious." She chose not to.

When did you ask me for this? This is news to me, Ron!

Infection requires the reproduction of the "infectious organism - with DNA, by its own DNA" (Crick and Watson) Prions do not contain DNA.


Just to give you another example of how a radio-active isotopes can be shed in the bodily fluids of a mammal, here is an example with cats treated for hyperthyroidism with Iodine 131. The cat shed the radioactive iodine in its saliva (when grooming itself or other cats) and urine.

With no "obvious pattern" varying levels of the isotope accumulated on the fur of the cat from licking itself. The high end measurements were above the New York State limits of removable activity for a non-controlled area (<1000dpm/100 cm2).

Vet Radiol Ultrasound. 2006 Sep-Oct;47(5):507-9.

Identifying removable radioactivity on the surface of cats during the first week after treatment with iodine 131.

Chalmers HJ, Scrivani PV, Dykes NL, Erb HN, Hobbs JM, Hubble LJ.
Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA. [email protected]

Because radioiodine (1-131) is excreted in urine and saliva, treated cats can accumulate I-131 on their coats from contacting soiled litter and grooming. This could result in removable radioactivity, which is a potential source of human exposure to radiation and specifically to internal contamination. The purpose of this study was to determine if there is removable radioactivity on cats treated with I-131. Daily wipe tests were performed for 7 days at two sites (both flanks, one site; and all four paws, one site) on six hyperthyroid cats treated with I-131. A y counter was used to determine the counts per minute (cpm) of the samples, which were converted to disintegrations per minute (dpm) to estimate activity. The results were compared to the New York State limits of removable activity for a non-controlled area (<1000dpm/100 cm2) to determine if the amount of removable activity was acceptable for a member of the public. The median value of removable activity was 241 dpm (range from 34 to 4184 dpm) for the flanks, and 308 dpm (range from 60 to 1890 dpm) for the paws. The amount of removable radioactivity on the surface of hospitalized cats treated with I-131 during the first week after treatment, occasionally and without obvious pattern, exceeded the New York State limit. Sporadic activity as high as 4148 dpm was found. It is prudent to advise owners to observe routine hygiene when handling cats after discharge to minimize the risk of internal contamination.

PMID: 17009517

 

[Kathy]

Isn't it interesting how Kuru showed up after the USA nuked the sh@% out of the Marshall Islands.

Gadjusek and Prusiner, both, have been said to have requested copies of Mark Purdey's peer-reviewed papers (reported by the publishers at Medical Hypothesis, and:

I asked Purdey if he thought the arrest and firing from his research position of the distinguished, US resident, Nobel Award CJD specialist, Dr. D.C. Gajdusek was also related to this mad cow situation. Purdey said that weeks before the arrest of Gajdusek Purdey was told by Ray Bradly of the Ministry of Agriculture that Gajdusek was seeking alternative hypotheses and specifically requested all of Purdey's papers. They were faxed to Gajdusek.

http://www.freerepublic.com/focus/fr/596777/posts
interview with Purdey, by Claire W. Gilbert, Ph.D., and more articles

 

[Kathy]

For someone who doesn't care what Randy or I (or anyone that disagrees with whatever you are stating at the time), you sure like to pay alot of attention to us. Always trying to discredit the things we say.

Transmissibility of the disease is not argued, we disagree on what the actual transmissible agent is which initiates the disease process. We also have a problem, because of your insistance that metals are not involved with these diseases, and that inhalation of fine and ultrafine metal particles can contaminate the brain initiating oxidative stress and other disease processes.

When I argued for iatrogenic transmission, ie: via injection of naturally derived beef growth hormones, you and flounder ignores or denied this possible route of transmission in cattle (especially in the UK). The UK banned naturally derived growth hormones in cattle for a reason, their use was transmitting the "agent" which initiated disease. The pituatary gland is a target organ for metals.

It is really sad that you and flounder make the bold statements that metals have nothing to do with this, or that OPs had nothing to do with these neurological disease processes. Do you care/know how many researchers you a presently insulting by these statements?

