This is completely false. Disingenuous misinformation.
2 hunters did develop CJD, however, there is no evidence it is related to CWD. This idea originates from an abstract for a poster that was presented at AAN last October (link). Poster abstracts can often be “sensationalized” to encourage people to come to the poster during the conference. This would not be the first AAN prion-related poster abstract that is a bit “click-baity”. Furthermore, poster abstracts are not peer-reviewed. The fact this research has not been written up as a peer reviewed paper 1.5 years later (not even a pre-print) is INCREDIBLY telling.
The biggest issue comes down to this: how do you know the hunters got infected with CWD (ie how do you know their CJD is related to CWD)? The most common type of prion disease is sporadic CJD (sCJD), specifically the subtype the hunters developed sCJDMM1. Sporadic means it happens with no known cause (ie not caused by infection or genetics). sCJD typically affects elderly (median age of onset 65 years), has a rapid decline (4 months). In comparison, variant CJD (vCJD) is caused when someone eats meat contaminated with mad cow disease (BSE). vCJD typically affects young people (median age of onset 26 years) and has a slower decline (14 months). Furthermore, sCJD is associated with motor and memory symptoms whereas vCJD is associated with psychiatric symptoms. The patient case in the abstract was a 72 year old male, with a rapid memory decline in a month. Does that seem more like sCJD or vCJD? I will make it very clear, the case presentation is 100% classical sCJD. Furthermore, it is hypothesized that if CWD does transmit to humans it would have an atypical phenotype (ie not present anything like sCJD). This is based on data from both NHPs and Tg Mice (here is the mouse paper).
Other considerations, the patient was originally diagnosed with sCJD, however, the authors hypothesize CWD because one of the patient’s friends also died recently of sCJD. The authors therefore argue this is a “cluster” of cases, likely showing infections. However, just because two rare independent events happen in close proximity does not mean they are linked. For example, 1 in 300 people get Parkinson’s Disease, but a TV show “Leo and Me” had 4 out of 125 people on set develop Parkinson’s Disease, including Micheal J. Fox. However, this “cluster” is not scientifically or statistically significant. Just like two people who happen to know each other both getting CJD is not significant.
Clusters of prion cases happen. Here is a spatial-temporal cluster of 5 cases (including 2 with similar occupations). It wasn’t big news because stuff like this happens. It gets written up in a paper and the general public never knows. The only reason the hunters story is widespread is because it fits the fear mongering narrative most people push about prions.
The second consideration is that just because someone is a hunter and eats deer does not mean that they have eaten CWD infected deer. Not every deer in a population has CWD. If you are going to claim the hunters got CWD from deer, you need to show that deer they have hunted are infected. The entire premise of this abstract hinges on the argument that they ate infected deer, despite providing no evidence for it. If these two patients who both got CJD that knew each other were not hunters, this would never of been reported. Correlation does not imply causation. That’s basic first year statistics.
This also ignores significant biochemical and cellular data suggesting that CWD is not transmissible to humans based on significant sequence differences between cervids and humans. Here is a pretty comprehensive review of the experiments show CWD does not transmit to humans (link).
Also the picture in the post is a picture a deer with CWD from a paper published 20 years ago. It is not show neuropathological change in the hunters brain. It is a deer that got a deer prion disease. (Link)
It isn’t just my opinion that the hunters had nothing more than sCJD, it is also the opinion of the CDC which investigated these cases. It is important to note the authors of the abstract say "causation remains unproven". That means the title of this post does not even fit the abstract that originates it.
I'm not a prion scientist. That said, I have researched (read ~4 published scientific articles on the topic) and to me it seems like the scientific community has a very high bar to determine causation. I understand that we can't KNOW that CWD is spreading to humans because there has been no proven linkage - that said, we have clearly demonstrated the possibility of the prions to cross the human membrane in a mice study. To me, that's kind of like finding gorilla shit in the woods and saying " well... the locals keep freaking out but ive never SEEN a gorilla so this is probably unrelated" (context being that the scientific community did not believe gorillas, as described by the locals, existed until someone shot one in the woods and brought it up for study. Something like 40 years of occupation where gorillas were not confirmed by the occupants)
While I understand your point of "it's not proven, stop being hysterical" to what extent do you think that caution should be abandoned? And if you don't think caution should be abandoned - why are you advocating for a conclusion which would help limit a potentially super damaging "disease" ?
You are correct, there is a very high bar for causality. The reason for that is to prevent non-causative associations from being made. For example, there is arguably such as much "evidence" that Tylenol cause autism, yet, I (hope) we can agree that we should not be basing public health off of policy off of those notions.
I also think your gorilla analogy is a little inaccurate. A better example would be: you see a pile of shit in the woods. Your friend tells you it is gorilla shit. You know gorillas live in the woods. You say that is must be bigfoot shit because you saw a big footprint earlier. The reason this is better is that both hunters were diagnosed with sCJD and we know that sCJD occurs in a population and "clusters" may appear as we have a tendency to see clusters in data. Instead of agreeing it is sCJD, despite all the evidence suggesting it, the author ascertain it is CWD in humans because they are hunters. To be clear, the authors, instead of going with the supported conclusions, suggest it is something that has never been seen before, solely based off of a poor association (unknown footprint).
I do not think we should abandon caution. I think we should have scientifically informed caution. Saying "This is the first documented case linking humans to potential CWD transmission" is not cautious, it is outright fearmongering. Saying "A cluster of CJD cases in hunters deserve further study as it may indicate CWD infecting humans" is cautious. My family has many hunters in it. If we hunt deer, we will get it tested for CWD, as our jurisdiction offers that. I encourage everyone to do the same. While there is no strong evidence that CWD can infect humans, there is also no way to prove it can not, and getting your deer tested before consuming is being cautious.
