So we have established that pesticides can cause thyroid disease, and diabetes.
We have also established that thyroid conditions and diabetes have very interrelated roles with copper and selenium. With thyroid conditions driving and being driven by selenium deficiencies. While diabetes is associated with copper deficiencies. We have overlap among all of this, as both conditions are autoimmune, and metabolism rooted conditions.
We have also seen that during and after big game population declines, we see copper and selenium deficiencies in these animals, along with other related mineral deficiencies such as cobalt(B12) http://www.ncbi.nlm.nih.gov/pubmed/18655403
Enter CWD: So CWD had been known in Colorado since the late 1960's, when deer populations first entered free fall. But the spread and increase of cases was slow until the late 1980's/early 1990's, when it became a much bigger problem than it had been in the past. Just like back then, we are now seeing increases in cases of CWD, and we are seeing CWD in places we have not seen it before.
Copper, Prions, and CWD: So CWD is a "transmissible spongiform encephalopathy". It is wasting condition affecting cervids. CWD has a shared etiology with other conditions such as diabtes, ALS, and other metabolic/autoimmune/degenerative conditions http://www.ncbi.nlm.nih.gov/pubmed/21571086
where the aggregation of misfolded proteins are at the root of the condition/disease.
The biggest difference with CWD is that its misfolded proteins, known as Prions are infectious, and the condition can be spread from one individual to another.
But the similarities at a certain level are striking. Especially between Diabetes and CWD as they share many of the same features, AND TSE's like CWD can be misdiagnosed as metabolic disorders like diabetes. From this: http://wwwnc.cdc.gov/eid/article/15/9/09-0253_article
"However, if CWD in humans appears like a wasting syndrome similar to that observed in the squirrel monkeys in our study, affected persons might receive a diagnosis of a metabolic disorder and never be tested for TSE."
The copper connection: http://www.copper.org/publications/n...2/mad-cow.html
So infectious prions share misfolding with diabetes, and they also have a shared role of copper deficiency. Prions are copper binding proteins that can bind to several copper molecules. Infectious misfolded prions are copper deficient, and have had those copper receptors replaced with manganese. Copper deficient misfolded prions are not infectious, IF their copper receptors have not been filled by manganese. Therefor you need two thing to occur to predispose for initiation, and therefor increased transmission. One is copper deficiency like is associated with many metabolic disorders, and second is an increase manganese to fill the voids left because of copper deficiencies.
CWD, Manganese, and magnesium: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801312/
So if you apply a herbicide like a sulfonylurea or Amidazolinone which can biochemically induce insulin resistance in mammals and therefor lead to diabetes, and therefor copper deficiency. You have the makings for part of this. In many areas that have experienced big game declines in association with copper deficiencies, herbicides in the Sulfonylurea and Amidazolinone classes have been documented to have been used.
So if you are half way there, and all you need is more manganese, how does that happen? Well one way would be if the area is naturally high in manganese like the area around Fort Collins CO where CWD was first discovered in North America. The other way would be by chemical means. If you use a herbicide like Tebuthiuron to take off sagebrush, then you would see the following plants that are grown in this area have an increased manganese content for as long as a decade after. http://www.jstor.org/stable/3986813?...n_tab_contents
Not only will the manganese content be higher, animals will preferentially eat these plants.
So what do you think would happen if you used large amounts of Imazapic(An Amidazolinone) and large quantities of Tebuthiuron in the same area? Well, I'd bet on the potential for CWD.
Now guys like Lost will tell you that I can't prove this, and I just read some stuff on the internet. So lets step back and look at what animals that have frequented a real life place where tens of thousands of acres were treated with Imazapic and Tebuthiuron. While you can't look at them and make a CWD diagnosis, they do have malformed antlers like are seen in copper deficient animals: http://jwildlifedis.org/doi/pdf/10.7...-3558-24.4.656
And they now have access to plants with higher concentrations of manganese, that are shown to be preferred by animals.
Lost can probably explain it better as he has "degrees and 15 years of field experience". Though he should probably start with an explanation of why he does not understand "normal reference concentrations" as they pertain to mineral concentrations https://en.wikipedia.org/wiki/Reference_range
This is how those look with HIGH levels of selenium http://www.ncbi.nlm.nih.gov/pmc/arti.../t1-cvj_01_70/
If an animal was deficient or high in selenium in 1960, or 2015, it would chart against the same "reference values" You would think that a guy with degrees in the field would understand this. Or maybe that's the problem, maybe people with degrees, like Lost, are just that,.....well,....Lost, yet leading the charge on the past 20 years of failed attempts at "wildlife management".