May 29, 2002

DEER DISEASE MADNESS

IMPLICATIONS FOR HUMANS

By Nicholas Regush

The plague is coming! The plague is coming! Mad Deer Disease, a chronic wasting disease, similar to Mad Cow Disease, may affect your brain.

Relax. It very likely won’t. The only thing it will affect is your peace of mind if you are going to be rattled by news headlines you are likely to see and hear before very long.

In fact, just mention Mad Deer Disease to almost anyone and I’ll bet it will immediately conjure up images of cows heaving and weaving from some form of neurological onslaught. That’s because Mad Cow Disease still has many people on both sides of the Atlantic wondering whether eating burger will result in a terrifying death and a brain full of holes to show for it.

Mad Deer Disease will also have people wondering whether an infectious agent will somehow manage to enter the food supply.

You’ll recall that most scientists believe that an infectious agent likely moved from sheep to cows.

How? The conventional wisdom says via the rendering of carcasses, to meat and bone meal in feed. The beginning of the Mad Cow epidemic was noted in 1986.

The human form of the disease began to turn up in Britain in 1995. Why? Because, according to the conventional wisdom, the infectious agent in cows was transmitted to humans by contaminated cooked meat products, had sufficient time to incubate and become destructive to the nervous system.

The key agent in the disease, again according to conventional wisdom, is a prion. Neither a virus, nor a bacterium, it is said to be an abnormally formed protein which can become infectious and capable of damaging the brain.

Now you may have noticed that I have already used the term "conventional wisdom" three times. That should clue you in on how outrageous I believe this theory of Mad Cow Disease is. In fact, I think this theory is worthless, shameful, has led to fear-mongering the likes of which we rarely see, and will ultimately prove to be a huge embarrassment for science and its increasingly lemmings-like behavioral patterns, more bluntly described as sucking up to the leaders of the pack.

Whether or not prions or mutated proteins actually exist, I’ll leave that to future metaphysicians to debate. As for their infectious nature, there is no appropriate scientific evidence that they infect anything. In fact, no one has ever fished out something known as an infectious prion. This is a theoretical concept. Nothing more! You can argue, if you want, for the notion of an infectious prion until the sheep or cows come home, but the available science is missing. All the huffing and puffing and scientific arrogance shown in regard to this type of criticism does not impress me one bit - because these princes and princesses of Ignorance do not know the difference between scientific evidence and speculation.

That’s why looking for an environmental explanation for Mad Cow Disease or any of the Mad-whatever-diseases (including deer, elk and mink) makes sense, if only to protect ourselves against putting all our eggs into one basket (which science has been doing).

I particularly like the innovative spirit of the theory put forward by David Brown of the University of Bath, who, on the basis of test tube experiments, points to metals such as manganese and copper as playing a triggering role in what is known as Mad Cow Disease. Brown thankfully parts company with the idea of an "infectious prion." He says the metal manganese can change a prion into its abnormal and dangerous form. And that this is especially true when the supply of copper to the cell is low.

Interesting. The prion part of this theory doesn’t sway me, but at least Brown is considering the possibility that environmental factors may be involved in Mad Cow Disease and its human form.

On a related front, an English farmer, Mark Purdey, theorizes that an organophosphate pesticide (Phosmet) was applied on the backs of cows along their spinal column, to fight off the warble fly.

When Mad Cow Disease erupted, Purdy found that it occurred on farms where the pesticide was used and not on those which, like his, wasn’t.

In his research in recent years, he has found that clusters of the disease, similar illnesses and a specific human form of the disease have occurred in geographic areas where the common factor in the environment (soil, water, vegetation) is manganese, and, in some cases, very large amounts of it, as well as low levels of copper.

Now isn’t it intriguing that there are low levels of copper in the soils in northeastern Colorado where Mad Deer Disease got started?

And in one small study, by Michael McDonnell, a Nebraska Elk researcher, when supplemental copper was fed to elk with the disease - let’s call it Mad Elk Disease, another chronic wasting disease - it stopped.

Let’s not get too excited about this, but let’s at least follow these sorts of clues. Why simply assume on the basis of questionable data that these types of diseases are transmissible?

Right now, Mad Deer Disease and Mad Elk Disease have the attention of government officials.

Deer are being slaughtered from helicopters. The chronic wasting disease has spread across 8 states and parts of Canada. It was actually first detected back in 1967 in Colorado.

One reason for the growing concern is that hunting is a $20 billion a year business in the U.S., Canada and Mexico. So, obviously this disease sooner or later was bound to be taken seriously.

Unfortunately government officials have been ditching themselves by not keeping an open mind about how disease develops and how environmental factors may play a role.