The Joe Rogan Experience - #1154 - Doug Duren & Bryan Richards

Episode Date: August 8, 2018

Doug Duren is a passionate hunter, farmer, land manager and conservationist. Bryan Richards is the CWD project leader for the U.S. Geological Survey's National Wildlife Health Center.

Five, four, three, two, one. Yeehaw, and we're live. My good friend, Doug Duren. Hello, Douglas. Hello, Joe Rogan. Good to see you as a whole. Oh, man, it is good to be here. And Brian Richards, your friend, wildlife biologist.

And, well, we're going to talk about a bunch of things, but one of the things that I wanted to talk about is this scary disease that, well when ted nugent was on the podcast uh he downplayed the uh consequences and effects of something called cwd or chronic wasting disease which has made it onto your farm and you live in wisconsin and you have this beautiful place that we visited when we did the meat eater television show and this is a new thing that this chronic wasting disease was just just it decimates the deer's health and kills them and the suspicion is that some of this at least comes from these high fence operations where people grow deer and treat them like instead of like a wild animal, they treat them like

a domesticated animal and have them all feeding off of the same pile of food and they share this disease. Is this all correct and accurate, Brian? Boy, you just started out about an hour's worth of conversation. So just a little bit. I'm a wildlife biologist with the National Wildlife Health Center, U.S. Geological Survey up in Madison, Wisconsin. And so one of the things that I spend a lot of time on is chronic wasting disease.

I wouldn't say that makes me necessarily an expert, but I've gotten to know a lot of people that I would call experts over the years. So I've gained a little bit of knowledge. So I don't even your statement there we could start a number of different places this disease it essentially just will describe what it does to these animals and why it's such of major concern it hasn't jumped to humans yet that we're aware of that we're aware of but it is a possibility a very real possibility we can't rule it

out at this point in time science Science is unable to rule it out. So, okay, that's a great place to start. Why would we care about this thing called chronic wasting disease? And I would argue, and some other scientists have argued, there's two major reasons. Number one is the impacts of this disease on members of the deer family themselves. impacts of this disease on members of the deer family themselves. And the other is that we cannot rule out the possibility that CWD could become a human health issue at some point down the road. Okay, so you kind of nailed those two. With regard to deer or members of the deer family, white-tailed deer, mule deer, elk, moose, and most recently it was picked up in reindeer in Norway, moose, and most recently it was picked up in reindeer in Norway, of all places. We could articulate some reasons, some rationale, why this disease might be thought of as being important.

The first we look at would be geographic spread. So CWD 20 years ago was thought to be this really novel thing in a very restricted geographic range in southeastern Wyoming, adjacent northeastern Colorado, and maybe a little spillover into Nebraska. Wildlife biologists, wildlife disease specialists looked at this disease. It was interesting. We didn't know much about it at that point in time, but it seemed to be very isolated there. What does it do to the deer? It kills deer. Right, but how does it kill them?

All right, so this is a member of a family of diseases called transmissible spongiform encephalopathies or TSEs. So big long words. Transmissible means it can go from animal A to animal B. Spongiform means looks like a sponge and encephalopathy means disease of the brain so you put it together and so this disease results in holes in the brain resulting in progressive neurological degeneration followed by death okay it's a it's a death sentence and there's no cure for it it's not like you can capture the deer and give them some sort of medication? No cure for these diseases. The suite of diseases, you know, there's members of this TSE group of diseases in humans. Most familiar is one called Creutzfeldt-Jakob's disease.

Right. So it's very similar to mad cow disease. They're in the same family. So it comes from prions? Well, I'd say prions. You could say prions. I don't know how to say it. I'll just read it.

That's an interesting, you know, there's a, it goes back and forth on whether it's prion or prion. Stan Proisner, who received a Nobel laureate for his work on these diseases, coined the term prion. And in his first publication describing these diseases, he did a phonetic spelling and it's prion. So other researchers, especially, you know, some from across the pond say it's got to be prion. And the main reason that, you know, some of them I've talked to about that is that it irks Stan Preusner when he hears it called prion. Oh, so we'll say prion. So I'll say prion from now on. Now, this disease, which people know as mad cow disease, obviously is transmissible to humans. And that's one of the reasons why people are very scared that this could potentially jump from deer into humans.

And correct me if I'm wrong, but it also is making its way into the actual plants that these animals eat. You're correct on both accounts. So with BSE, mad cow disease, that was an interesting disease where it resulted from, in essence, turning cows into cannibals. Which also exists in New Guinea, right, with cannibals, Jacob Kreutzfeld. With Kuru, which is a human disease, TSE, likely started when one individual developed Kreutzfeldt-Jakob's disease. That individual died.

And as is the practice, was the practice in the Foray tribe in Papua New Guinea, they practiced ritualized cannibalism to honor the dead and to help release the spirits from deceased family members. and to help release the spirits from deceased family members. So they would feed upon the corpse and the bodies of their deceased. So when one individual died of probably some variant of Creutzfeldt-Jakob's disease, then the causative agent, the prion protein, which is concentrated in the central nervous system and lymphatic systems of, you know, of disease patients, this was fed back to other members of the family and the extended family.

And so when they got sick and died, fed it again. So we saw that with Kuru. In the 19, I believe it was in 1960 or around there, it was realized that this cannibalistic behavior was likely the result, you know, or the, rightly, the cause of disease transmission. Cannibalism was outlawed. And at that point in time, you broke completely the disease transmission cycle. So no more new cases of Kuru, but they had lingering cases with an extended incubation period up to 40 years later before Kuru finally burned out of that population. Whoa. So now with BSE or mad cow disease, we were doing exactly, in essence, the same thing.

Not exactly the same thing, but in essence. So in an effort to maximize production and reduce the amount of waste, when they butchered cattle, we would take all the offal, O-F-F-A-L, you know, the hide, the bones, the parts that are inedible, and we would render them, cook them at high temperature and typically, you know, high pressure as well. And it turns into a slurry, a high protein slurry. You skim the fat off the top of that and then dehydrate the rest of it, and you have kind of a meat and bone meal, a high-protein supplement. Realizing that cattle grow faster and produce better when they're on a higher-protein diet, it seemed reasonable to use waste material from cows to feed back to cows. So at some point – It doesn't get better. turning cows into cannibals.

So at some point in time, a cow developed a TSE, a prion disease. Whether it came from scrapie, the TSE of sheep, or a rose on its own is unknown. But that cow died. It was rendered into meat and bone meal, and this high-protein feed was then fed out to hundreds to thousands. And correct me if I'm wrong, but these prions, they could survive up to more than 1,000 degree temperature. Yeah, surviving is kind of a strange term, Joe, in that they're not alive to start with. It's a protein.

They can persist. They cannot be inactivated. So, yeah, you'd have to cook pretty hot. These prions are not necessarily a living thing like a disease or a virus or a bacteria. Well, they're a disease-causing agent, but they are incredibly unique. So they're an etiologic agent like a virus, a bacteria, or, you know, a parasite could be causing disease. But all these other things have genetic material. They're alive, which allows them to change rapidly, to evolve over time.

So the whole concept that you have a protein, a protein that all mammals produce in a normal form, can be converted after production into a disease-associated form that has these radically different characteristics. One that you mentioned was, you know, resistance to heat treatment. A normal prion protein, and we have billions of them circulating in our bodies right now, have a specific purpose, a cellular purpose. We don't know exactly what it is, but it's likely involved in some sort of intracellular communication. It's a string of around 250 amino acids, so a relatively short protein. It does whatever it does, and then the body recycles, breaks that chain of amino acids

down into its component parts and recycles it. Turns out that normal cellular preamp protein likely has a half-life of maybe four to six hours. Okay, so you're producing them relatively constantly. Then there's the disease-associated form, and all disease-associated prions start as the normal cellular prion. So they're converted from one three-dimensional form to a different form, okay? And this different form has these radically different characteristics. One is heat resistance. Another is UV light resistance. I mentioned that the normal cellular prion protein has a half-life of maybe four to six hours.

The disease-associated ones can persist in the environment for years and potentially up to decades, okay? And when you say persist in the environment, you mean on the ground, on leaves? How would they persist? Yeah, all of those things, Joe. So if a deer sheds infectious agent, this prion protein, and so from the time a deer is infected, it's probably around two years before it develops clinical signs of disease, goes downhill, loses its fear of humans, dramatic weight loss, all of those things.

That incubation period, it's probably shedding infectious agent for the vast majority of that time period. So it looks healthy, but it's able of transmitting disease. We'd call that a typhoid Mary syndrome. The two deer that were positive on our farm, two bucks, two and a half year old bucks, we had them tested. As you know, for the last several years, we've been getting, initially we got our only bucks tested. And then the last three or four years, we've gotten all the deer tested. They were two-and-a-half-year-old bucks, looked perfectly healthy.

And these are the first ones that you tested that tested positive? When we tested in excess of 35 deer over the last, well, more than that, probably more like 50. Now, during the incubation period, would they still test positive? At some point, they will. At some point. So they could be spreading infectious agents without testing positive? At some point they will. At some point. So they could be spreading infectious agents without testing positive? Yes. Oh, fuck. So it's probably between three and six months out when we can test an animal, test positive, but it's likely shedding infectious agent, at least at lower quantities prior to that point in time. And so it's shedding infectious agent. It's capable of

transmitting disease, okay, long before it looks clinically ill. And so that's one of the real challenges with this disease from a management standpoint. They look perfectly healthy. They act perfectly healthy. But they're starting to have that progressive neurological degeneration that we can only see very near the end of disease. So correct me if I'm wrong, but this seems like we could potentially be facing a ticking time bomb of many, many, many deer that are wandering around out there right now that look totally normal, that are spreading this stuff all over the place. And they're acting normal. They look perfectly healthy. normal, that are spreading this stuff all over the place, and they're acting normal. They look perfectly healthy. And then, obviously, with this multi-year incubation period, this could just cascade. And I think we've seen evidence of that now. We talked about being isolated disease. It

was picked up in Wisconsin at the end of 2001. As of today, CWD has now been picked up in 25 states in captive and or free ranging populations in white-tailed deer, mule deer, elk, or moose, two Canadian provinces. In addition, it was picked up in South Korea. And that was real interesting. It was in captive elk, and those elk still had Canadian ear tags in them. So we pretty much know how CWD, you know, those elk didn't swim across the Pacific pond. Most recently, it was picked up two years ago in free-ranging reindeer in Norway. And subsequent to that, it was picked up in a small handful, like three or four moose and a red deer in Norway and a single moose in Finland. There's a real concern over in Norway with reindeer.

So reindeer are very gregarious. Whitetail deer are caribou reindeer. So not unusual to see them in herds of hundreds of animals. So very, very different than what we see with white-tailed deer, mule deer, elk, or moose. We don't see those huge herds. Well, with elk, you can in the wintertime. But anyway, it's thought that this gregarious behavior might really facilitate transmission in reindeer, right? So when it was picked up in reindeer, Norway said, you know, maybe we should do something. It's an interesting story in that, you know, Norway's got experience with scrapie and sheep. And so they have a long history. What is scrapie? Scrapie is the same as,

well, it's the same family of diseases in sheep. It's actually the first one that was described, scrapie, we've known about since the early 1700s. A disease of domestic sheep. And it's called scrapie because of the behavior these animals, once they enter the clinical phase of disease, display. And they seem like they itch bad. And so they'll go up to fence posts and other objects, and they'll literally rub their hide off of their body. So that's the name scrapie. And it's the same progressive neurological disorder followed by death. And you think about it. So as this disease creates vacuoles in the brain, it's killing off neurons.

And so without those neurons firing, you fall into that progressive degeneration. And yet at some point, your body can no longer survive. And that's what's really spooky about how this thing kills. So anyway, go back to Norway. When they detected CWD... Brian, try to keep this a little bit closer to you. Sorry, you're very soft-spoken. Oh, no worries. I can hear myself plenty well. I know. The problem is the recording. Sorry. Okay. No worries. So when they picked up CWD and reindeer in Norway, the researchers over there had witnessed our lack of success on this side of the pond over the course of the last 20 years. They took it very, very seriously. So they took kind of some harsh medicine. They announced their plans that they were going to eliminate a herd unit.

