My weekly posts are now appearing on The Unz Review(http://www.unz.com/). By accepting Ron’s invitation, I hope to reach a bigger audience and bring myself closer to other writers in the area of human biodiversity. When people work together, or simply alongside each other, minor differences can be ironed out and major differences narrowed or at least accepted good-naturedly. One thing I’ve learned is that academic debate can leave a legacy of hurt feelings. The impersonal can become personal, partly because people feel attached to their views and partly because views themselves can have personal impacts.
Working together also creates synergy. It becomes easier to identify research priorities, contact interested researchers, and end up with publishable findings. At present, most HBD research involves trawling through the literature and offering new interpretations. That’s fine, but we need lab work as well. This point came up in a 2006 interview with geneticist Bruce Lahn:
A lot of researchers studying human population genetics and evolution are strictly data miners (i.e., they generate/publish no original data). There are limitations to such an approach, as it depends on the available data and prevents certain analyses from being performed. Do you expect to see more research groups turning into pure data mining labs in the future? Or will there still be a place for independent labs generating their own data (for example, resequencing a gene in multiple individuals to study the polymorphism)?
Given the explosion of genomic data in the last decade or so, which shows no sign of slowing down any time soon, there is likely to be a proliferation of pure data miners just because there is a niche for them. But I suspect that many interesting findings will still require the combination of data mining and wet experiments to provide key pieces of data not already available in public databases. In this regard, labs that can do both data mining and wet experiments can have an advantage over labs that can only do data mining. (Gene Expression, 2006)
Lab work will probably have to be offshored, not because it’s cheaper to do elsewhere but because the “free world” is no longer the best place for unimpeded scientific inquiry. A Hong Kong team is conducting a large-scale investigation into the genetics of intelligence, and nothing comparable is being done in either North America or Western Europe. Cost isn’t the reason.
A few suggestions for research:
Human variation in IQ-enhancing alleles
We know that human intellectual capacity has risen through small incremental changes at very many genes, probably hundreds if not thousands. Have these changes been the same in all populations?
Davide Piffer (2013) has tried to answer this question by using a small subset of these genes. He began with seven SNPs whose different alleles are associated with differences in performance on PISA or IQ tests. Then, for fifty human populations, he looked up the prevalence of each allele that seems to increase performance. Finally, for each population, he calculated the average prevalence of these alleles at all seven genes.
The average prevalence was 39% among East Asians, 36% among Europeans, 32% among Amerindians, 24% among Melanesians and Papuan-New Guineans, and 16% among sub-Saharan Africans. The lowest scores were among San Bushmen (6%) and Mbuti Pygmies (5%). A related finding is that all but one of the alleles are specific to humans and not shared with ancestral primates.
Yes, he was using a small subset of genes that influence intellectual capacity. But you don’t need a big number to get the big picture. If you dip your hand into a barrel of differently colored jelly beans, the colors you see in your hand will match well enough what’s in the barrel. In any case, if the same trend holds up with a subset of 50 or so genes, it will be hard to say it’s all due to chance.
Interaction between age and intellectual capacity
These population differences seem to widen after puberty, as Franz Boas noted a century ago (Boas, 1974, p. 234). It may be that general intelligence was largely confined to early childhood in ancestral humans, as a means to integrate information during the time of life when children become familiar with their surroundings. With increasing age, and familiarity, this learning capacity would shut down. When modern humans began to enter environments that had higher cognitive demands, natural selection may have favored retention of general intelligence in adulthood, just as it favored retention of the capacity to digest lactose wherever adults raised dairy cattle and drank milk.
After doing a principal component analysis on covariance between the above IQ-enhancing alleles and performance on IQ and Pisa tests, Piffer (2013) was able to identify three alleles that show the highest loading on the first component. Ward et al. (2014) have found that possession of these three alleles correlates with educational performance of 13 to 14 year old children. We now have a tool to measure the interaction between genes and age in the development of intellectual capacity, particularly during the critical period extending from pre-puberty to early adulthood.
Some human populations seem to have arrived at similar outcomes through different evolutionary trajectories. East Asians, for instance, resemble Western Europeans in their level of societal development, but this similar outcome has been achieved through a different mental and behavioral package, specifically lower levels of guilt and empathy with correspondingly higher levels of shame and prosocial behavior. In short, East Asians tend to enforce social rules more by external mediation (e.g., shaming, peer pressure, family discipline) than by internal control (e.g., guilt, empathy).
This difference probably reflects a mix of learned and innate predispositions, since natural selection favors whatever works, regardless of how hardwired it may or may not be. To the extent that these predispositions are hardwired, East Asians may be less able to cope with the sort of aloneness, anonymity, and individualism we take for granted.
It would be easy enough to study the neurological effects of social isolation on East Asians, and there is already suggestive evidence that such effects include unusual outbursts of psychotic behavior. It would be harder, however, to determine whether this malfunctioning has a heritable component.
