Various shenanigans within the Indonesian palaeoanthropology community have hindered evaluation of all the evidence surrounding the diminutive adult female skeleton found in Liang Bua cave on Flores in 2003. Her skull was damaged after prolonged examination by a leading national figure in the science, and now further excavation in the cave has been blocked indefinitely. Whether she is indeed a member of new species of hominin, Homo floresiensis, or merely an individual modern human dwarfed by some genetic defect, as some claim, seems closer to resolution (Morwood, M.J. and 10 others 2005. Further evidence for small-bodied hominins from the Late Pleistocene of Flores, Indonesia. Nature, v. 437, p. 1012-1017). During the 2004 field season at Liang Bua the Australian-Indonesian team unearthed remains of nine other individuals of similarly diminished stature. They included another jaw bone that is virtually identical to that of the first ‘hobbit’: neither have the chins that unify all fully modern humans. Significantly, the new piece of lower jaw is dated at some 3 ka older than the original, so the chances of both being from physiologically unfortunate modern humans are remote.
The new finds also include stone tools, more advanced than any found in association with one of H. floresiensis’s possible ancestors, H. erectus. Whoever they were, the ‘hobbits’ also butchered prey and cooked meat. There is negative evidence in support of the new species hypothesis too: compared with human sites of the Late Pleistocene, Liang Bua is conspicuously lacking in evidence for any form of art. But the idea is not proven. It would take a definite association between fossils and tools, as for instance in a burial, to show that the implements belonged to ‘hobbits’ rather than having been introduced by a fully human visitor. Moreover, should any evidence for moderns be found in Liang Bua or other caves of interest, the possibility of mixture of cultures and fossils would leave things up in the air.
It is worth noting that Indonesian scientists are not the only ones prone to obstructive tactics as regards hominin sites. They have long been a bone of contention throughout Africa, where both local and visiting scientists have tried to throw spanners in their colleagues’ research ambitions.
See also: Dalton, R. 2005. More evidence for hobbit unearthed as diggers are refused access to cave. Nature, v. 437, p. 934-935; Lieberman, D.E. 2005. Further fossil finds from Flores. Nature, v. 437, p. 957-958.
Congenital disease, human migration and population growth
The way in which genetic features are inherited has become a key feature in distinguishing human populations, the time and route of their migrations as separate groups, and when they merged with other groups. The most familiar outcomes are those based on mitochondrial DNA and lines of female descent that show with little room for manoeuvre, that all of us descend from Africans alive around 150 to 200 ka. Studies of the male Y chromosome help fine tune the record to show short periods when either populations fell so low that human survival passed through only a few small bands (e.g. around 70 ka) or Big Men corralled most women for their own purposes (the now famous case of Ghengis Khan’s genes still dominating the genetics of Central Asian people). Dennis Drayna of the US NIH outlines yet another revealing feature of genetics with historical connotation in the October 2005 issue of Scientific American (Drayna, D. 2005. Founder mutations. Scientific American, v. 293(4), p. 60-67).
Disabling congenital diseases, such as cystic fibrosis and sickle-cell anaemia, together with adverse reaction to alcohol and the ability of adults to tolerate the lactose in milk, are all passed down generations in different ways. Understanding the genetic processes involved obviously stems from medical research on genetic mutations so as to identify groups that are at risk. From it has emerged details on the structure and location of the responsible genes in chromosomal DNA. The feature that unites the four examples above is a special repetition of the same kind of mutant structure. Inherited conditions involve either different mutations in a single gene, or the identical change at a specific location. Of the latter, it seems the most common is an innate tendency in DNA for the same mutation to affect a specific gene – so called ‘hot-spot’ mutation, which occurs in unrelated individuals. More rare is a defect that is embedded in a length of DNA (a haplotype) whose structure is identical in all those who carry the mutation. That common identity suggests that the mutation arose once and has been passed down subsequently; a ‘founder’ mutation.
Since a ‘founder’ mutation arose at some time in the past it can potentially be used to trace population history, and so passes into the realm of palaeoanthropology. The fascinating and most useful feature is that the greater the separation in generations from the individual in whom the mutation occurred, the more restricted becomes the haplotype, in terms of its relative length in DNA. That phenomenon is a consequence of sexual recombination among descendants. In the founding individual, the whole chromosome is the haplotype, and the mutated part becomes increasingly ‘diluted’ with time. Measuring its length today harks back to the time of foundation. What has become clear is that not all founder mutations have any obvious consequence, and instead of being in as few as one millionth of a population, the general case for those causing disability and therefore conferring an adverse effect on natural selection, a few percent of people can carry them. Such abundance indicates either neutral effects or some subtle benefit to fitness. Diseases ascribed to them appear when both parents contribute the mutation: most are recessive.
A good example is a mutation of the HFE gene that confers above normal iron absorption, which is a decided advantage in protection against anaemia from iron-deficient diet. An individual with two copies vastly overcompensates and iron accumulates to deadly levels in their cells. Studies of its incidence in global populations indicate that it arose in Ireland, western Britain and Brittany and then spread south-eastwards. It appears to be a Celtic trait, although not from their original heartland in Central Europe but at the limit of their original migration more than 2000 years ago. Its haplotype is quite long and suggests a founder around 800 AD. There are no records of significant late Celtic migrations, and quite possibly the spread was through wide-ranging Vikings who dominated parts of the western British Islands at that time. A more fascinating case is the founder mutation that prevents people who carry it from tasting bitterness. Most people do experience bitter tastes, and that is very handy for avoiding toxic plants. About 25% do not. Maybe the mutation involved conferred some advantage, but the fact is that the haplotype is exceptionally short, representing a foundation at about 100 ka. It occurs in Africa along with 6 variants of the bitter-taster gene, yet beyond that continent only one taster and the non-taster forms occur commonly. That tallies with the hypothesis of the major movement out of Africa to populate the rest of the world with modern humans, around 75 ka ago. The surveys go intriguingly further: should descendants of those African migrants have bred successfully and regularly with earlier Eurasian hominins (Neanderthals and Erects), then non-African versions of the bitterness detecting gene ought to be present among non-African populations. Not one ‘alien’ haplotype has been detected, and this novel approach seems to have lain to rest that particularly intriguing bit of sociology.