They were going to kill every reindeer in an entire herd unit in Norway. The idea is to eliminate the host population. It's called stamping out, and it works in a pen. This is the first time it had been done realistically in a free-ranging population. The whole idea is we don't have effective tools for management of disease. They were very fearful of what would happen if this spread throughout that reindeer population and throughout other reindeer herds. And like Alaska, they have multiple herds. Like last year, I hunted caribou with Steve up in the Forty Mile River area. And so they're very localized. But at least they have a range that they move through.

And in Norway, they have two or three different herds. Many more than that. So I don't know exactly how many herd units they have. But the point was that you could isolate one of the herds. So the idea is before this gets any worse, before it gets any farther, let's take it out. So they had a hunting season. They allowed hunters to take as many as they could, which was a little over 1,000 reindeer. Then they came in with government agents, sharpshooters.

But isn't there a concern that the hunters could eat something with CWD and then catch it? Well, that's always a concern. But we can talk about human health. Let me finish this one up with Norway. They literally took the bull by the horns. They decided to do what was very unpopular, what we have not been able to do in North America. And so after the hunting season, government agents, sharpshooters took an additional 1,400 reindeer.

So they killed every reindeer in this herd unit. And they're going to keep it fallow, allow no reindeer in there for a minimum of five years. So it says every bit of promise of being the first large-scale success with dealing with this disease in a free-ranging herd. Pretty different than what we've been able to accomplish over here. Five years, is that, I mean, with it being in the soil and dirt and from what i was reading wood and everything else is that um so at some point there becomes a the the prions um diminish in population or they die out or whatever the proper word i mean they're not living so they don't die but five years viable anymore yeah five years is probably a pretty, it's a guesstimate, okay, with regard to how long these prions remain viable in the environment and in the substrate.

So it's a good first guess. And what they'll do then is slowly allow reindeer to repopulate. And as they do, they'll be harvested periodically and every one of those will be tested. harvested periodically, and every one of those will be tested. So, I mean, it'll be a long-term experiment into, you know, successful management, and it will also learn quite a bit about whether, how far along the environment was contaminated. So, another thing, they caught this disease very early. So, after killing off, you know, 2,400 reindeer, I think they had around 20 positives. So, very low prevalence, suggesting the disease was very, very new in this system. So if you're going to be successful with a disease where animals are

shedding infectious agent out into the environment, it persists for years to decades, do it early. You know, if you're going to get on it, detect it early, get on it fast, get on it hard. Why the decision to let human beings consume them? get on it hard. Why the decision to let human beings consume them? Well, at this point in time, we really don't have any evidence that humans can get CWD. Could that potentially, though, be an incubation period issue, just like it is with deer, maybe extended with humans? Because you were talking about, how do you, was the correct pronunciation? I was pronouncing it wrong. Kuru. No, no, no. Or? Jakob Kreutzfeld. Oh, Kreutzfeld-Jakob's disease Or Kreuzfeld-Jakob's disease. So that has a long incubation period in human beings, correct?

Likely, yeah. And mad cow, same thing. Extended incubation period. Kuru could, you know, some of the cases it looks like we're up maybe even to 40, maybe even 50-year incubation period in individuals. That is crazy. year incubation period in individuals. I want to talk about Kuru for a minute because every time I talk to this guy, I mean, I've learned a lot from him about all kinds of things and diseases. But yesterday we were talking about Kuru and one of the things that was interesting to me about it is that these tribes, the women and children contracted it first.

Yeah, isn't that interesting? contracted it yeah that's interesting and the reason why was the man ate the meat and the women and children ate the internal organs internal organs and yes as where it's concentrated as kuru took off you know it was one of the features as the researchers in the you know in the 50s and you know 1950s were looking at the population. Very few adult males had Kuru, and it was more focused in the females and the children. And so it came back to that ritualistic, you know, cannibalism. And he hit it right on the head.

The women and children got the internal organs, including the brain, that had the highest concentration of the prion protein. The men, if they consumed anything, consumed the finer cuts of meat, which have a lower concentration, but not nil. That's just one of those social things that just kind of stuck with me, you know? It is kind of. It's a pretty interesting story. So a bunch of people reached out, and some were very angry after Ted Nugent was on the podcast.

And I don't know how CWD got brought up. I don't know what the context was. I don't remember. But I remember him saying that winter kills more animals than CWD does. And many people were very angry that this was a gross simplification of what could be a ticking time bomb. I guess I would, yeah, I'd have to agree with that. There's another disease out there called epizootic hemorrhagic disease, EHD. And periodically you'll have significant outbreaks of this disease. And in northern latitudes where the disease has not been present as often, you can see dramatic mortality.

80%, 90% of a herd can be killed in a single event. But a very distinction between these diseases, EHD is spread by midges, little black noceums. A bug. A bug. A bug. It actually transmits the disease, the virus from animal A to animal B or from the environment to animal A, either one. So while you have these pretty dramatic die-offs, as soon as the weather changes after the first frost, the first hard frost kills off the midges,

and within about two weeks, the disease cycle is broken completely. So it has significant impacts on a localized level periodically. But the disease cycle, there's a definite end to the disease cycle. And then it's no longer present for that period of time or for a period of time. Yeah, the virus may persist in the environment. But once the transmission cycle is broken, the mortality stops. And isn't there some genetically engineered food plots that they're putting together now, different types of seed that inhibits midge growth and inhibits EHD? I'm not aware of that, but I wouldn't doubt it. And I think there's also some stuff they're doing that bolsters the animal's immune system.

They're supplementing some of the food with, I don't know what they're using, but it bolsters the animal's immune system and makes them less susceptible to it. And populations that have been exposed to EHD over time definitely develop a herd immunity to it. And is EHD transferable to humans? No, not that we've ever seen. There's no evidence that it is. This is a disease of deer. And, you know, it also can get into livestock.

So even if people get bitten by these midges, there's still no concern that we could potentially get EHD? Not EHD. No. So contrast that, this disease, E ehd with a very definite end to the transmission cycle first frost kills off the midges with cwd there's no known ecological factor which signals the end of the transmission cycle so that's why we see prevalence or the proportion of animals that are positive in individual you and individual herds. It just keeps

going up, up, up. In captive facilities, the Hall Farm in Wisconsin, where CWD was first detected in 2002, the place was depopulated in 2006, prevalence was nearly 80%. So four out of five deer in that captive cervid facility had it. Wow. More recently, we had a farm, a deer farm in Iowa, where disease had gone undetected for some period of time. And when the herd was depopulated, again, about 80% prevalence. But this was a big herd. So there were over 200 positives in this single high-fenced enclosure. And so winter's not going to change that. It grows.

So no stop. There's no known feature which stops the transmission cycle. And so when you say that something like EHD kills a lot of deer, yes, it does. But the disease transmission cycle stops. transmission cycle stops. With CWD, we don't know anything that stops it. It's, EHD is more like the flu. Have you had it on your farm? EHD, never. No, no. Let me rephrase that. Not that I'm aware of. And so when I learned about EHD and, you know, comparative diseases, you know, chronic wasting diseases, like none other. As it develops within the herd, as it develops within the animal, it just continues to grow. So it'll start out as a very small problem. There's some maps of how it developed or how it spread in southwest Wisconsin.

And we're on the front edge of it now. And it's all, correct me if I'm wrong, Brian, but it's like, it's almost like the way it develops within the deer, taking that period of time before it becomes clinical and the deer dies, it's almost as if that's reflective of how it moves through the landscape. It moves very slowly, but once it's there, it's there. Now, I have read about hunters eating meat from some sort of diseased deer and getting sick and dying. What would that be?

Misreporting? Would it be? Possibly. I mean, I shouldn't say that. I mean, I don't know. There have been instances where people that hunted deer later died of a prion disease, likely developed Creutzfeldt-Jakob's disease. Okay. And so was it the deer that gave it to them? Well, there's no epidemiological evidence that this occurs at this point in time. And we've hinted about some of the human health issues.

So there's a few things we can look at. In areas where CWD is known to exist, do we see higher mortality rates from Creutzfeldt-Jakob's disease, the prion disease of humans, than we do elsewhere? The answer is no. Okay. So from an epidemiological standpoint, there's no evidence that CWD has crossed over that species barrier into humans. Now, we can take a look at a number of science experiments that have been conducted. And at least in some of these studies, in experimental models, we have evidence that the CWD prion protein can cause human normal prions to convert to a disease-associated form.

But now these are models. It's not quite the same as pumping CWD into the brain of a human patient and seeing what developed. So the science suggests that there is a small, non-zero chance that CWD could become a human health issue. There's also some of the more recent science that's been conducted suggests that this barrier, we call it the species barrier, and it really is a very robust barrier. One would think that keeps CWD from crossing into human hosts. That barrier may not be as tough as we think it is. And that barrier may be changing over time. And is that because one of the things we've talked about before is that they've discovered different strains of CWD? Yeah, it sure is. Oh, Jesus.

So, yeah. Like I said, man, it gets worse. It's fascinating. It's fascinating stuff. You've got to get to that point, that fascinating point. It's definitely fascinating, but it's scaring the shit out of me already. So, yeah, the idea of strains is really interesting. With scrapia, I mentioned that disease is sheep. We recognize some 30 different strains, and it's

still all that same identical strand of amino acids, and it's shaped, that tertiary form must be slightly different, and it manifests slightly differently in sheep. So now with CWD, there's at least two recognized strains that have been published in peer-reviewed literature. There's probably more strains out there. In fact, it's kind of interesting. There was a paper done a couple years ago, which looked at the actual architecture of this disease-associated prion protein. And there's a portion of it that's referred to as a loop structure. And it's just kind of, you know, if you take a rubber band or a piece of yarn or something and ball it up into a three-dimensional shape, there's a little loop hanging off the side of this disease-associated prion protein.

And in deer, in CWD, that loop is very, very rigid. It's very inflexible, shall we say. In humans, it is more of a flexible loop as opposed to the rigid loop. And it's thought that this difference in that architecture is partially controls that species barrier. So I was telling Doug. I read the paper yesterday. It's pretty neat stuff. Actually, it was really interesting.

So now it turns out mice, experimental laboratory mice, their prion protein has the same structure as the human prion does. So you cannot give CWD to a normal laboratory mouse. They just don't get it. And it's likely this difference, some of this difference in their prion structure, this one cannot convert that one to a different form. So some researchers in Alberta identified a strain of CWD, which came from wild deer. So it's not something they engineered in the laboratory. They have a strain from wild deer that does give mice CWD.

Oh, fuck. So most of the strains out there, mice can't get, but they discovered one that mice do get. So researchers from a few years ago, and lately I've seen it in the popular media, that, hey, this difference in this loop structure is going to keep people from getting CWD. Well, all the assumptions that people can't get CWD are based on this idea that CWD is CWD, and it will always be exactly the same thing. But our experience with scrapie strongly suggests that even though there's no DNA in these things, that they do change over time. They morph over time into slightly different disease characteristics and etiologic agents. Now, in the hunting community, is there skepticism about this?

Is Ted Nugent's ideas, are these unique? Or is this a common thought? Or is it a convenient thought for them because they don't want it to be real? It's a challenge. Of education? Yeah. Obviously, just in whatever period of time that we've talked here, it's really complicated. Right.

And to get to the – you almost want to stick your head in the sand and just forget about it. You know, besides the sort of things that, you know, your friend that we were talking about before, like I was doing on the farm, of, you know, managing deer in a particular way for a particular kind of deer, which might be contrary to the spread of the disease. Well, geez, nobody wants to hear that I can't do what I want to do management-wise. And what we're talking about management-wise, we're talking about my friend John Dudley's farm in Iowa, is that he only shoots the big, mature males, and he lets all the other deer grow to a very large size so he has a really healthy population of big deer on his farm.

