I have been writing
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
Not-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) can be brought
about 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.
