Now another group of researchers led by Peter J. Obendorf of RMIT University in Melbourne, Australia, is proposing that the hobbits were modern humans that suffered not from a genetic condition, but an environmental disorder known as myxoedematous endemic cretinism. Their report appears in the current issue of the Proceedings of the Royal Society B. The team argues that the largely complete skeleton, known as LB1, exhibits a number of distinctive features that are associated with cretinism, including an enlarged cavity for the pituitary gland and primitive wrist morphology. They further note that the environmental factors that lead to this form of cretinism--namely, iodine and selenium deficiencies, and the use of cyanide-producing foods, such as cassava--were potentially present on Flores.
The story doesn't seem to have received much press coverage here in the U.S., but is getting a fair amount of play overseas. Peter Brown of the University of New England in Armidale, Australia, who led the initial description of the little Floresians, has been quoted in a number of publications, including the BBC, as saying:
"The conclusions in this paper are not supported by the facts," he said. "The authors have not examined the original fossil, have little and no experience with fossil hominids and depend upon data obtained by others."
The news stories I've read don't contain much in the way of detail from outside commenters. So I thought I'd ask a few hobbit experts not involved in this particular piece of research what they thought about the new work. Suffice it to say, their responses were pretty damning.
First off, I e-mailed Matt Tocheri of the Smithsonian Institution, who published a paper in the journal Science last year describing LB1's wrist bones. His findings are considered by some researchers to be among the strongest evidence yet that the hobbits were a species distinct from our own. He had this to say about the authors' assertion that the hobbit wrist--in particular, the trapezoid bone--supports the cretinism claim:
"In the paper we published in Science, we provided the descriptive,
developmental, and quantitative details that demonstrate that
pathological disturbances do not turn a human wrist (normal or
pathological) into that of a chimpanzee or gorilla. We also
provided the comparative evidence that demonstrates that early
hominins (including LB1) retain wrist morphology inherited from the
Pan-Homo last common ancestor, whereas Neandertals and modern
humans share derived wrist morphology most likely inherited from
their last common ancestor. The speculation that LB1 has a
bipartite trapezoid is falsified by looking at the figures we
published in Science. A bipartite human trapezoid would have half
of all the trapezoidal articular surfaces missing while the
scaphoid and capitate would show the articular areas of the missing
half; but they do not, and all three bones articulate with one
another fully (just like in an African ape). Moreover, cretin
skeletons may sometimes show a bipartite scaphoid as the new paper
contends (this is because of how the scaphoid tubercle ossifies)
but LB1 does not have a bipartite scaphoid and is otherwise normal
(as are the capitate and trapezoid) but normal for an African ape
or primitive hominin.
60 or so million years of primate evolution provide the world with
a considerably large amount of evidence that the wrist of modern
humans and Neandertals is a recent acquisition in our shared
evolutionary history. Moreover, the evidence indicates this
acquisiton occured after the hobbits split from our hominin family
tree. New hypotheses of hobbit pathology arise every week, and
they will continue to disappear just as quickly afterward. The
phylogenetic evidence of the wrist is just not that easy to explain
I then asked paleoneurologist Dean Falk of Florida State University, who has studied the brain of LB1 (as revealed by a cast of the impresson it left on the braincase), what she thought about the allegation that the pituitary was enlarged. Obendorf et at. estimated on the basis of photographs published in one of Falk's papers that the cavity that housed the pituitary--the so-called pituitary fossa--was abnormally large, a sign of pathology. Falk sent me the following prepared statement:
"The Obendorf et al. paper prompted us to take another swim
through LB1's CT data in the region of the sella turcica, where the pituitary
lives. We had actually done this before when we examined LB1's skull for
pnematization. Earlier, we determined that we could not measure
the pituitary fossa precisely because of damage to the anterior and posterior
borders of the fossa. Now that we've reexamimined the CT images, we can tell
you that there is absolutely no way that the length of the pituitary fossa could be
12.9 mm. We used a measurement of 12.9 mm, which extended far beyond the
existing damaged borders of the fossa. The maximum length the fossa could
have been, in our opinion, is 9 mm - and we emphasize that this is a maximum
estimate. We also measured the 3D-CT reconstruction of LB1's endocast, of
which the authors' only examined a published 2D image of the 3D specimen,
which is a radiological no-no. As with the 3D-CT skeletal measurement of
the fossa, the 3D-CT endocast measurement of the fossa was far less than
She added that she and her colleagues "saw nothing in the images to indicate anything abnormal about the relative size of the pituitary gland or its fossa."
Ralph Holloway of Columbia University, another expert on fossil hominid brains who has studied LB1's endocast, had this to say:
"...the pituitary fossa on my endocast is, to my mind, tiny, and I don't get much more than about 6 mm in dimensions, either [anterior-posteriorly] or in breadth, so I don't understand where they have data to make such a claim. Of course, this area on my endocast is not the best preserved, but even still, I cannot see where it was possible that the pituitary fossa showed enlargement. Indeed, as I mentioned in my 2006 presentation at the AAPA meetings, I thought the smallness of the pituitary might have signaled some pathology!"
So there you have it. No love for the cretinism theory so far. I've got a couple more requests for comments out, so if I receive any additional responses, I'll post them here.
Update 03/06/08 6:00 p.m.: Paleoanthropologist David Frayer of the University of Kansas, a proponent of the idea that LB1 was an abnormal modern human, says he thinks that a growth disorder known as Laron syndrome is a better fit with the hobbit's features than cretinism is. (An Israeli team published a paper last year positing that Laron syndrome could explain the hobbit's traits.) But there are other reasons to think LB1 does not represent a new species, he remarks. Frayer also notes that he thinks the oft-repeated claim that 12 individuals are known from the hobbit site is misleading, because most of them are represented by fragmentary bones or teeth that don't reveal much about body size and brain size. LB1 is the only hobbit whose brain size is known.
Edited by katewong at 03/06/2008 1:19 PM
Edited by katewong at 03/06/2008 1:21 PM
Edited by katewong at 03/06/2008 3:02 PM
Edited by katewong at 03/06/2008 3:04 PM
The views expressed are those of the author(s) and are not necessarily those of Scientific American.