Now, what are you doing in your place i understand you're just on a mass call well i feel like i'm on the front edge uh well i don't feel like it i am on the front edge of the spread of this disease and there's some in wisconsin in wisconsin in southwest Wisconsin. So 15 years ago, or 16 years ago, when CWD was discovered, there were a lot of changes in hunting structure. And there was an effort by the Department of Natural Resources to eradicate the disease in the core area south of the Wisconsin River, about 70 miles from us. In 15 years, the disease has moved 70 miles north. That effort that the DNR started became political. And quite honestly, that many years ago, I would have likely been a little skeptical. Well, I know I would have been skeptical. You want me to do what?

They wanted to kill all the deer in a particular area. You know, that many years ago, had they come to my farm and said, we're going to kill all the deer here and all the neighboring deer, I would have had some real hard questions. I have no idea how I would have reacted to it. I continued to do, like, buck management. And, you know, you were there when we were still doing that. And we can talk about how bucks contribute to the spread of the disease and that sort of thing.

Uniquely versus doe? We see different prevalence or curves depending on the demographic faction of deer. Adult males, the ones with the big antlers, the gears on the wall over there, tend to have higher prevalence, sometimes maybe two, three, four times as high as other segments of the population. So highest prevalence in adult males, followed by adult females, and then by juvenile animals. So it's likely behavioral reasons why we see that in adult males. So adult male deer, during the rut or breeding season, they greatly expand their home range. They contact multiple female or family groups of females. Earlier in the fall,

especially with the white-tailed deer, adult males tend to gather in these bachelor groups. So there's a lot of social contact, grooming, things like that. So because of their behavior, they contact more animals at different times of the year. And this number of contacts, it's believed, is likely responsible for them becoming infected at a higher rate than other members out in the herd. So now if you are an adult male, then you're in this group. You also have a higher likelihood of being able to transmit disease to other animals because you're out there during breeding season, right? Is there any evidence that any of these deer have transferred this to livestock

or that it's gone into agriculture, to food sources, to corn and what have you, that could be consumed by people even that are vegetarians? Okay, interesting question. So with regard to transmission into cattle, it's basically the same situation as with humans. No evidence that it has, but in an experimental sense, we can push it over that species barrier. Okay. Now, interesting you bring up plants because we have shown research that we've done at the National Wildlife Health Center has shown that if you grow some plant types in a slurry, a concentrate of prion protein, that those prions can be uptaken through the roots and deposited into stems and

leaves. Okay. And so that's one possible mechanism. A second is that some prions themselves, the disease-associated prions, tend to form very tight chemical bonds with various surfaces. And I showed him a paper on the way out here yesterday where they bind to just about anything. They bind to plants as well. So that deer that's out there with CWD positive, shedding infectious agent out into the environment through its urine, through its saliva, through its feces. So if a deer urinates, a deer with CWD, urinates on plants, the prions have a tendency to bind to those plants, form a chemical bond. It's not just dried on, it forms a chemical bond to the plant. So they literally become part of the plant.

It's, yeah. Okay. So a deer could eat those plants, and that could be one of the possible transmission mechanisms. So that's the second one. The third one has, you know, is speculated about and some folks have looked at, and it has potential impacts for agricultural commodities. So when CWD was, you know, 20, 30 years ago, it was really, really rare. It probably couldn't happen. But now it's in 25 states, vast geographic areas.

We have just south of where he lives, in adult males, nearly 50% prevalence. So when you kill that big buck, take a coin out of your pocket, flip it in the air, and that's the odds that that deer has CWD. And when he says just south, it's 15 miles. So now let's go out west. 50% of them.

Yes. So let's go out to— 22% prevalence overall in the county at this point. Let's go up into the big agricultural areas in Saskatchewan or out west. So you've got a mule deer herd out there with CWD and let's say maybe 20% overall of that herd is CWD positive. You've been out in some of those big wheat fields and hay fields. How many mule deer are standing out there before sunset? A shitload.

Yeah. Okay. So take that amount times 20% or that amount, whatever percent have CWD, figure out how many times does the deer defecate or urinate on a daily basis. And that's a bunch. And now think about the possibility that when you harvest those agricultural foodstuffs and roll it up into big bales, that you might have fecal material rolled up into those big bales. Not just might, right? I mean, most likely. We'd need a graduate student that we could have, you know, pick apart large bales of hay to really prove that. But I mean, it's almost certainly. So now we're putting those on semi-trailers and moving them across borders. And are those are those – is there a possibility that these agricultural commodities, then deer could come up to them and be infected by contact? We don't know.

It's important to say that Brian's a scientist. These other folks studying that are scientists, and they don't – it's evidence evidence and it suggests and they get attacked for that. By people who don't want it to be true. Well, and, you know, that's how science is attacked anyway, right? Because it's hard to, speaking in absolutes is a real hard thing to do, you know. And so you'll hear him say the evidence suggests, the information is this. And I just think that's a real important distinction to draw here when you're having those kind of discussions. You know,

there are people who want absolute proof. Proof is hard in a biological world because there's so many factors out there. We can't control for them all. But there are certain tactics that have been used quite successfully. It goes all the way back to smoking. You know, when tobacco companies were attacking science. And the whole idea is to sow the seeds of doubt. There's actually a documentary on it called Merchants of Doubt. We've seen that. We see the same thing going on with CWD. So you mentioned it earlier. Hey, you know, CWD,

it's not so bad. What about winter kill? What about EHD? So instead of focusing on that, saying don't look here, look at this one. This one is worse. Why aren't you doing something about this one? So it's a simple diversion. Another tactic, which is, I mean, there's a body of science around this.

But this is a non-scientific approach to this because these are unrelated issues. Like EHD does kill animals. Winter kill most certainly kills animals. But we're not talking about the same circumstances. Right. We're trying to divert the conversation. Right. Another thing that's very easy to do is, you know, is cherry-picking the literature that's out there.

We saw a real great example of this about a year ago where there's a lot of letters to the editor being sent into newspapers in areas where CWD is. And I think it's an attempt to change the conversation. So they were very careful to use citations from peer-reviewed literature. they used was they found that in researchers in Wisconsin found that CWD was not having a significant effect on mortality rates when they studied the disease so this is a true statement taken directly from peer-reviewed science what they didn't identify was that that when they studied that disease was between 2003 and 2007, 10, 12, 11 years ago. Early on. The next sentence in the paper was,

our study can use as a baseline for comparison at a later point in time should disease change over time. So you mentioned that exponential growth curve and how early on, back in 2003 to 2007, this area, disease prevalence was probably lower than 5%. Now it's shot up in that curve, and it's probably in that 25, 30, 30-plus percentage range. So you're cherry-picking literature to make your arguments that even scientists say this is not having a big effect when they studied it they're just not saying when they studied it so as a non-scientist what i'm looking at here is everyone's always terrified of the next pandemic disease and this is one of the reasons why i felt it was so important to discuss this because you know people would say they look at it casually good don't eat animals, don't eat deer. This is not that.

This is something that has the potential to reach large-scale agriculture. One of the things about your farm, and we talked about this when we were there, is these animals are farm animals almost because they're absolutely free-range. They're absolutely wild. When you talk about the deer on your place, you don't have them controlled in any way, but they're feeding off of your corn. They're eating all this stuff that people eat. They're eating, I mean, that's what they eat. That's one of the reasons why the deer populations are so enormous in farmlands is because it's a massive food supply. It's a perfect environment. Yeah. And it's also one of the reasons why they're so delicious. They're so well-fed. They're so nutritionally balanced diets.

But what terrifies me is this potential for a pandemic disease also comes with an incubation period. And that we are looking potentially at, like if you just objectively look with no hysteria and no hyperbole, you look at the history of diseases. Diseases mutate, and many of them come from animals. This is why swine flu and avian flu and all these different things have actually come from either farm animals or wild animals that have somehow or another managed to transmit diseases that have morphed and mutated and become dangerous and deadly to human beings. This, to me, seems like a ticking time bomb. It has a potential. One switch, one way or the other, like you've observed, or they've observed rather, with mice,

and this could potentially infect human beings and spread across, I mean, the entire country, like wildfire? Well, we're seeing that spread right now in deer. So in deer, we're seeing clear geographic spread. We're seeing clear increases in prevalence. And in areas where the disease has been present the longest, we are seeing population level impacts. There's locations in Wyoming where we've demonstrated, where we've proven that CWD is driving population decline in deer. So that encapsulates why we should be concerned about deer. And is this in mule deer? That's in mule deer and in white-tailed deer.

And the mule deer have an extended range in terms of like their migration. That's one of the things that we've realized, I believe, over the last decade, right, is that mule deer travel far more, far longer and far longer distances. On average. On average, yes, they do. Than we ever thought before. Even whitetails can. There's an interesting research tidbit, the state of Minnesota, you know, they've got what appears to be a fairly recent CWD outbreak in the southeastern part of the state. So their researchers are really trying to get ahead of this and figure out what could move this around.

So they went in and captured deer in an adjacent area, put radio telemetry collars on these to see, well, just how far do they go? This was in an article just about a week ago, a popular media article. So it's not published yet, but they had a doe, single doe, collared that went 80 miles. Pretty long distance. Now, 80 miles circular or 80 miles point to point? 80 miles as the crow flies from point A to point B. Oh, in one direction. Christ.

So in that 80 miles could potentially be spreading CWD if it was an infected deer. Sure. Throughout crops, throughout, I mean, and this is. And then there's that exponential growth. So once it's there, sure, it takes a long time for it to become a large problem. And we're seeing that in Richland County. It crossed the river. Testing has been, you know, surveillance testing has been going on.

It crossed the river river and it just keeps moving up and it could be in again all these different plants all these different berries people could be eating these berries eating these plants fruits vegetables all these different things and they could be potentially consuming these prions. Well, I think it's very clear that there's exposure. And I talk with Doug quite a bit about the difference between exposure and disease transmission. So it is certain that lots of humans are exposed to disease-associated prion protein from CWD and likely from plant materials as well. Whether that will result in transmission of disease across that species barrier is an open question. We absolutely cannot

say it will. We absolutely cannot say it will not. It's an open question. And one thing we can identify very clearly is that the rate of exposure is increasing exponentially. As disease has a larger geographic footprint and prevalence goes up, more and more hunters are just by simple math being exposed to that positive material. So we're rolling the dice. And when you do biological experiments, I mean, there's a certain likelihood that you'll see outcome A or outcome B. So if you keep rolling the dice enough times, you might see an alternative outcome. We cannot rule that out. at the farm, meat eater podcast number 70.

Brian, you put it as the chances are very small at this point that it can, and this is what the CDC and the World Health Organization says as well, the chances are very small, minuscule even, but they're not zero. even but they're not zero and uh i'm assuming that we continue to that continues to be the you know the concern and i know you're talking a lot of joe about about and i get it because after all humans um but i've actually begun to focus more on the effect on the resource, on the deer. I mean, I tested positive animals. We properly disposed of the meat, which is a whole other line of discussion. I'm still eating venison, but I'm not eating meat. Are you testing the animals that you eat?

Every one of them. We test every deer killed on the farm. Now, how long when you raise a cow, how long before you kill it? How long do you wait? I do grass-fed beef. This is actually kind of interesting. You were talking about the deer, the whitetail deer on our place eating corn and beans and GMO corn, GMO beans, alfalfa, whatever they want to eat. I control what my grass-fed beef eat. I mean, you've met some of my cattle.

The one says hello, by the way. It's always so high. Anyway, but it's very controlled. So even though my deer aren't – Could be infected. Your cow will not be. Well, and that they're not organic. Right. My cattle are. Right. Because it is controlled.. Right. My cattle are.

Right. Because it is controlled. How ironic. Oh, yeah. I mean, you have farm animals in captivity that are organic, purely eating grass, as nature intended. And you've got deer eating Monsanto corn. Yeah. Yeah, believe me.

