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Friday, September 9, 2011


I have been reading about a disorder that intrigues me, Kuru (which means “shaking”) widespread among the Fore people of New Guinea in the 1960s. In around 3-6 months, Kuru victims go from having difficulty walking, to outbursts of laughter, to inability to swallow and death. Kuru, and (what we now know to be) related diseases, e.g., Mad Cow, Crutzfield Jacobs, scrapie) are “spongiform” diseases, causing brains to appear spongy. (They are also called TSEs: transmissible spongiform encephalopathies). Kuru clustered in families, in particular among Fore women and their children, or elderly parents.
They began to suspect transmission was through mortuary cannibalism.  Apparently this was deemed a way of honoring the dead, and was also a main source of meat permitted women. It seems that men also took part, but got first dibs on eating the muscle. Ending these cannibalistic practice all but eradicated the disease, which had been of epidemic proportions.

No one expected at the time that understanding the cause of Kuru would falsify an established theory that only viruses and bacteria could be infectious (the “central dogma”).  Some would say it led to a “revolution” in molecular biology.  The reasoning is of a standard form: There is some hypothesis H from which we derive some expected experimental results, E.  Here, H is the generalization:
All infectious agents have nucleic acid (equivalently, there are no anomalous pathogens).

If the experiment is done properly and yet results conflict with E, we may say there is an anomaly for H.  The anomaly can be abbreviated as not-E.  The anomaly here is that Kuru (like scrapie in sheep) is transmitted by a protein alone (by changing a normal protein shape into an abnormal fold). The first clues that no nucleic acids were involved in transmitting Kuru came from the fact that it is not eradicated with techniques known to kill viruses and bacteria.  Stanley Prusiner called the infectious protein a prion (he received a Nobel prize for his work on prion disease in 1997).  The anomalous results would not go away, and were demonstrated by experimental transmission to animals, mostly hamsters and mice.  It is generally accepted that hypothesis H is thereby falsified. The argument form is the familiar modus tollens:

If H then E
Therefore H is false.

The argument is deductively valid: it is logically impossible for the two premises to be true while the conclusion false.  One would get a logical contradiction.  Strictly speaking, however the empirical data do not logically contradict H. It is logically possible, despite strong evidence against this, that some nucleic acid is somehow involved.  Still, the data warrant denying H: the central dogma has been given a very good opportunity to be retained, and it has not been. Experiments on prion transmission rarely fail to give us results incompatible with H.  Instead, results are in sync with the “protein only” hypothesis: they are regarded as at least practically impossible under the assumption that H is true.  We might say they are statistically inconsistent with H. 
The “protein only” anomaly (the not-E) is "reproducible at will" (as Popper would say).  Or, to adapt what R.A. Fisher says in relation to the test of significance, a phenomenon (that is anomalous for H) is experimentally demonstrable when we know how to conduct an experiment which will rarely fail to give us a result that is statistically inconsistent with H.  A lot of negations, but clear enough.  Note: it is not that infectious protein events are “very improbable” in their own right (however one construes this); it is rather that these events are counter to, and forbidden under, the assumption of the hypothesis H.
The underlined portion of the last sentence, obvious as it is, is my main point just now.

Popper, K. 1959, LSD, 203.
Fisher, R.A. 1947, The Design of Experiments, 14

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