Microcephalin – Why does its Eurasian allele increase brain volume?
Almost a decade ago, Bruce Lahn was among those who discovered that a gene involved in brain growth, Microcephalin, continued to evolve after modern humans had spread out of Africa. Its most recent allele arose some 37,000 years ago in Eurasia and is still largely confined to native Eurasians and Amerindians (Evans et al., 2005). Interest in this finding evaporated when no significant correlation was found between the Eurasian allele and higher scores on IQ tests (Mekel-Bobrov et al, 2007; Rushton et al., 2007). Nonetheless, a later study showed that this allele correlates with increased brain volume (Montgomery and Mundy, 2010).
The time of origin corresponds to the entry of modern humans into seasonal temperate environments. It also corresponds to the beginnings of Upper Paleolithic art—realistic 3D representations of game animals on stone, clay, bone, and ivory. The common denominator seems to be an increased capacity to store spatiotemporal information, i.e., the ability to imagine objects, particularly game animals, and how they move over space and time. If IQ tests fail to measure this capacity, it may be worthwhile to test carriers of this allele for artistic or map-reading skills.
ASPM – Does the Middle Eastern/West Eurasian allele assist processing of alphabetical script?
ASPM is another gene that regulates brain growth, and like Microcephalin it continued to evolve after modern humans had spread out of Africa, its latest allele arising about 6000 years ago somewhere in the Middle East. The new allele then proliferated within and outside this region, reaching higher incidences in the Middle East (37-52%) and in Europe (38-50%) than in East Asia (0-25%). Despite its apparent selective advantage, this allele does not seem to improve cognitive performance on standard IQ tests. On the other hand, there is evidence that it is associated with increased brain size (Montgomery and Mundy, 2010).
At present, we can only say that it probably assists performance on a task that exhibited the same geographic expansion from a Middle Eastern origin roughly 6000 years ago. The closest match seems to be the invention of alphabetical writing, specifically the task of transcribing speech and copying texts into alphabetical script. Though more easily learned than ideographs, alphabetical characters place higher demands on mental processing, especially under premodern conditions (continuous text with little or no punctuation, real-time stenography, absence of automated assistance for publishing or copying, etc.). This task was largely delegated to scribes of various sorts who enjoyed privileged status and probably superior reproductive success. Such individuals may have served as vectors for spreading the new ASPM allele (Frost, 2008; Frost, 2011).
Tay Sachs and IQ
Ashkenazi Jews have high incidences of certain neurological conditions, particularly Tay Sachs, Gaucher’s disease, and Niemann-Pick disease. In the homozygous state these conditions are deleterious, but in the heterozygous state they may improve intellectual capacity by increasing neural axis length and branching. Cochran et al. (2006) argue that this improvement could amount to about 5 IQ points.
There was in fact a study in the 1980s to determine whether Tay-Sachs heterozygotes suffer from mental deficits (Kohn et al., 1988). The authors found no deficits but did not elaborate on whether performance was above-normal on the neuropsychological tests. They did mention that about two thirds of the Tay-Sachs heterozygotes had education beyond high school.
The raw data seem to be long gone, but it would not be difficult to repeat the study with a view to studying above-normal mental performance in heterozygotes and non-carriers.
Boas, F. (1974). A Franz Boas Reader. The Shaping of American Anthropology, 1883-1911, G.W. Stocking Jr. (ed.), Chicago: The University of Chicago Press.
Cochran, G., J. Hardy, and H. Harpending. (2006). Natural history of Ashkenazi intelligence, Journal of Biosocial Science, 38, 659-693.
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.
Frost, P. (2008). The spread of alphabetical writing may have favored the latest variant of the ASPM gene, Medical Hypotheses, 70, 17-20.
Frost, P. (2011). Human nature or human natures? Futures, 43, 740-748. http://dx.doi.org/10.1016/j.futures.2011.05.017
Gene Expression. (2006). 10 Questions for Bruce Lahn.
Kohn, H., P. Manowitz, M. Miller, and A. Kling. (1988). Neuropsychological deficits in obligatory heterozygotes for metachromatic leukodystrophy, Human Genetics, 79, 8-12.
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.
Montgomery, S. H., and N.I. Mundy. (2010). Brain evolution: Microcephaly genes weigh in, Current Biology, 20, R244-R246.
Piffer, D. (2013). Factor analysis of population allele frequencies as a simple, novel method of detecting signals of recent polygenic selection: The example of educational attainment and IQ, Mankind Quarterly, 54, 168-200.
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.
Ward, M.E., G. McMahon, B. St Pourcain, D.M. Evans, C.A. Rietveld, et al. (2014). Genetic variation associated with differential educational attainment in adults has anticipated associations with school performance in children. PLoS ONE 9(7): e100248. doi:10.1371/journal.pone.0100248