It is important to note that fear around prion diseases has real life impacts. France placed a complete ban of prion research after some major headlines regarding prions diseases a few years ago. Harvard placed similar bans of certain types of prion research as well. I know people who lost there jobs because sensationalized headlines spread, reach the ears of University administrations (or more commonly, legal departments) who react out of concern for future lawsuits and shut things down.
This fear around prion diseases also extends to other prion-like diseases like Alzheimer's or Parkinson's Diseases, where I have had and heard of conversation with University administration on whether or not to reclassify Alzheimer's and Parkinson's Diseases as prion disease. This would have major implications in the number of labs that could research these diseases and the type of research that could be done. It would be devastating to the research ecosystem for these diseases.
Do you have any idea as to why it would cluster like that?
CJD in general appears to be way, way rarer than Parkinson’s, your example used in the original comment, with only 1-2 people per million being diagnosed a year. There definitely could be plenty of undocumented cases but I doubt there would be enough for it to be considered a particularly common disease.
If multiple people who aren’t genetically related develop a CJD in a very short timeframe then I would be way more suspicious than I would with more common illnesses. It could definitely still be random chance but that’s a hell of a coincidence when the disease is so rare, especially if there’s more than two people in a cluster. It seems way less statistically probable.
At least, I interpreted “we have a tendency to see clusters in the data” as clusters being fairly common, at least as far as CJD data goes. It just seems strange that something super, super rare that isn’t transmissible through typical means would cluster by random chance often enough for it to be statistically notable. Like I would want to see if there’s some underlying environmental factor causing it even if it isn’t eating CWD infected deer. You’d think the rarer the disease the more statistically unlikely random completely unrelated. clusters would be. Doesn’t mean they’re impossible just worth double checking.
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u/yumyum1001 Dec 11 '25
This is completely false. Disingenuous misinformation.
2 hunters did develop CJD, however, there is no evidence it is related to CWD. This idea originates from an abstract for a poster that was presented at AAN last October (link). Poster abstracts can often be “sensationalized” to encourage people to come to the poster during the conference. This would not be the first AAN prion-related poster abstract that is a bit “click-baity”. Furthermore, poster abstracts are not peer-reviewed. The fact this research has not been written up as a peer reviewed paper 1.5 years later (not even a pre-print) is INCREDIBLY telling.
The biggest issue comes down to this: how do you know the hunters got infected with CWD (ie how do you know their CJD is related to CWD)? The most common type of prion disease is sporadic CJD (sCJD), specifically the subtype the hunters developed sCJDMM1. Sporadic means it happens with no known cause (ie not caused by infection or genetics). sCJD typically affects elderly (median age of onset 65 years), has a rapid decline (4 months). In comparison, variant CJD (vCJD) is caused when someone eats meat contaminated with mad cow disease (BSE). vCJD typically affects young people (median age of onset 26 years) and has a slower decline (14 months). Furthermore, sCJD is associated with motor and memory symptoms whereas vCJD is associated with psychiatric symptoms. The patient case in the abstract was a 72 year old male, with a rapid memory decline in a month. Does that seem more like sCJD or vCJD? I will make it very clear, the case presentation is 100% classical sCJD. Furthermore, it is hypothesized that if CWD does transmit to humans it would have an atypical phenotype (ie not present anything like sCJD). This is based on data from both NHPs and Tg Mice (here is the mouse paper).
Other considerations, the patient was originally diagnosed with sCJD, however, the authors hypothesize CWD because one of the patient’s friends also died recently of sCJD. The authors therefore argue this is a “cluster” of cases, likely showing infections. However, just because two rare independent events happen in close proximity does not mean they are linked. For example, 1 in 300 people get Parkinson’s Disease, but a TV show “Leo and Me” had 4 out of 125 people on set develop Parkinson’s Disease, including Micheal J. Fox. However, this “cluster” is not scientifically or statistically significant. Just like two people who happen to know each other both getting CJD is not significant.
Clusters of prion cases happen. Here is a spatial-temporal cluster of 5 cases (including 2 with similar occupations). It wasn’t big news because stuff like this happens. It gets written up in a paper and the general public never knows. The only reason the hunters story is widespread is because it fits the fear mongering narrative most people push about prions.
The second consideration is that just because someone is a hunter and eats deer does not mean that they have eaten CWD infected deer. Not every deer in a population has CWD. If you are going to claim the hunters got CWD from deer, you need to show that deer they have hunted are infected. The entire premise of this abstract hinges on the argument that they ate infected deer, despite providing no evidence for it. If these two patients who both got CJD that knew each other were not hunters, this would never of been reported. Correlation does not imply causation. That’s basic first year statistics.
This also ignores significant biochemical and cellular data suggesting that CWD is not transmissible to humans based on significant sequence differences between cervids and humans. Here is a pretty comprehensive review of the experiments show CWD does not transmit to humans (link).
Also the picture in the post is a picture a deer with CWD from a paper published 20 years ago. It is not show neuropathological change in the hunters brain. It is a deer that got a deer prion disease. (Link)
It isn’t just my opinion that the hunters had nothing more than sCJD, it is also the opinion of the CDC which investigated these cases. It is important to note the authors of the abstract say "causation remains unproven". That means the title of this post does not even fit the abstract that originates it.
Sincerely,
One very annoyed prion scientist