Thanks for the additional information. Now, here is an example of a
supposed fraud that actually turned out to be real, like Haeckel's drawings.
In 1968 a neuroscientist by the name of Georges Unger working at the Baylor
College of Medicine claimed to have isolated a peptide that would transfer
scotophobia (fear of the dark) to animals that did not display that behavior
[Unger, Galvan and Clark. _Nature_ 217, 1259-1261 (1968)]. He had taught
rats to be scotophobic (not a normal condition for rats), then harvested and
pureed their brains before injecting the extracts into mice. The mice then
displayed scotophobia without having been trained. Unger isolated the
peptide and demonstrated that it too would induce scotophobia in mice. He
named the peptide _scotophobin_. Four years later he announced that he had
sequenced and synthesized the peptide, and that the synthetic peptide also
induced scotophobia in mice [Unger, Desiderio and Parr. _Nature_ 238,
198-202 (1972)]. Unger then went on to isolate other fear-inducing peptides
before he died in the mid-Eighties.
The same pattern as for N-rays and polywater was repeated, with some
researchers being able to reproduce Unger's results in mice, goldfish and
hamsters (to name a few species), while others could not. [See Wilson.
_Nature_ 320, 313-314 (1986) for a short review.] Some researchers
questioned the accuracy of Unger's structure for scotophobin, some suggested
that the synthetic peptide could induce scotophobia but that no natural
scotophobin had ever been produced, some suggested that scotophobin simply
increased an animals overall level of activity so it only seemed like it
avoided the dark, and some suggested the whole affair was simply another
case of wishful thinking. It wasn't long before scientific historians were
comparing scotophobin with N-rays and polywater. Even today there are
historians, scientists and textbooks who claim scotophobin was a fraud and
that it did real harm to neuroscience. The parallels with Haeckel and his
drawings are too strong to ignore.
However, unlike N-rays and polywater, the transfer of scotophobia by
scotophobin was verified as a real phenomenon by the discovery of the
peptide's mechanism of action. A series of papers by Satake and Morton were
published in the journal _Pharmacology and Biochemistry of Behavior_ in 1979
[10(2):183-188; 10(4):449-456; and 10(4):457-462] which showed how
scotophobin could induce scotophobia.
In the first paper, the authors demonstrated that the pineal gland was the
likely site of action for scotophobin. They noted that scotophobin
increased dark avoidance, increased shock sensitivity and suppressed the
norepinephrine-induced aggregation of chromatophores in goldfish. The
researchers also noted that goldfish that had undergone a pinealectomy were
reported to show the same results. Finally they noted that chromatophore
aggregation was controlled in part by pineal melatonin.
In the second paper, the authors demonstrated that scotophobin inhibited the
pineal enzyme hydroxyindole-O-methyl-transferase (HIOMT) which is necessary
in the biosynthesis of melatonin (a neurotransmitter). HIOMT converts
N-acetylserotonin (NAS) to melatonin by the transfer of a methane group
(methylation) from the methyl donor S-adenosylmethionine (SAM), producing
S-adenosylhomocysteine (SAH). Norepinephrine (another neurotransmitter),
which decreases dark avoidance, is known to induce this reaction, whereas
SAH, serotonin (another neurotransmitter and precursor to N-acetylserotonin)
and NAS itself increased dark avoidance. This suggested that increased dark
avoidance was linked to an increase in NAS levels in the pineal and that
inhibition of HIOMT by scotophobin would cause this increase. To test this
hypothesis they measured pineal melatonin levels in the presence and absence
of SAH and scotophobin. The former, being a known inhibitor of HIOMT, did
indeed reduce melatonin levels; scotophobin did the same, reinforcing its
role as an HIOMT inhibitor. The authors later verified that scotophobin
directly inhibited purified HIOMT.
In the third paper, the authors determined the actual mechanism of
scotophobin. HIOMT binds SAM first, then binds NAS in close proximity,
creating a transitional compound by binding NAS to SAM directly. The
unstable compound then breaks about into melatonin and SAH, which are then
released. Scotophobin competitively binds to the HIOMT-SAM complex, thus
preventing the binding of NAS and the creation of product. The authors
noted that part of scotophobin's structure was similar to the structure of
NAS, thus reinforcing this model.
The point of all this biochemistry is to point out that, despite past and
present claims, Unger could have hardly committed fraud considering that the
peptide he had claimed to isolate did indeed have a specific biochemical
mechanism that induced scotophobia in chordates possessing a pineal gland.
How NAS induces dark avoidance I have not been able to discover, but that
does not invalidate Unger's specific claims. What is doubly interesting,
however, is that there is good evidence to show that Unger had made a
mistake when determining the structure of scotophobin. Yet despite this
mistake, his specific claims were verified and are now part of
neuroscientific theory, even though scotophobin has not received the
_popular_ recognition it should have.
The take home lesson with regards to Haeckel and his drawings is that it
demonstrates that Haeckel could have been inaccurate, yet his drawings still
correctly portray the basic elements of his biogenetic law and
recapitulation. It also demonstrates that if the biogenetic law and
recapitulation have some basis in reality (which they do) the inaccuracy of
the drawings will not prevent scientists from discovering that basis.
Unfortunately, it also demonstrates how powerfully self-deceptive people can
be once they decide a scientific phenomenon is a fraud, and how they
perpetuate that self-deception even when there is proof that can be easily
found that refutes their belief.
So while N-rays and polywater teach us the folly of excess credulity,
scotophobin and Haeckel teach us the folly of excess skepticism.
Kevin L. O'Brien