World distribution of the recent Microcephalin allele. The prevalence is indicated in black and the letter ‘D’ refers to the ‘derived’ or recent allele(Evans et al., 2005)
Almost a decade ago, there was much interest in a finding that a gene involved in brain growth, Microcephalin, continued to evolve after modern humans had begun to spread out of Africa. The ‘derived’ allele of this gene (the most recent variant) arose some 37,000 years ago somewhere in Eurasia and even today is largely confined to the native populations of Eurasia and the Americas (Evans et al., 2005).
Interest then evaporated when no significant correlation was found between this derived allele and higher scores on IQ tests (Mekel-Bobrov et al, 2007; Rushton et al., 2007). Nonetheless, a later study did show that this allele correlates with increased brain volume (Montgomery and Mundy, 2010).
So what is going on? Perhaps the derived Microcephalin allele helps us on a mental task that IQ tests fail to measure. Or perhaps it boosts intelligence in some indirect way that shows up in differences between populations but not in differences between individuals.
The second explanation is the one favored in a recent study by Woodley et al. (2014). The authors found a high correlation (r = 0.79) between the incidence of this allele and a population’s estimated mean IQ, using a sample of 59 populations from throughout the world. They also found a correlation with a lower incidence of infectious diseases, as measured by DALY (disability adjusted life years). They go on to argue that this allele may improve the body’s immune response to viral infections, thus enabling humans to survive in larger communities, which in turn would have selected for increased intelligence:
Bigger and more disease resistant populations would be able to produce more high intelligence individuals who could take advantage of the new cognitive opportunities afforded by the social and cultural changes that occurred over the past 10,000 years. (Woodley et al., 2014)
Bigger populations would also have increased the probability of “new intelligence-enhancing mutations and created new cognitive niches encouraging accelerated directional selection for the carriers of these mutations.” A positive feedback would have thus developed between intelligence and population density:
[…] the evolution of higher levels of intelligence during the Upper Paleolithic revolution some 50,000 to 10,000 ybp may have been necessary for the development of the sorts of subsistence paradigms (e.g. pastoralism, plant cultivation, etc.) that subsequently emerged. (Woodley et al., 2014)
What do I think?
I have mixed feelings about this study. Looking at the world distribution of this allele (see above map), I can see right away a much higher prevalence in Eurasia and the Americas than in sub-Saharan Africa. That kind of geographic distribution would inevitably correlate with IQ. And it would also correlate with the prevalence of infectious diseases.
Unfortunately, such correlations can be spurious. There are all kinds of differences between sub-Saharan Africa and the rest of the world. One could show, for instance, that per capita consumption of yams correlates inversely with IQ. But yams don’t make you stupid.
More seriously, one could attribute the geographic range of this allele to a founder effect that occurred when modern humans began to spread out of Africa to other continents. In that case, it could be junk DNA with no adaptive value at all. There is of course a bit of a margin between its estimated time of origin (circa 37,000 BP) and the Out of Africa event (circa 50,000 BP), but that difference could be put down to errors in estimating either date.
No, I don’t believe that a founder effect was responsible. A more likely cause would be selection to meet the cognitive demands of the First Industrial Revolution, when humans had to create a wider range of tools to cope with seasonal environments and severe time constraints on the tasks of locating, processing, and storing food. This allele might have helped humans in the task of imagining a 3D mental “template” of whatever tool they wished to make. Or it might have helped hunters store large quantities of spatio-temporal information (like a GPS) while hunting over large expanses of territory. Those are my hunches.
I don’t want to pooh-pooh the explanation proposed in this study. At times, however, the authors’ reasoning seems more than a bit strained. Yes, this allele does facilitate re-growth of neural tissue after influenza infections, probably via repair of damaged DNA, but the evidence for a more general role in immune response seems weak. More to the point, the allele’s time of origin (39,000 BP) doesn’t correspond to a time when humans began to live in larger, more sedentary communities. This was when they were still hunter-gatherers and just beginning to spread into temperate and sub-arctic environments with lower carrying capacities. Human population density was probably going down, not up. It wasn’t until almost 30,000 years later, with the advent of agriculture, that it began to increase considerably.
The authors are aware of this last point and note in it their paper. So we come back to the question: what could have been increasing the risk of disease circa 39,000 BP? The authors suggest several sources of increased risk: contact with archaic hominins (Neanderthals, Denisovans), domestication of wolves and other animals, increasing population densities of hunter-gatherers, and contact by hunter-gatherers with new environments. Again, this reasoning seems to push the envelope of plausibility. Yes, Neanderthals were still around in 39,000 BP, but they had already begun to retreat and by 30,000 BP were extinct over most of their former range. Yes, we have evidence of wolf domestication as early as 33,000 BP, but livestock animals were not domesticated until much later. Yes, there was a trend toward increasing population density among hunter-gatherers, but this was not until after the glacial maximum, i.e., from 15,000 BP onward. Yes, hunter-gatherers were entering new environments, but those environments were largely outside the tropics in regions where winter kills many pathogens. So disease risk would have been decreasing.
I don’t wish to come down too hard on this paper. There may be something to it. My fear is simply that it will steer researchers away from another possible explanation: the derived Microcephalin allele assists performance on a mental task that is not measured by standard IQ tests.
Evans, P. D., Gilbert, S. L., Mekel-Bobrov, N., Vallender, E. J., Anderson, J. R., Vaez-Azizi, L. M., et al. (2005). Microcephalin, a gene regulating brain size, continues to evolve adaptively in humans, Science, 309, 1717-1720.http://www.fed.cuhk.edu.hk/~lchang/material/Evolutionary/Brain%20gene%20and%20race.pdf
Mekel-Bobrov, N., Posthuma, D., Gilbert, S. L., Lind, P., Gosso, M. F., Luciano, M., et al. (2007). The ongoing adaptive evolution of ASPM and Microcephalin is not explained by increased intelligence, Human Molecular Genetics, 16, 600-608.http://psych.colorado.edu/~carey/pdfFiles/ASPMMicrocephalin_Lahn.pdf
Montgomery, S. H., and N.I. Mundy. (2010). Brain evolution: Microcephaly genes weigh in, Current Biology, 20, R244-R246.http://www.sciencedirect.com/science/article/pii/S0960982210000862
Rushton, J. P., Vernon, P. A., and Bons, T. A. (2007). No evidence that polymorphisms of brain regulator genes Microcephalin and ASPM are associated with general mental ability, head circumference or altruism, Biology Letters, 3, 157-160.http://semantico-scolaris.com/media/data/Luxid/Biol_Lett_2007_Apr_22_3(2)_157-160/rsbl20060586.pdf
Woodley, M. A., H. Rindermann, E. Bell, J. Stratford, and D. Piffer. (2014). The relationship between Microcephalin, ASPM and intelligence: A reconsideration, Intelligence, 44, 51-63.http://www.sciencedirect.com/science/article/pii/S0160289614000312