CWD Positive. What would you do??

jmez

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Couple that with the Czub research showing transmission to macaques through infected venison muscle meat (read the actual release by Czub and not the con job about monkey cannibalism a certain farmed deer advocate put out to every outlet that would print it),

Can you provide a citation for this study? As I understand it was a short abstract presented at a Prion Conference as a point of interest. There was no actual data presented with the information. Even if there was data it is unsubstantiated and unpublished. Since that announcement nothing else has been published or released. If they already had the information then the actual study should have been published by now. Until it is published and peer reviewed it shouldn't be tossed around as fact.
 

rmiller

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...so because the study is ongoing the prudent path is to pretend a well respected researcher in the field said nothing? I noticed you don't address the peer reviewed research I mentioned by Davenport and Manuelidis....Why, if you're concerned with the science? Not being a scientist myself, I feel I can make the "lots of smoke from different directions = fire" leap, rather than exposing myself and others to a potentially irretrievable problem. As someone said earlier in the thread "Beef is cheap." I would add, as I live in the second most endemic area on the planet, so is antelope, bear, duck, pheasant, etc. when compared to brain rot. I also feel somewhat duty bound to share as much information as possible with folks who are potentially feeding it to their kids and unknowingly spreading it throughout the landscape. You are free to do otherwise.
 
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Unfortunately, the "Alzheimer's is different and couldn't be PrP related" Argument doesn't quite have legs. Due in part to the fact that, statistically, Alzheimer's prevalence is growing at a rate that far outstrips the growth of our senescent population. The most damning evidence is, ironically, evidence that it's likely that a large chunk of "Alzheimer's" isn't Alzheimer's.
An intensive autopsy study by Laura Manuelidis (Head of Neuropathology at Yale, if that counts for anything other than an appeal to authority) turned up about 13% of brains diagnosed as Alzheimer's as having distinct CJD pathology.

Back of the envelope math - ~500,000 new "Alzheimer's" cases this year X 13% showing TSE pathology = 65,000

So, assuming the researchers at Yale aren't telling tall tales, the research points toward human TSE prevalence in the US at about 185X higher than the oft quoted 1 in a million figure.

Couple that with the Czub research showing transmission to macaques through infected venison muscle meat (read the actual release by Czub and not the con job about monkey cannibalism a certain farmed deer advocate put out to every outlet that would print it), plus the study by Kristen Davenport at CSU showing in vitro conversion of human prion proteins by CWD PrP and you have about all the correlative experimental evidence you're likely to get.

Oh, and I nearly forgot the documented increase in CJD diagnoses in Wisconsin in lagging proportion to the growth in CWD prevalence being written off to better surveillance.

Does anyone here remember John Gummer going on television and having his daughter eat a hamburger to show that BSE was of no oncern to humans. That was six years before the first confirmed vCJD case.

If you're waiting for the human studies showing definitive causation, that study is you and everyone willingly and unwillingly exposed to it. It ain't legal to run experiments like that on humans in a laboratory setting. Probably for reasons with which most here would agree.

Seems pronghorns and bear are getting more exciting and delicious by the day...

Thank you for the somewhat terrifying Czub study. . . Slide show gave me enough reason to purchase preg checking gloves, go gutless, and test every animal until further research is completed!
 

jmez

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Thanks, as I thought. You didn't need to add you aren't a scientist, that is obvious. Carry on saving your brain!

I read the entire Davenport study, you missed the mark and conclusion of the author as well.
 
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rmiller

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Thanks, as I thought. You didn't need to add you aren't a scientist, that is obvious. Carry on saving your brain!

I read the entire Davenport study, you missed the mark and conclusion of the author as well.

...but you're unwilling to share your take on the Davenport study, or your authoritative credentials for your differing opinion (Lesser conversion than BSE must mean we're all clear)...I guess you showed me.
 

jmez

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Not unwilling to share anything. Here is her conclusion.

We found that human rPrPc can be readily converted to an amyloid state by CWD prions and that the NTD facilitates this conversion. As there is little evidence for the susceptibility of humans to CWD, the biologic significance of our observation remains to be determined. However, the role of the NTD in this in vitro phenomenon may be important to the in vivo mechanism as well. RT-QuIC, transgenic mouse bioassay, and PMCA measure different outcomes. This report compares the efficiency of initial amyloid formation, while bioassay and PMCA reflect total accumulation of protease-resistant PrPSc, which may explain the difference in the apparent susceptibilities of full-length human rPrPc in these models. The molecular underpinnings for species barriers and transspecies prion conversion remain a complex yet important problem in prion biology. We propose that an interaction between the amino-terminal domain and the globular domain facilitates in vitro susceptibility of human rPrPc to conversion by CWD prions. Such an interaction may be important in assessing the susceptibility of humans to animal prion diseases.

They are identifying where the change in the prion occurs, NTD or amino terminal domain. Nothing in this study concludes that CWD is transmissible to humans. Scientist can do a whole lot of things in a test tube that can never be replicated outside of the test tube. She is aware of this and her conclusion is worded accordingly.
 

rmiller

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It reads to me as if she might be open to the idea of the in vivo process being reflective of the in vitro process...unless she mistakenly spelled that out. As we're talking about a study on the effect of pathogenic PrP on human proteins, what other in vivo environment might be of concern, if not human? Do we have an population of human PrP transgenic mice roaming the prairie, eating deer poop that we're concerned about? At any rate, thanks for the utter lack of synthesis. Happy sciencing.
 

BFR

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I’m kind of on the fence, I have family back east in CWD areas that hunt and eat deer and don’t bother testing them. Been doing it since before it came up and have no problems. Most studies I’ve seen say the meat is OK but other studies say it’s possible to cross over, well he’ll, anything is “possible” except a politician telling the truth. Anyway, my solution is to not hunt in CWD areas until it’s settled or I have no other choice.
 
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No way I would eat a know infected animal. We have good evidence that the 1986 BSE outbreak in the UK was caused by a transmission of the prions in feed supplements for cattle which contained TSE infected products (most likely scrapie sheep) . We also have good evidence that BSE was transmitted to humans causing vCJD. So this prion crossed 2 species barriers. Why would anyone believe a very similar prion would not jump a single species barrier and cause vCJD in humans or into cattle to cause BSE and then into humans. Read up on BSE and then make a informed decision based on a very similar disease and its transmission.


I do not think we are taking this seriously enough.
 
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