When I argue against the "infectious" prion, I am not saying that the research on prions should stop. I am asking for deeper investigation and complete characterization of the prions. It appears Manuelidis and others are finally moving deeper into this process.

Neurotoxicology. 2006 May;27(3):437-44. Epub 2006

Free radical generation of protease-resistant prion after substitution of manganese for copper in bovine brain homogenate.

Deloncle R, Guillard O, Bind JL, Delaval J, Fleury N, Mauco G, Lesage G.
Universite Francois Rabelais de Tours, Bio-Inorganic Chemistry Laboratory, Faculty of Pharmacy, 31 Avenue Monge, 37200 Tours, France. [email protected]

The exchange between copper and seven transition metals is studied in a bovine brain obex homogenate according to the redox status of the medium. In reductive conditions, almost all the studied metals can substitute for copper when it is in the reduced form Cu+. This substitution is reversible, since copper uptake as Cu++ is restored in an oxidizing medium but only Co++, Ni++ and Mn++, in this decreasing order, can substitute perfectly for copper in bovine brain homogenate. To study free radical effects on bovine brain proteins, at first a copper substitution was processed in order to inhibit superoxide dismutase-like protective properties against free radicals in copper metalloproteins. Manganese was selected since a brain copper decrease correlated with a manganese increase is well-known in transmissible spongiform encephalopathies. Results for bovine brain homogenate, initially negative in the Western blot Prionics test, indicate that the substitution of manganese for copper in a reducing medium and exposure to UVA-induced free radicals produce proteinase K resistant prion. These findings suggest that an impairment in brain metal homeostasis leading to oxidative abnormalities may be involved in transmissible spongiform encephalopathies.

PMID: 16481041

Angew Chem Int Ed Engl. 2006 Sep 28;

Charge-Induced Molecular Alignment of Intrinsically Disordered Proteins.

Skora L, Cho MK, Kim HY, Becker S, Fernandez CO, Blackledge M, Zweckstetter M.
Department of NMR-based Structural Biology, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Gottingen, Germany, Fax: (+49) 551-201-2202 http://www.mpibpc.gwdg.de/abteilungen/030/zweckstetter.

PMID: 17009286

ScientificWorldJournal. 2006 Feb 28;6:295-310.

Anticholinesterase toxicity and oxidative stress.

Milatovic D, Gupta RC, Aschner M.
Department of Pediatrics, Medical School, Vanderbilt University, Nashville, TN, USA. [email protected].

Anticholinesterase compounds, organophosphates (OPs) and carbamates (CMs) are commonly used for a variety of purposes in agriculture and in human and veterinary medicine. They exert their toxicity in mammalian system primarily by virtue of acetylcholinesterase (AChE) inhibition at the synapses and neuromuscular junctions, leading into the signs of hypercholinergic preponderance. However, the mechanism(s) involved in brain/muscle damage appear to be linked with alteration in antioxidant and the scavenging system leading to free radical-mediated injury. OPs and CMs cause excessive formation of F2-isoprostanes and F4-neuroprostanes, in vivo biomarkers of lipid peroxidation and generation of reactive oxygen species (ROS), and of citrulline, a marker of NO/NOS and reactive nitrogen species (RNS) generation. In addition, during the course of these excitatory processes and inhibition of AChE, a high rate of ATP consumption, coupled with the inhibition of oxidative phosphorylation, compromise the cell's ability to maintain its energy levels and excessive amounts of ROS and RNS may be generated. Pretreatment with N-methyl D-aspartate (NMDA) receptor antagonist memantine, in combination with atropine sulfate, provides significant protection against inhibition of AChE, increases of ROS/RNS, and depletion of high-energy phosphates induced by DFP/carbofuran. Similar antioxidative effects are observed with a spin trapping agent, phenyl-N-tert-butylnitrone (PBN) or chain breaking antioxidant vitamin E. This review describes the mechanisms involved in anticholinesterase-induced oxidative/nitrosative injury in target organs of OPs/CMs, and protection by various agents.

PMID: 16518518