As just one example of the type of work junkscience does, take a look at this article Milloy wrote discussing the recent mad cow scare. While prions are certainly not completely understood, it seems likely that they are at the root of many diseases, including mad cow disease (bovine spongiform encephalopathy; see this Science article and its associated commentary). In an attempt to show that prions couldn't cause disease Milloy says,
"Despite Pruisner's Nobel Prize, however, it has not been scientifically established that prions cause any sort of disease ... Despite almost 10 years of intense research into the causes and potential ramifications of mad cow disease, the prion theory still does not satisfy the basic scientific test known as Koch's Postulates for whether a particular microorganism, such as a prion, causes a specific disease, such as mad cow."Milloy goes on to list Koch's postulates, one of which is that "the organism [infectious agent] must be isolated and grown in pure culture away from the host organism" (from Freeman's Biology, 2002). If we go with the hypothesis that the infectious agent of prions is solely a protein, not whole cells, it would be physically impossible to culture prions in pure culture separately from other cells. Thus prions will never satisfy Koch's postulates (at least as I understand them). This is not necessarily a problem, however, as many other parasites also fail to satisfy Koch's postulates, though we clearly understand that they can cause serious physiological problems.
In questioning whether humans can get variant Creutzfeldt-Jakob disease from cows infected with mad cow (which is still somewhat open to question, I'll agree), Milloy says, "There is, in fact, no evidence that the 150 victims of nvCJD even ate infected beef, but it is assumed they did because no other explanation has been developed for how they could have contracted nvCJD."
Considering that known incubation times for Creutzfeldt-Jakob disease range from 1 year to more than 20 years, it seems near impossible to determine with certainty whether victims ate infected beef (data from CJD cases caused by neurosurgical procedures or treatment with Human Growth Hormone derived from cadavers; from this article). Can you remember the manufacturer and lot number of all the ground beef products you ate in 1985?
So if we can't know whether the vCJD patients ever ate infected beef, why do we suspect beef infected with mad cow disease was the cause? Here's some of the reasoning,
"Cases of vCJD in Great Britain and France raise the possibility that BSE has been transmitted to humans (6, 7). All but one of the 20 vCJD patients are 40 years of age or younger; the only other group of young CJD patients are those who received pituitary HGH during childhood. The neuropathology of vCJD patients is unusual, with numerous PrP amyloid plaques surrounded by intense spongiform degeneration (Fig. 4). These atypical neuropathologic changes have not been seen in CJD cases in the United States, Australia, and Japan (87). Macaque monkeys and marmosets both developed neurologic disease several years after inoculation with bovine prions (88), but only the macaques exhibited numerous PrP plaques similar to those found in vCJD (89)." (from Science)I've also looked at some other examples of Milloy's work, and they all seem similarly unconvincting.
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Importing comments:
Radagast
I appreciate the feedback, and I apologize if I have confused the issue rather than clarifying it. I based much of my post on the Science article I cited, and that article made it clear that no solid link between BSE and vCJD had been found. I searched briefly for further information, but after finding nothing other than non-experimentally backed statements saying only that vCJD was caused by BSE, I decided to take the safe route and say it was open to question.
I would love to know which references you're citing regarding the "glycosylation results". Are you referring to Collinge et al's 1996 Nature paper and Hill et al.'s 1997 Nature paper (which I just recently found)? If so, I'm curious how they respond to Prusiner's statement (in the Science article cited), "However, the utility of measuring PrP glycoforms is questionable in trying to relate BSE to vCJD (94) because PrPSc is formed after the protein is glycosylated (37) and enzymatic deglycosylation of PrPSc requires denaturation (95)." I haven't been able to get the full text of the two papers, so I don't know if they address the issue in the articles, or if I'm misunderstanding the whole thing.
I agree that there is a strong distinction between what the infectious agent is, where it comes from, and how it is transmitted. Do you (or anyone else) know of references examining the potential routes of transmission?
February 20, 2004, 10:13:04 PM PST – Like – Reply
John
"In questioning whether humans can get variant Creutzfeldt-Jakob disease from cows infected with mad cow (which is still somewhat open to question, I'll agree),..."
What is open to question about the glycosylation results?
"So if we can't know whether the vCJD patients ever ate infected beef, why do we suspect beef infected with mad cow disease was the cause? Here's some of the reasoning,..."
None of the evidence cited has anything to do with the route of transmission. Have you thought for 10 seconds about the dozens of different products from bovines with which you come into contact outside of eating?
To summarize, the evidence that prions were transmitted from bovines to humans is very solid. There is zero good evidence regarding the route of that transmission. Milloy conflates them to make the doubts about the route look like they argue against the source, while your conflation of the two points is almost as bad.
February 19, 2004, 8:48:29 PM PST
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