It's kind of crazy. Yeah, yeah, believe me. It's kind of crazy. Yeah, yeah, yeah. And, you know, before anybody out there gets the idea that my cattle are confined in a little barnyard or anything. No, it's a big, large area. Big pasture. They are, you know, free-ranging within that pasture, you know, the pasture raised. So, short answer, with grass-fed beef uh i just sent four in unfortunately none of it was ready i was going to bring you some but uh they just went in on monday

uh i would like to see him go through the security checkpoint carrying you know bags of beef with him but 26 so they were uh two So they were two years old and two years old in two months or three months. Now with the incubation period that you were discussing earlier, you're talking about a two-year incubation period with deer

before they potentially show any effects. So these animals would fall into that line between birth and slaughter that that would be inside that incubation window for deer. It could be potentially larger for cow. Is that correct? BSE, I think the incubation period is between three and five years.

And so that's why one of the precautionary measures for BSE in the United States is we don't allow those older-aged cattle into the human food chain. What does BSE stand for? Bovine spongiform encephalopathy, a.k.a. mad cow disease. So that's one of the precautionary measures is not allowing cows to get old for mad cow disease. Well, and from my standpoint, they're prime at 26, 27 months. Right. And so when they are in an incubation period, they're still capable of distributing the disease though, correct?

Well, that's with CWD and with scrapie and sheep as well. With BSE, and let me clarify, if CWD went into a cow in a natural world, we don't know exactly what it would look like. We know what it looks like when we inject it into the brain of a cow, but we don't know what it would really look like. But BSE is quite different in that similarly with the human prion diseases, an individual with Kuru could not give Kuru to another human being. They had to consume it. So there was that artificial process involved. Same thing with BSE.

So there's that artificial process involved. Same thing with BSE. A cow with BSE can't give BSE to another because they're not shedding that infectious agent out into the environment. So when they stopped it, when they stopped feeding cows to cows, there's still transmission of vehicle. CWD is a different animal. CWD and scrapie are different animals. This is like BSE times 10 on steroids. Well, they're contagious.

Kind of freaking me out a little bit. Because these animals are shedding, okay? That infectious agent. Cows with BSE are not shedding infectious agent. CWD-positive deer and scrapie-positive sheep are. These two diseases are unique in the world of TSEs. TSEs, pre-hand diseases, are unique amongst themselves, but scrapie and CWD are in a different world of their own. Okay, what, if anything, can be done?

can be done? Well, I try to break this stuff down to the most basic levels so a guy like me can understand it. Buy time, pay for science. That's sort of one of the things. Slow the spread of the disease. There's a lot of work being done.

All kinds of studies being done, different organizations and the government, unfortunately, in Wisconsin, not as much as we should be doing. We're, you know, we're a hotbed of it. I think that in Wisconsin, quite honestly, that we've become an example of how not to handle the disease. And a lot of the other states have begun to you know take that idea that if you don't have it you don't want it so let's do what we can to stop it from coming here that's why you're seeing things like let's not transfer carcasses that you know there's bans on being able to transfer carcasses in Wisconsin in some cases you can't take it to another county. You can take the finished meat, so you have to bone your meat in the area, and then you can take it home, which is a bit of a problem for some folks. We're beginning to stop the movement of captive deer from one farm to the other, but that's just recent,

and there have been hearings on that lately. So people resist that, right? Sure. If your economic vitality depends on selling and moving live deer, you're going to be opposed to restrictions on your economic activity. But that is one of the primary infection sources. It's one of the infectious sources. He'll always correct you when you say something like primary.

What Doug's getting at is... No bullshit. He wants them. He's going to break it down. It's a world I live in. We think of... There's two mechanisms, primary mechanisms if we lump them together for how CWD moves. One is deer to

deer to deer to deer, that slow diffusive process of moving out on the landscape. That's really hard to deal with. The other one is this anthropogenic or human-assisted movement where humans are moving infectious material. And that might be how it got from Colorado to Wisconsin in the first place. It's highly unlikely that a mule deer or a whitetail deer got up, woke up one morning in Colorado and decided to, you know, go 900 miles across the Mississippi River and settle in, you know, western Dane County. And back in the day, my dad and a bunch of his buddies used to go out to Colorado, or Wyoming is actually where they went, and they hunted elk and mule deer,

and it brought the whole damn thing back. I mean, just what you did, right? You put it on the back of the truck and off you went. And then processed that. I mean, I can remember doing it in a garage in Casanova as a kid, you know, working there with knives. This is a great thing. Well, what do you do with the bones and the, you know, the non-meat stuff when you're done?

Well, back in the day, it still happens. We take it out and put it in what we call a bone pile, a coyote pile or something like that. It's dumped on the back 40. Yeah. Where that still could have infectivity if it was a positive animal. So how it was brought to Wisconsin is… Who knows? But anyway, he's absolutely correct.

The 25 states that don't have CWD don't want to get it. They want to do everything they can. What states are these? What is it, eastern states? Southeastern states and some of the far western states haven't picked it up. If you go to our website, you'll see a map there that shows the current known distribution of where the disease is. So the other states really don't want it.

They don't want it bad. So it makes sense to look at these anthropogenic factors, human-assisted. Identify the possible mechanisms, how humans could bring CWD to you and stop them, either with regulatory frameworks or with education teaching hunters that it's a risk to move carcasses around is likely much more effective than just putting a rule in place that says you can't do it and there are unscrupulous people who purchase deer from these high fence operations and release them in the wild because they want big racks and animals. People don't know, there are these high fence operations.

I shouldn't even call them high fence operations because some of them are wild animals that are contained in a fence. These are farms. They're farms that grow deer, and they grow deer with special protein feeds so they have enormous racks. So you have these really perverse species, perverse examples of a deer. And people look at that and like to someone who enjoys wild animals, you see those and you're like, it's like a stripper with triple F tits. It's like, what the fuck did you just do? Like these, they don't look real.

They don't like they have like 80 points yeah instead of like an eight point buck which is you know very typical or a ten point buck you're like wow look at that monster that's a natural animal that lives in the wild they they have these things that they don't even look like deer they look like some some cartoon they're bred specifically for like that stripper with the triple f tits there are dudes who go i'm digging that yeah but it's obvious to all who are in the know like you go over a guy's house and he has one of those over his wall you're like did you just walk right out to that thing and put a pistol in its head like the deer hunter yeah you know like what what is that? That's not even a wild animal. That's some weird science project.

Well, and genetics play a role. And Brian will correct me when I start to veer off the science thing here. But genetics play a role in bigger deer. Yes. And your friend John Dudley would say the number of – he's doing it. The number one way to get big antler deer is it's not in space flight. Let them grow. Let them get old.

Let them get old and give them plenty of food. Yep. Yeah. Genetics have a role in it too. There's three factors in production of antlers. It's genetics, age, and nutrition are really the key three there. But now a lot of places will identify these as genetically superior. Well, that's kind of a misnomer. When you get back to the definition of fitness, genetic fitness,

there's only one measure of genetic fitness, and that's how well represented you are in the next generation, okay? So let's take an example where we took one of these, you know, 80 point whatever, So let's take an example where we took one of these, you know, 80-point whatever, and let's release it out into the wild. And during breeding season, it comes across a prime 3 1⁄2 or 4 1⁄2-year-old eight-pointer. You know, this physical specimen that you've witnessed them. They're unbelievable. So now if you put those up against each other in a mortal battle, I know who I'm putting my money on.

The wild animal. Absolutely. Yeah, for sure. Every time. So these animals, while they're bred very much like livestock for very specific characteristics, big antlers, these don't necessarily translate into something that would be more fit out in the wild. Well, let's also point out that the reason why you're bringing this up is these animals actually do fight to the death. And it happens all the time. They kill each other in combat. That's the reason why they have those antlers in the first place. They don't have them to protect themselves against wolves like caribou do. They literally have them to fight

with. You know, female caribou have antlers as well them to fight with you know female caribou have antlers as well and they have these antlers so that they could try to fend off animals that are trying to eat them there's a big difference between that and elk and deer they have them for combat that's why once the breeding season's over they shed them and then they start all over again yeah there's an interesting example if you look to to history it's an animal called the ir elk. Those things were incredible. They're extinct now. Okay. They were twice, three times the size of our normal elk and their antlers were measured in feet instead of inches. Okay. And so during their evolutionary time period,

when they were on the face of the earth, it was when, you know, animals were larger, predators were larger. These things got gargantuan, okay? Then they disappeared from the landscape. And at least, you know, the author Stephen Jay Gould, there you go. Stephen Jay Gould has offered up that likely what occurred was a change in the habitat, that climate changed over time, and that forests grew up. habitat that climate changed over time and that forests grew up. If you're in the plains and you have antlers that are seven, eight feet wide, you can walk around. But now when trees start to grow up, how can you survive when the world around you changed? And you'd have to literally walk with your head turned sideways. And Irish elk went extinct. So there's a very real example of how a phenotypic characteristic, these mega antlers, really in the long term were not in the best interest of the species. Jamie, pull up a photograph of these farm deer antlers.

Just type in Google ridiculous farm deer antlers and you get a sense of what we're talking about for the people that are watching this on YouTube. Because until you see it, you don't understand how gross it's gotten. Yeah, I think one was called Goliath that I remember. Well, there's a perfect example. That is a perfect example. What in the fuck is that? Because that's not a deer. That thing is crazy what they've done to that deer. It's a product of selective breeding for specific characteristics that some people will pay a lot of money for. Yeah, and there's certain high fence operations that you can go online and they, you know, this is what, like, go back to that photo you just had with that guy standing there.

Drawing. Oh, it's a drawing. Yeah. Duh. You went to it so quick, I thought it was real. Look at that thing. I mean, that is just insane. Look at the one behind it, though.

Yeah. Very normal-looking deer. Yeah, yeah. It's probably a one-year-old. Yeah. Yeah, there's these places that have these animals, and some people will take these animals and then they import them they purchase them import them and then release them into the air quotes wild and

then they'll hunt them and then they'll pretend that that's a wild animal that they shot and this is uh this is a source of cwd they are, okay, so a deer has to have CWD in order to be a risk, right? So it's been shown, I mean, in the lower 48, we're just, I think we're at 100 captive deer and elk facilities that have been shown to be CWD positive. So we can definitively identify that the captive cervid industry has been a part of moving CWD across the landscape. We know that CWD-positive deer have been moved by the industry, even across international and state lines. The ones in Korea are a great example.

Right, and we had a recent one where a CWD-positive farm in Wisconsin, it can do tracebacks where this animal came from. It turned out it came from Pennsylvania, a game farm in Pennsylvania. And then doing testing in that source herd, they found additional positives there. So definitively. So now, while I'll say that, very clearly the captive industry is a portion of the equation. They're not the whole equation. No.

They're not the whole equation. Where did it originate? You said the first testing of the positive testing of this stuff was? It was first described in 1967 in a research facility in the state of Colorado. That's not to say that was the first instance of CWD. It was the first time it was described in research. So this is pre-deer farms? I think deer farms have been around for a long time.

If you Google tame deer, you'll find some from the late 1800s when photographs became possible of deer following people around. So we've domesticated animals for a long, long time. But as an industry, probably really came into vogue in, you know, maybe the 60s and 70s. And more recently now it's grown, you know, that industry has grown exponentially. I used to work for Texas Parks and Wildlife before I worked for USGS. And one of the things I did was I administered the deer breeding program for the state. So when I started this, I didn't start the program, but when I came into that role- What do you mean you administered it?

Well, deer breeders in the state of Texas, like many states, need a permit from a state agency to conduct those activities. And so I was administrating that program. I think there were around 120 licensed breeding facilities, white-tailed deer breeding facilities in the state at that point in time. Ten years later, when I left Parks and Wildlife in Texas, there were around 600 or 700. So it just grew exponentially. And now I believe there are around 1,000 captive deer facilities in the state of Texas. Pennsylvania, there's around 1,000 of them.

Ohio's got several hundred. Wisconsin's got a couple hundred. So like I say, they're part of the equation. But I don't want to place all the blame for CWD moving it around because there's other possibilities for how this disease moves around. Doug hit on one of them, and that's the idea of carcass movement. It hasn't been proven that this occurs, but it's certainly, when you look at it from a scientific standpoint, it's very easy to identify. So if, you know, I butcher my own deer, so if I kill a deer that happens to have CWD, I butcher my own deer, I've got to do something with this stuff, okay? You know, the meat component in a deer is probably around 30%, 35%, something like that.

So I've got a lot of other stuff. Landfills, it turns out, are very loathe to accept this material. You know, it's almost taboo now. loathe to accept this material. You know, it's almost taboo now. Oh, it might have CWD, so we don't want it at our landfill because the effluent might be pumped out onto a farmer's field and they could come back and, you know, they see it as a liability. So I've got my deer bones and awful, the rest of the material, and I drive to the dump, which is, you know, 25 miles away. I said, no, we're not taking that. Well, now what am I going to do with this stuff? So I could double bag it a little bit at a time and put it

out in the trash. Or maybe on the way home, I'm driving past a state-owned, a state park or a state natural area or a wildlife management area, and I see a trail go down there. And I drive down that trail and, hey, there's a pile of deer bones and dare heads here whoops and did I knock that over sorry about that Joe so it's easy to see how inadvertently just hold your thought when you're not on a microphone just just that's and it is one of the one of the concerns is how are we uh you know how what kind of hygiene do we have with the the carcasses and it is something that we're talking about a lot more in wisconsin now and it and it's become an issue and one of the interestingly i'm in the county deer advisory committee for richland county and we

it's a citizen group and we have some say in season structure and then how many antlerless permits there are there's a lot of things we don't have any say in which is you know fine I'd rather leave it to the biologists but because there are hunters involved I'm happy to be one of them. One of the things that happened in our in our spring hearings is that we had folks come in and say, you know, we're concerned about chronic wasting disease and we don't want to spread it on the landscape. But when we put the bones out on the curb, they aren't taking it. On the Wisconsin DNR CWD website, there's a list of haulers who will take it. So there are some that will take it.

There are some who don't. But the problem is, where are they taking it? Well, they're taking it to clay-lined landfills. And how it's being handled, there's some question. But it can be isolated so the effluent isn't being taken out and pumped down the fields. It's something that we can do something about. There's clear science. We noted how prions bind to various surfaces. They bind to clay particles very, very tightly. And so one of the researchers at UW-Madison, his name's Joel

Patterson, was looking at this issue 10 years ago to try and figure out, can it be safely done? Turns out if you put about an eight inch clay liner underneath, you know, one portion of your landfill, you can put all the deer and all the prions there that you want to. And while the prions will then migrate down, you know, over time through the soil, when they come in contact with the clay particles, they bind and they don't go anywhere. and they don't go anywhere. So it can be completely safely done. So there's a way to dispose of these materials very, very safely.

But the thought of it, the risk associated with it, the liability, some landfill owners are just like, nah, we'd rather not. And interestingly, because we're challenged about this, what are we supposed to do? And you can't incinerate it, right? Because they'll... Well, it ends up being a budget issue. In Wisconsin, everything's a budget issue. And the DNR is having issues with that.

And it is something I'd like to talk about a little bit. But when this all first happened 17 years ago, they were incinerating deer and it became a problem. But there are landfills that are taking it and there are haulers who will take it. They have dumpsters that they use specifically for it. They're lined with heavy mill plastic. They're very specific to deer bones. but some haulers aren't doing it. So I contacted the head of solid waste for the state of Wisconsin and asked, well, how is this? I go

on your website and I see some take it and some don't. And her response was, we have no legislative authority to require them to take this. So some are doing it voluntarily, and actually one solid waste hauler said to me, geez, we're putting a hell of a lot worse stuff in the landfills than some deer bones. But it's simple hygiene. So one of the efforts that we're working on in southwest Wisconsin right now is to, and it's a funding issue, is to place dumpsters in areas where, you know, like I'm volunteering to have one on my farm. It's a question of who's going to pay for it. And if it comes down to it, I'm going to pay for the damn dumpster or about 500 bucks for

a 20-yard dumpster. But so that then, you know, people can and throw their put their bones in that dumpster and then they'll be properly disposed of because we have a hauler near us who's said we're willing to bring them there um you know to bring the dumpster there and then dispose of the bones properly like they do with uh uh at one of the lockers that one of the butcher shops that you know processes deer they the setup, which is actually when I saw it. I was like, why aren't we doing that countywide in various places so that people aren't chucking them in the ditch? I mean, otherwise, you're holding on to the damn bones until you find out whether the things, if you're being completely careful about the hygiene, which I've been trying to do.

You've got a pile of bones in the old milk house down there until you find out whether it's positive or not. And I'm literally keeping the deer bones separate so that when I find out that deer A was non-positive, well, okay, I can put those out or something like that. So that's one of the things. There's a difference between what we can. So that's one of the things. There's a difference between what we can – there's natural spreading of the disease. And then there's human, like, putting them on trucks and moving them around or taking the bones around and doing that stuff. This carcass thing, is it really a low-hanging fruit? The idea that we can't fix this one? I mean, that's ridiculous.

And it's easy. It seems easy to me. I mean, it's just a matter of will and money and then and education obviously um that we're we're providing opportunity for this i'm i've been working with the dnr a little bit on this we're in some discussions about um two things one is uh self-service kiosks to make getting your deer tested easier, where you essentially cut the head off the deer and leave it in a kiosk with some information about where it was. And they're fairly simple. They've been doing this for a couple of years on an experimental basis. But again, it becomes a budget issue. So we're hoping that what we're going to be able to do is start something called Adopt-A-Kiosk,

essentially, that hunters and sportsman's groups will gather those heads and then take them into the testing facility and therefore keep the budget money targeted at doing the actual testing. doing the actual testing. Right next to that self-service kiosk really should be a dumpster that you can throw your deer bones into, whether you know whether it's positive or not. Otherwise, you are holding it. The other thing that the DNR suggests that we do is if you kill the deer on your farm,

leave the bones on your farm. Makes sense to me. If it is positive, disease is already there, and so you're not taking as great a chance of moving it. That's not an optimal solution to leave that stuff on the ground surface. An optimal

solution is dig a hole, but it's pretty hard to dig sometimes in December in Wisconsin. If the dumpster thing doesn't end up working out with me, there will be a hole. I mean, last year, I just kept the bones separate, and the ones that we actually took

from the one deer, they went into the dumpster at the locker. This all seems to me, sorry to interrupt, but this all seems to me like band-aids on massive gunshot wounds. It is, but go back to what I was saying before. Let's buy time. Right.

Because this shit's spreading, man. Yeah. Let's buy time and pay for science. Not, ah, there's nothing we can do about it. Or the other one, that it's always been here, which I think the guitar player talked about. Is there any consideration whatsoever that there could potentially be a cure? Absolutely. Absolutely. See, we hit on a couple of things. I think it's important to talk just very briefly about some very generic disease management practices. Number one, and this

would be wildlife disease, human disease, livestock disease, prevention. Number one, if you don't have it, don't get it. Do everything you can. That's why we get vaccinated, Prevention, number one, if you don't have it, don't get it. Do everything you can. That's why we get vaccinated, okay, for various diseases. If you do get disease, do everything you can to keep from moving it artificially. So that's why we don't want to move the carcasses around. That's why, you know, we don't want to move captive deer around.

That's why when we had an Ebola outbreak in 2015 in Liberia on Ivory Coast, we stopped commercial airline flights. We didn't want people inadvertently moving it out. So prevent, don't move it around, conduct surveillance around areas where it is to see what's going on. And states are doing that very well, largely. The next one is a tough one. Do something about disease. Manage disease to try and knock down prevalence incidents and get rid of the disease. So that's challenging. But two other things. Number one is support research because if we don't have a cure today, we won't have one tomorrow either. How is research funded right now? either by states or by the federal government. And there's not a ton of money. The last one is being transparent with your stakeholders, being open and communicative with them. So with many diseases, we have good therapeutics, okay? We can treat some diseases. CWD and other prion diseases, we have no therapeutics, we have no treatments right now. But people are certainly working towards them. Now,

it's likely it's going to be very challenging to create a therapeutic, something that treats a prion disease, because treatment would then mean you would have to get past the blood-brain barrier. And once you start this cascading interaction of normal prions to disease-associated prions in the central nervous system, it's going to be really, really challenging to stop that. I mean, it's a roller coaster going awry by the time it gets up into the brain. So then you're looking at preventative measures. The idea of vaccines is number one. And number two is looking at animals that through their genetic profile are resistant to disease. And there's some advances on each front. So we can talk about vaccines for a moment. So people, individual scientists, research outfits

have been trying to develop vaccines for TSEs, for prion diseases for a long time. Okay. None have been successful. There's no human prion disease vaccines. There's nothing for BSE. There's nothing for scrapie. But there's research ongoing, and there have been some advances. There's a Canadian research group that had a vaccine candidate for CWD. They thought it looked very promising, so it went to a field production stage. And they actually tried deploying this vaccine in a captive facility in Wyoming, a research facility. It turned out that this vaccine was not ready for prime time. And actually

after giving this vaccine to some elk, giving a placebo to other elk, and then leaving him in a CWD contaminated facility, actually the vaccinated animals got CWD faster and at a higher rate than the non-vaccinated animals. So it turned out to be almost an anti-vaccine. Okay, so it didn't work. So instead of being inert, there was some sort of active CWD in the vaccine? Is that what it is? No, it just, for whatever reason, it predisposed the animals so it it was a massive failure but even from failures you learn okay so they're working now and based you know they learned a lot in that experiment there's another research group centered out of the university of new york who published a paper i think in 2015 was their most recent work and they've got a vaccine candidate that provides some degree of

protection, quote unquote, protection from disease. Now, all but one of the animals that they gave this vaccine to and then challenged with CWD got CWD. Okay. So that's not good news. But the average incubation time was extended at something like 300 days. Okay, so they're on the right track. They have a mechanism that is somehow interfering with the conversion from normal host prion protein to the disease-associated form. So very valuable. Now, will they get there? We don't know. We don't know.

But think about it. Even if we do create a vaccine that works, that prevents CWD, and prevent as opposed to slowing, there's a very big distinction. So if you have a vaccine that makes the average course of disease three years instead of two years or four years instead of two years, they still have CWD. Are there any deer farms that have 100% percent negative cwd deer in them like none of them test positive the vast majority of deer farms have never had cwd the vast majority absolutely so there is a potential that you could isolate these populations of completely CWD-free deer, and if there's some sort of a mass die-off, you could reintroduce these deer into the wild? Well, okay. So, again, you're looking at the difference.

I'm not talking about just a giant die-off. So, you're looking at the difference there between a herd that is CWD-free, which means it likely hasn't been exposed to CWD, versus animals that are CWD resistant through genetics. So to date, we have not seen any deer that are genetically completely resistant. There are different genotypes of the prion protein gene out there that do impact the length of disease and also seem to have some impact on how often the frequency that these animals get disease. But even the genetically resistant deer

do get CWD. Okay. And they transmit it. They get it at a lower rate. They likely transmit it. They're likely shedding infectious agent. So instead of that kind of garden variety two-year incubation period, it might be closer to a five-year incubation period. So now, on the one hand, you're going, great, most deer died before they're five years old anyway, so this would be a good thing. But on the downside, you're talking about a population of animals that have CWD with all these other side effects. They're shedding infectious agent out into the environment, this, that, and the other, and, you know, cause a potential risk to human and other health impacts on the landscape. not so certain that this is a success story. Just like a vaccine that results in a longer course of disease where their deer can get CWD, but they die from something else. A population of resistant

animals that has a high prevalence of CWD, I guess I don't see that as a desirable endpoint because of the other consequences and potential repercussions it would almost be more desirable if it killed them instantly a shorter incubation period would be preferable yeah because then you have the i mean it's almost like engineering deer to survive longer gives them more potential to spread it absolutely so now um recently so there's claims that and there's research going on in some of the conservative farms, the deer farms, that they've identified genetic markers, ones that are not published in the literature yet, that are affording a higher degree of protection from disease. But until it's published in the peer-reviewed literature and really tested, it's a speaking point until that point in time.

So we don't know if they'll get there. We've got to put a fence around Wisconsin, Doug. Giant one, 30 feet high. Well, it's already in the northern Illinois, northeast aisle. Well, all the places that have it. 25, so we're half and half. Yeah. Well, Alaska doesn't.

Does Alaska have it? Not that we know of. No, Hawaii. No. No, okay. So lower 48, Alaska have it? Not that we know of. No. Hawaii? No. No. Okay. So lower 48, 25. It's more than 50% then.

More than 50% of the states have it. Wow. 25 out of 48. Yep. So this is something that it just can't be dismissed. This is not something that's a hoax. This is not. So the reason why people were upset,

what Ted said on the podcast, there's a very good reason. Well, look, if I want to, you know, I play guitar. And if I want to learn some kick-ass Detroit guitar riffs, I'm going to listen to Ted Nugent. If I want to learn about CWD, I'm going to listen to Brian Richards and guys like him. Well, the thing is, Ted does know a lot about hunting. He knows a lot about wildlife.

He knows a lot about conservation. He knows a lot about conservation. But it appears that he's very misinformed or under-informed about this. Let me try and put this in perspective. Okay, so you have a disease which is contagious. It's always fatal upon clinical presentation. Always fatal, 100% fatal. Yeah, deer don't survive. Humans don't survive prion diseases.

When it enters the central nervous system, it's a death sentence. Okay? So it's contagious. It's fatal. Neurodegenerative disorder. It's got to be a horrible way to die. Okay?

So that's a pretty significant set of clinical signs or symptoms in an individual animal. Okay. Now let's look at the geographic spread, rampant geographic spread. So it has a ever-expanding geographic footprint. In areas where it has been known the longest, we now have prevalence in a cohort of animals, adult males of around 50%, and in adult females around 30%. Can you name any other disease of humans, fish, domestic livestock, dogs, wildlife, anything else that has that set of characteristics

and that degree of penetrance into the population, and you go, eh, that's no big deal? I'm not aware of one. There isn't one. Now, this is obviously very, very significant, which is one of the reasons why i wanted to have you guys on i wanted to ask jamie to pull up uh some photos of of clinical cwd deer or elk i think you had some and then you kind of took them down photos of the ones that are they're sick yeah yeah that so again 24-month plus or minus incubation period in the last six to eight weeks are clinical.

You know, I got to tell you, man, I killed this deer, and it tested positive. Whoa. Yeah. Tested positive. Oh, that is awful. That one's not CWD. That one could be.

Not the one before. No, that one. What is that? That's got some of the— That was called—that's's not CWD. That one could be. Not the one before. No, that one. What is that? That's got some other. That was called, that's cutaneous fibromas. They're tumors that grow on the surface of the skin. Pretty grotesque looking. What's the cause of that?

It's a virus. Is it fatal? Well, if you get those warts and those fibromas on your eyes and they block your vision, it would be. But otherwise, it's a stressor on animals, and you can actually eat them. They're fine, but I don't think I would. Chronic wasting disease. That image that Jamie's got up there, the larger image, scroll down. Is that?

That's likely CWD, yes, absolutely. Pick the one that's on the row underneath the second one from the left that one that the buck there that's yeah that's that's a photograph no no you had that one there so that was taken by a game warden um michael uh hopper is his name with in in the state of kansas and he's, you know, this disease has a pretty decent footprint in Kansas. This game warden, he gets calls about deer acting funny. And so he's taken a number of good pictures. If you can zoom in on that photo, I don't know if you can, look at what's coming out of that deer's mouth. See that stream of saliva? Yeah. Yeah. That's all filled with infectious material. So that's one of the clinical signs is this hypersalivation. That's a wild deer.

That's a wild deer. So it's almost like this disease is trying to spread itself. It's pretty efficient. Yeah. Yeah. But by doing that, by forcing these animals to have all the saliva excretion, this is a very effective means of transmitting this disease throughout the environment. The set of characteristics of this whole disease where the protracted incubation period, shedding infectious agents through bodily fluids for the majority of that incubation period, the infectious agent persists in the environment for years out to decades. I mean, if you wanted to stack the deck for a disease, you couldn't come up with a better

set of characteristics. Plus, they look perfectly healthy. So we have no idea that they're diseased until later on in the disease progression. Now, is there a prevalence in, or is there a higher prevalence in deer versus moose versus elk or anything else? We tend to see higher prevalence in the deer species, white-tailed deer, mule deer, in isolated areas than we do in either elk. Moose, there's only been, you know, worldwide, there may have only been 10 positive news okay to date and it's likely and it doesn't seem that they're less susceptible it's just that they're likely haven't been exposed because they're not in the same systems and there are there moose tend to be solitary solitary just fewer in

Wisconsin they can you know periodically a single a single yearling will wander down from northeastern part of Minnesota, but very, very rare. What about wolves? Have wolves contracted it yet? Wolves are an interesting story. So to date, there's no evidence that any canid, any member of the dog family has ever developed any TSE. They never got BSE as far as we know. No evidence that any canid, any member of the dog family has ever developed any TSC. They never got BSE as far as we know. No evidence that any canid has gotten CWD. Now that could be a real observation. It could also be that we haven't done enough science on it. Okay. But there's certainly exposure. As opposed to cats, in the BSE situation, both great cats and domestic cats got a TSE, it was referred to as feline spongiform encephalopathy, and it was from consuming BSE-contaminated meat. Okay?

Very similar to how humans... Mountain lions. Yeah, great cats. Which most certainly consume deer on a regular basis. Now, with CWD in North America, again, we have no evidence that any mountain lion or any great cat or small cat has contracted CWD. In fact, it's very interesting. In a research study in Wyoming that I was a part of, it turned out that the highest source of mortality for CWD-positive deer was mountain lion predation. And so somebody's going, aha, CWD doesn't always kill deer. Well, but it predisposes them. So think about that progressive neurological degeneration

and think about how mountain lions hunt. They're ambush hunters. So if you're a deer and you're not quite right, you know, I mean, this disease is developing in your brain. You're progressing progressive dementia. It's not at the point where we are humanized, which really are very, very poor. We can't see disease yet, but disease is progressing. And an ambush predator can leverage that and take advantage of that in that weakness in the prey. See the same thing in Colorado. Studies have identified that CWD positive deer tend to get hit by cars more often than CWD negative deer. It's very logical. So now let's extend that to wolves and ask the question, could wolves be a management tool for CWD? Okay. Wolves are present in Northern Wisconsin, you know, a lot of other locations.

And at some point, wolves and CWD will meet. So there's been mathematical models developed, which are, there's a lot of assumptions built in those models, but it leaves it as an open question. Could a large coursing predator whose vision and senses are much more acute than ours could they take advantage of this disease in earlier stages and so when disease meets geographically wolves could wolves slow or maybe stop the progression of disease because they're because they're taking the weak and the... The sick and the old. Right, but they still wouldn't stop the excretion,

and they still wouldn't stop all of the bodily fluids. Right, so could they slow the spread or stop the spread? Maybe. Could they reverse disease? You could likely take all the predators you could find, wolves and mountain lions, and dump them into Iowa County, just south of where Doug lives, and they likely would not be able to eliminate disease. But as disease spreads geographically at the intervase, could predators be an effective tool to slow or stop disease from spreading?

to slow or stop disease from spreading? It's an interesting question, especially when states are contemplating more aggressive control measures, opening up hunting and trapping seasons to reduce population densities of wolves. So we don't have good tools. And I'll leave it an open question. Do we want to take that potential tool

and take it out of the toolbox? And what about, okay, so a wolf, well, a coyote by us, you know, they're eating deer die in our woods. We found a dead one last time Steve was there, and I was very suspicious of it being a CWD because it was a two-and-a-half-year-old buck. It was laying there, and it turns out it was probably hit by by a car but it was fairly well consumed by coyotes by then um and i cut the head off of it and sent it in and it came back non-positive um what happens when that coyote which is going to travel well they aren't traveling huge distances but say he's eating a cwd positive deer on on the durian farm and he's running over to Bunker Hill seven or eight miles away because they do that. And he takes a dump over there. Yeah, we've done that.

Science has been done. And so it turns out if you take CWD, CWD positive material, you put it in the front end of a coyote, it comes out the back end of a coyote and it's still capable. It's still infectious. There's still infectivity in it. that's capable of transmitting disease. Now, you said mice don't get it. Rats eat coyote poop, correct? Yeah. Yeah, so they don't get it, though.

Not that we're aware of. But they could potentially spread it in their urine because they would be carrying it. So that coyote, you have to ask, so he could eat CWD positive material. He could poop it out X number of hours later, and he might be a mile or two away. So that's a fairly local geographic phenomenon. They could be spreading infectious material. Now you have to ask yourself more questions. When they defecate on the landscape, is a deer likely to encounter and

consume that material? Well, maybe not now, but it might be fertilizer two years down the road for plants that the deer could eat. But I think that's quite restricted. It's a localized geographic phenomenon. Okay. And that's something that we can do a hell of a lot about. It's hard to. okay and that's something that we can do a hell of a lot about it's hard to same thing um with with crows you can put cwd in the front end of a crow or probably other scavengers and cwd comes out the back end about four hours later so you could ask yourself the question how far does a crow fly in four hours and is a deer likely to consume crow poop so these have been shown to be possible in a laboratory environment, but how much they really apply out in the field is of question. So we go back.

We know that deer to deer to deer to deer, we see that slow diffusive process on the landscape. That's the biggie that's going on just south of him and now is past him. Then we have that anthropogenic movement, you know, humans moving at long distances and the potential for agricultural commodities to be involved. I mean, there's likely other things like crows and coyotes, a proof of concept in a laboratory, but whether they're really happening in the field is an entirely open question. And if they are, how big are they as compared to these other features? So why not do the, you know, and some of the detractors will also say,

well, you can't stop deer from doing deer activities, right? Licking branches, licking each other, those normal deer activities. But if we're concentrating them in an area, let's say a mineral lick, where every deer in the area comes through there and licks that. Or a feeder. Or a feeder. You know, a bait um and and we've seen bait i mean i've seen bait piles where there's a pile of corn there's a pile of apples well they're all eating off the same pile you got all these deer coming into that that's something we can do something

about there are all these natural movements that we can't do anything about. But if we can slow the spread by stopping these unnatural gatherings of deer and these unnatural spreading of the disease, why wouldn't we do that? Yeah, there's a few things. You keep honing in on, there's these anthropogenic factors. And then what can we do where disease is, truly is? The things you're talking about, the baiting and feeding, artificial congregations of animals. Where TB is in Michigan, you can't bait and feed. And in Wisconsin, some of the other states where CWD is, you can't bait and feed deer. The idea is you're artificially congregating them. So remember that single deer, we saw him up there on the screen, who's shedding copious amounts of saliva. So if that deer goes up to a pile of corn on the ground,

he's sharing, spreading infectious agent into that corn. It can persist on that corn for a long, long time. Decades. Healthy, naive, susceptible animal comes up and eats that corn or licks that mineral lick. And it's likely that that animal is ingesting a viable infectious agent and can transmit disease. The analogy there is daycare. If you want to get your kids sick, your three-year-old kids sick, what's the best place to do it? Send them to daycare.

Daycare, the analogy there is that pile of corn on the ground. So if every child that ever goes to daycare is perfectly healthy, they're not little disease factories. But we know that's not the case. So they're a great place, and schools are a great place to spread disease, and then those kids come home and share it with you, and then you can share it with others, right? Same thing there so these artificial congregations if all the deer are healthy well then they can't be a place to transmit disease but we know that's not the case so it's one of those risk factors we can control but now you hit doug you know we get back to this

area where disease is established is there anything we can do? And there's certainly things we can try, right? We haven't exhausted the toolkit yet. Mike Samuel at UW is now retired. He looked at this from a mathematical perspective, and he's trying to leverage the idea that adult males have higher prevalence, right? So they are sinks for disease, they're gathering disease, and then they're shedders of disease as well. So what if in our harvest regime in hunting season,

we focused on adult males, okay? We hammer the bucks because they're the ones most likely to have disease. So we would lower prevalence in that we're reducing the proportion of the population with the highest prevalence of disease. The idea is if you knock that segment down enough that you would interrupt disease transmission cycles and you could actually lower herd prevalence over time now you still have the persistence in the environment but on from a modeling basis it works all right so now think about the deer hunter out there listening to me today listening this show today oh now they want us to go out and kill all the bucks

so it's not going to be a very desirable from a a hunter's perspective, tool. So all the tools we have, you consider these like medicine for a disease. They're very bitter. It is a bitter pill. You were there when we were still wearing the sombrero if you shot a smaller buck or whatever, and we had a management idea that we wanted to grow some bigger bucks, but at the same time we were pretty lenient about it. We're not doing that anymore.

The deer I shot last year were deer that seven, eight years ago I wouldn't even take another look at. I shot the first buck I had an ethical shot at. Are they giving you more tags? No. There's resistance in the hunting community to that. That's unfortunate. It is unfortunate.

I'm not one of those people. I'm part of the County Deer Advisory Committee. We're giving more doe tags or antlerless tags because the other part of it, sure, we have a population, the bucks, because they're sinks, as he said, and they're spreading the disease and they're traveling more. You know, a doe and her family tend to kind of stay in one area a little bit more where the bucks have a bigger range. But the other thing is population. So one of the things that, for a couple of different reasons, I i mean you saw the number of deer that we have in our place um in richland county we have in excess of 75 deer per square mile of habitat and i know there's places in the country that are higher than that but um you know it's sort of a it's a big population and i'm i have issue with it for

a few different reasons one of them is disease the other one is that when i have too many deer, my little oak trees are getting, because they love those little oak trees, and they're getting chewed off and I'm trying to do multiple things. I'm not just trying to raise deer on our farm and on our woodlands. So, you know, that's one of the issues. So there's this demographic issue that Mike Samuel had been working on, but then there's the population issue as well. We're given four – when I was a kid, when you bought a buck license, you and four other dudes would get together and then fill out this form and send it in in, like, August to get what was called a party tag,

and you could shoot one doe between four people because we had um they were trying to manage the herd to have more deer because again when I was a kid seeing deer was a big deal it's exact opposite now so now you buy you get a buck tag and you get four antlerless tags with every tag that you buy in our county. What changed from when you were a kid? Where the population exploded? Well, management was a big part of it. And the management exploded.

I mean, I'm going to be 60 years old, Joe. It wasn't exactly. You look great. Well, thank you very much. As do you. Thank you. And Brian, you look pretty good too. Pretty good?

What the fuck? Jamie, on the other hand, over there. I don't know. He's the young buck amongst us. No kidding. No kidding. But, I don't know, of course. That's a pretty long period of time. And when you're controlling, because you don't have many deer,

and you're managing to increase the deer herd and you have a mentality out there that well i'm not going to shoot a doe because you know and they're having two fawns and this year at least in my area we're seeing a lot of does having three fawns that's you can see how how that growth of the herd would be pretty dramatic. Yeah, if you want a herd to grow, stop shooting does. If you want to take a herd down, shoot does. I remember back in grad school in Illinois, they gave away these little pins that hunters collected. And when you brought a doe into the registration station, you got a pin that said,

I shot a doe so the herd won't grow. People collected these little mementos. That's interesting. So during that time frame, like I said, I grew up a couple counties to the north and west of where Doug was. And in the 1960s, I mean, there weren't a lot of deer around there. And watch, as I grew up, we didn't shoot many does. The regulations in the state didn't allow you to shoot does.

By 1980, on opening day, I remember I counted 160 deer on opening day. Fifteen years before that, probably saw three, something like that. So exponential growth in the deer population over that point in time. The deer management program worked really well. Oh, yeah. We know how to grow deer. And then along with all of that that we've already talked about, the agriculture and the – The agriculture expanded.

Well, I don't know about agriculture. Food opportunities expanded. But, yeah. But, you know, it was always there. Absolutely. So it had the potential for all of the – you know, for this explosion. So there's an interesting – you know, I talk with folks in the state of Michigan, and they've got a relatively recent issue with CWD. And there's user groups out there that are trying to advise the state on how to manage CWD.

One of the groups is talking about, it's called antler point restrictions. The idea is a yearling buck, 18 months old, has fairly small antlers. And then as they get older, they typically get successively larger antlers. So a group is out there right now as an active proponent of implementing antler point restrictions and promoting antlerless harvest at the same time, okay, as a disease management tool. So as we noted, you know, lowering the population in the areas that already have CWD is beneficial in that if we have a herd of 500 animals with 10% prevalence, that's 50 positives, of 500 animals with 10% prevalence, that's 50 positives, versus a herd of 20 animals with 5%, which would be one, and that's a dramatic difference. The prevalence is the same, but we have fewer positives out there, right? So lowering populations overall does make sense with regard to disease, okay? But now the other part of antler point restrictions is allowing males to get older.

And they argue that that will keep hunters engaged. And if hunters are engaged, they'll shoot more does and keep the population down. And that'll be a good thing. But, you know, we've already discussed how adult males tend to have the highest prevalence of CWD. And so now you're talking about promoting, pushing more males into these older age groups in an area where CWD is already known to exist. And so from a biological perspective, from a numerical modeling perspective of disease, I fail to see how this can work.

So will it keep hunters engaged? That's a sociological question that I can't really address. But from a purely biological disease-driven process, promoting more older-aged animals, older-aged deer in a population with CWD, I cannot figure out how that could be beneficial. That seems the opposite. I'm hoping that through this podcast, this information becomes more digestible because I think that in order to get what you just laid out over two hours, in order for someone to get that by reading, it's like they're not going to do it. Most hunters are just not going to do it. So I have a feeling that, like what Ted Nugent had said, that this is a – his perspective is possibly way more prevalent than should be.

And because this information is not that digestible, I think that there's – I know you talked about it on meat eater episode 70 and then now today this is going to reach a lot more people and it's in a very digestible form where they can just sit down and listen to it and hopefully we can get the word out on this in a way that it's not

getting out now so people understand the consequences of this this is a real issue and this is not simply like hey we don't want to do this because this could negatively impact our hunting opportunities. We might not have any hunting opportunities in 10 years or 20 years. This literally could devastate the entire population of deer. This is not a simple thing. This is an incredibly complex thing with a terrible disease that is 100% fatal

and is absolutely spreading. No question. Some of the, you know, the take-home points I always think, and I get regularly asked by hunters, well, what can I do? Okay, well, what do hunters do? They sit at deer camp and they shoot the crap around, you know, whatever, libations or whatever. And they shoot the crap around, you know, whatever, libations or whatever. And they're going to talk about things like CWD and good. So let those conversations be driven by fact and science as opposed to rumor and innuendo. Right. That's what we're doing here today. And that's why I think this public information is so important.

There's other things it can do. We talked to, you know, Doug hit on a bunch of them. You know, hunting is part of promoting a healthy deer herd. Hunt deer. Keep populations low. Test your deer and manage those carcasses. Don't leave them out on the landscape. There's another category, though, of things that can be done.

You know, in deer camp, what's the easiest thing to do? It's blame the DNR for everything, the Department of Natural Resources. Okay, it's almost a sport to kick around at night and see who can insult the DNR the worst, right? So with regard to disease, though, is that really an effective use of your time? It might be fun, but it's likely not effective. Because think of these state management agencies that deal with deer. It might be the Agriculture Department or the Natural Resources Department. They're very, very restricted in what they can do. They're within a legislative, they operate within a legislative framework. Okay. So if you really want to impact

change in how a government agency goes about its business, should you talk to the local biologist or should you talk to the elected leader who establishes the legislative framework that that agency works underneath? It's important to put pressure on our elected representatives. And we've seen change in that in, well, Wisconsin being a great example. Our management used to be science-based. Wildlife biologists making decisions about deer management. It's politically based now. Politicians are deciding. You'll often hear that in Iowa County, Wisconsin,

where this first effort started. Well, see, it didn't work up there. DNRs, you know, they had this idea, and it didn't work to stop the disease. It didn't get a chance to work because people— Social and political pressure... Social and political stuff. ...forced the DNR to vacate their plans and their aggressive measures. And even more recently, there was a court case.

The state of Missouri, the Missouri Department of Conservation, tried to implement some restrictions on the captive cervid industry to stop importation of live deer, seeing them as a risk factor. The deer breeders sued the state, went through, you know, the court system, and it was decided by the Supreme Court in the state of Missouri about three weeks ago that, in fact, all deer are, you know, represent wild deer, and that the Department of Conservation was well within their constitutional and legislative authority to implement measures designed to protect the integrity and viability of that deer herd for future generations. So the Supreme Court

said, yes, Department of Conservation, you do have the right to restrict import of animals into captive cervid facilities to protect the integrity of the herd. And the legislative part of it is really important, and I can't put too fine a point on it. Laws can be changed, and there's pressure to do that under a lot of different reasons. I've been a part of changing some legislation that had to do with forestry, and I know how it's done. And, you know, one of my favorite quotes from L.O. Leopold is, ethical behavior is doing the right thing even when no one's watching, and the wrong thing is legal.

So just because it's legal doesn't mean it's the right thing to do and it doesn't mean it's the ethical thing to do. Is there any potential to changing the limits, tag limits, or making them more widespread if they understand the issue with this and they understand that one of the main tools of handling this in a more effective manner and slowing the spread of this disease through the population of deer is reducing the population itself. I mean, even these hunters would resist this because it would limit hunting opportunities.

This could potentially be a large tool in the toolbox of conservation and stopping this spread. Short answer on that is yes. As I said, I'm on the County Deer Advisory Committee. We have the opportunity to give out as many tags as antlerless tags as we want. What about antler tags? Because that's the issue, right? One.

That's it. One per person? And that is legislatively controlled. But even with this disease, which that might be the number one tool to slow down the spread. We used to have a policy in Wisconsin called earn a buck. And it was not particularly popular with a lot of hunters because, you know, I want to shoot my buck. And I don't want to have to earn a buck. You to shoot a doe uh or less deer to earn a buck tag um and it wasn't particularly popular that's really a mild way to put it well it was vehemently opposed vehemently

opposed by a very noisy group of hunters just like and again with my experience with working with the legislature a small group of people making a hell of a lot of noise with a certain amount of money can change things it wasn't popular it was popular with me as well again you hunted on my farm um we shoot way more antlerless deer than we shoot bucks um When Earn a Buck was in place, we'd have a stack of buck tags because we were shooting so many does. That was because it was politically or socially became a political issue. It was rescinded. And so now what we found in Richland County is we can give,

we could drop antlerless tags from a helicopter, shoot as many as you want, and we're still going to kill. About the same number of does. About the same number of does. There's a little bit, there's been a little bit of an uptick. But when we had Ernebuck, we killed a shitload of them. You know, three times as many. as many and um it becomes a and i understand especially like casual hunters like you know gun hunters are a good example and bow hunters are you know different example because they're they're not as casual but they're more interested in and you know killing the big big buck a

generally um uh gun hunters yeah you go out there for two or three days. I mean, you were there. We froze our asses off. I mean, it's like, well, how long am I going to stay out here? We have a really short season. We initially had much longer season. When the CWD management first started, we had a much longer season. I loved it.

I got to hunt with folks that maybe had their own place to hunt, or I invited folks from the community to come in and hunt. Friends from different places came down and hunted. But again, a small, noisy group – and I don't know if small is – I don't know what the numbers are on that. But made that go away. So now we're back down to the nine-day season. That doesn't make any sense to me. Like, who gave in to that?

The politicians did. But why don't the politicians understand? And they're doing it from an ignorance, from a point of ignorance. They don't understand. Political pressure. Political pressure. I've got to hope that something like this podcast gets to them.

I sure hope so, man. I mean, I'm sure why we came out. This is a terrifying scenario. So the Wisconsin experience was really important. And the data shows that the first couple years of this aggressive management with Earn a Buck was actually forcing the population down. But it was very unpopular. And so political pressure was applied. and that tool was taken out of the toolbox, thrown on the ground. Immediately when you stopped doing earn a buck and you stopped

having longer seasons, the population trends reversed and started going back up. So it was easy to label, hey, the DNR failed. Their effort to eliminate disease by having aggressive seasons failed. Like Doug said, we don't know that because we stopped. We pulled the plug on the tool. Alberta, when CWD started really blossoming in Saskatchewan, Alberta was like, we don't want it. And they found their first handful of cases right on the border between Alberta and Saskatchewan, they raised the odds a little bit. They started harvesting deer from an aerial platform called a helicopter. Okay? That helicopter with government agents sharpshooting deer to try and basically eliminate deer in a buffer zone between Saskatchewan and Alberta, knock the diseased deer out, and create a buffer zone where disease wasn't.

Well, that was not very popular either. It went over like a fart in church. And landowners and outfitters went to the ministry and said, we can't possibly have this. And that program had every chance of being successful, and the rug was pulled out from underneath them okay so now it's a matter of time here we are uh you know years later and the western states you know montana colorado wyoming where disease has been a long time their wildlife health professionals i have put together a set of uniform management recommendations for the

Western states. Okay. And they're promoting the things that we've been talking about, reducing those artificial congregations of animals, implementing a harvest structure to focus on males. Okay. The male focused the most, the social group with the highest prevalence and also kind of what i guess i would refer to as hot spot shooting when you see a new spark of disease out there on the landscape get on it don't allow it to become established your only chance to be successful to eliminate disease is very very soon before it gets established and starts you know spreading so now we're seeing in wyoming Wyoming and Colorado and Montana, they're actively talking. They're talking to the media.

They're talking to their commissions. And they're talking about implementing these regulatory structures, at least on an experimental basis, recognizing that doing nothing is no longer an option. And that's one of the things that was learned from the Wisconsin experiment, for lack of a better word, that our failure, I mean, you know, the analogy that I often use is, you know, we had this car. And it was, you know, a pretty decent car, this pretty decent model of how we were going to control the disease. But, you know, they kind of let the oil go out of the car and they ran it in the ditch and banged it around and then brought it up and said, damn, this Ford doesn't run worth a shit. And you can't actively try to defeat something and then say it doesn't work. You really have to let it, you know, in the 15 years that I've learned about CWD,

is that not only is there a lot being learned about the disease, but there's been a lot learned about how to manage it, both on a scientific level, but on a social level as well. And I can tell you, man, if you don't have it, you don't want it. You know, 15 years ago, I felt, and there's so much more known now than there was 15 years ago um you know i feel like we it's not too late in wisconsin i mean we can keep slowing it down and we can protect the rest of the state but um we got a lot of work to do and um it takes a will but it really does take the medicine is very bitter i think it takes information too because i don't think people are really aware of the extent is very bitter i think it takes information too because i

don't think people are really aware of the extent of this disease or the danger of it or all the ramifications of it i agree i agree i'm surprised in my area intelligent people that i know that are casual hunters you know so it's getting to be deer hunting time you know i'll talk to them what i'm like ah they don't really well you know they don't know they don't know yeah that yeah yeah and that really is one of the things so you know i appreciate so much the opportunity to come out here and talk about it and and brian and and mike samuel um are going to come to richland center in september uh which is you know the the uh capital or county seat of Richland County, and we're going to do another presentation on chronic wasting disease,

and we're advertising it widely. And more of that information has to get – education is a big part of it, Joe. You're exactly right. Yeah, I just don't think there's enough digestible education. And I think this sort of form is one of the most digestible all you have to do is you put it on your car you drive around you listen to it you put it in your headphones you're at the gym you'll get this information you'll get it in a in a way that you're probably not going to sit down and go through these studies yeah i appreciate it as well

i mean i'm pretty uh not very savvy on social media and things like that i wasn't even sure what a podcast was when when you know steven renault you know asked me to come on and do meat eater and so we did that and um i i understand now it's been downloaded like 650 000 times okay which for a scientist you know i've been an author on a lot of peer-reviewed papers, and I can guarantee you they haven't been read. You take a couple zeros off of there, and that's probably the readership on those things. So from an impact, being able to get a message out to people, this type of forum really, really is helpful.

And getting it down, like you say, down to a level that, you know know hunters can understand and digestible i think is very very important because we talked about how misinformation active misinformation to try and you know hey it's not so bad or look over here don't look at this look over there you know these diversionary tactics are very very successful they were very successful with tobacco they were successful with other scientific endeavors today. And also the simplistic perspective that, hey, look how many deer get killed by winter. It's way more than CWD. Stop crying wolf. Yeah.

It's a diversionary tactic. Here's the other thing that I'd like to bring up about that. I've killed some big deer. And I get it. Guys want it. People want it. Hunters want to do that. They want to kill.

It's what they look forward to. They look forward to hunting season. It's only one time a year. Yeah. And you get to do that as we're not just hunters. We're conservationists. What we do is going to affect the future. And we have an obligation to do what's best for the resource and what's best for the future.

And I'll tell you this. Last year, I shot a two and a half year old buck opening day and uh this is a nice little eight pointer and i celebrated that deer i enjoyed that deer i remember that moment just as much as the 200 inch buck that i killed. It's different, but it concerns me that at times we get so wrapped up. And I was one of them, man. I feel like a recovered alcoholic sometimes about the whole antler thing. Like, hi, I'm Doug, and I used to be an antler.

It's a 12-step process. Well, and there is a part of that. But remember what the joy of hunting is and the reason for it and how important it is to make sure that that continues into the future. There have been some folks who really sounded huge alarms about this. And you talked about it a little bit. Yeah, 20 years from now, it could be, well, it might take a generation or two, but it really could become that.

I want to be able to eat the meat. And I want to know that in future generations, you know, 100 years from now, and that farm is still there and it's still in the Durham name. It's been in my family for 115 years. I want to know that 100 years from now that my descendants and their friends and their family are going to be able to come there and still enjoy that. And in order for that to happen, just like when I'm managing my oak trees, so that 100 years from now there's going to be those big oak trees there again. 100 years from now, we have to do what we need to do now in order for this opportunity to be there for the future. Our hunting heritage is huge, not to mention the economics of deer hunting.

In a place like Wisconsin, there's over 650,000 people that hunt deer. They pump in excess of $1 billion every year into the economy of the state of Wisconsin surrounded by hunting. If we put that on a national basis, there's millions of hunters and more billions of dollars spent. So it's not a small thing when you think about, you know, the economics of hunting. But the heritage of hunting is very, very important. I mean, I've been hunting my whole life. Yeah. You know, now I hunt primarily one

county west of him and, you know, CWD is coming. I'd say I'm sitting in my tree stand three years ago and CWD is in the next county over. Two years ago, the first CWD positive deer in Crawford County, Wisconsin was detected less than two miles to the southwest of the tree that I'm sitting in. Last year, CWD had been detected in a second deer in Crawford County, this time one mile to the northeast of where my tree stand is. I find myself looking at deer differently. I'm looking for those subtle cues of disease, and it's changing the experience. I get calls pretty regularly from hunters who are like, you know, really?

It's a coin flip out there? I'm not so sure I want to hunt there anymore. I know because I'm on that deer advisory committee, a group of hunters came in who bought land south of us, you know, 20 miles south of us, in a significant portion. And they bought it to manage it for bigger bucks and population and all that. They came into the County Deer Advisory Committee and talked to us about what they're doing. They shot 43 deer on that property last year. So what they're doing, they shot 43 deer on that property last year.

All of the bucks tested, all of the antler bucks tested positive for CWD. About 25% of the does and some of the fawns. So a doe fawn who has CWD and she's going to be clinical and die in two years, she's never going to have fawns of her own. That's a population issue. But what I, you know, and I hope those guys are listening, what I applauded about them is what they've done is really worked with bringing in other people. And I'm going to do the same in our place.

Bringing in more people to hunt, to take more deer, and to do what they can to manage it. Because they saw it. Well, you know what? They're not seeing big old bucks anymore because they're dead. They're dying. They're finding them, but they're finding them dead. We've seen that in Wyoming. We look at the long-term impacts of disease.

I talked a little bit about population impacts, driving populations down. The other thing we would identify is changes in that demographic structure. So you, you know, when you're hunting for the big antler deer, you're looking for animals that are four or five years old, mature or over-mature animals. In an area where CWD is established at high prevalence levels, those animals are not going to exist or will be extremely, extremely rare. They're rare now. There's an example of a real large ranch out in Wyoming. It was about 100,000 acres, and they managed historically exclusively

for these over-mature mule deer, you know, the ones with the antlers, you know, like that monstrous mule deer. Even in the good times, they probably killed maybe three of them a year, something like that, on that vast acreage, because, you know, there's a lot of sources of mortality. They're not anymore because, you know, those deer aren't living that long. Think about it, a math question, math quiz for Duren here. So in this population with super high prevalence, so let's say at 18 months of age, yearling deer, let's say they have 20%

prevalence, and we have that. We've demonstrated that. At two and a half, it's probably 30% prevalence. At three and a half and four and a half and above, it's close to 40, 45, 50% prevalence. So this is a two-year disease, right? So half your prevalence dies every year. So if you have 20% prevalence, half of those deer are going to be dead the next year and half the year after that. Okay. So over time, you would expect these cohorts to diminish. So the math question is, in that population, how many five-year-old bucks are there?

Because disease penetrance grows over time. The answer is not many. It's not many. Come on, man, I'm supposed to answer that. Sound the alarm. Yeah, no, and that really is the case. And it's, you know, again, that's why I wanted to bring Brian along, because he's going to provide the science, and I'm going to try to break it down to, you know, Doug's level,

and hopefully that, you know, folks can understand. And I know I get emotional about it, but, you know, part of it is. You care. Yeah, well, my dad would have been 94 years old today. And he's the guy that I started deer hunting with. You know, he died a couple years ago. And he grew up with that farm. You know, it was my great-grandfather's farm.

And that area and the driftless area, and you've heard me talk about the driftless area before and how important that area is to me. And this is a big, you a big part of that area. It is an emotional thing for me, which is why I then look at the science and what can we do about this. And I think about, you know, I think about Elder Leopold. What would Leopold do right now? I mean, what would he be thinking about this? You know, my old man would be thinking about this.

You know, I know what my dad would be saying. He always thought my antler thing was uh bullshit he every time he'd see a buck on the trail camera go shooter he just he was just like he was just an old school buck hunter man he had an antler on it you shot it um so all those things are in my head as i think about this and uh you know it's know, the emotion's important, and I get the emotion part from all of these folks. And I understand that some of them want to kill big bucks, and, you know, maybe because I have killed a couple of big ones, it's not as important to me.

Maybe it has something to do with being 60 years old. Well, it's also you understand the consequences. I mean, this is a real serious issue. Forget about the ego of killing a big buck or, you know, this desire to achieve something that's more difficult than shooting a young one. There's more at stake here. Yeah. So you brought up an interesting thing. What would Leopold do? And, you know, I mean, kind of a Leopold disciple, you know, father of modern wildlife ecology, started the first program of wildlife ecology at University of Wisconsin. In the 1940s, populations of deer in the northern part of Wisconsin were growing by leaps and bounds.

And they were dramatically changing the landscape, you know, denuding the landscape, you know, eating eastern white cedar. And deer in northern latitudes tend to yard together in the wintertime. And so Leopold knew that this was deleterious to the long-term viability of that ecosystem. Unsustainable. He took people out, landowners out and hunters out into these deer yards in the spring to show them how there was nothing to eat within reach of a deer on its hind feet. And there were bodies of dead deer that had starved through the wintertime in order to demonstrate to them the consequences of mismanagement of deer herds. So he was a

real proponent of showing people the results of doing things the wrong way and education. So I think, you know, it comes back back it's what we're trying to do not saying that you know we're leopoldian or anything like that but education getting information out getting accurate information out is maybe one of the biggest things we can do i think you guys did that here today so thank you thank you for being here brian thank you doug for organizing this putting it together i'm really happy we got a chance to talk and scared the shit out of me. Thanks for the opportunity.

My pleasure. Thank you, guys. Thank you.