Saturday, June 25, 2011

Human nature or human natures?

A new article of mine has just appeared in the journal Futures. All comments are welcome.


Most evolutionary psychologists share a belief in one key concept: the environment of evolutionary adaptedness (EEA), i.e., the ancestral environment that shaped the heritable mental and behavioral traits of present-day humans. It is usually placed in the African savannah of the Pleistocene, long before our ancestors began to spread to other continents some fifty thousand years ago. Thus, later environments have not given rise to new traits through genetic evolution.

This belief rests on two arguments: 1) such traits are complex and therefore evolve too slowly to have substantially changed over the past fifty thousand years; 2) because the same time frame has seen our species diversify into many environments, recent traits should tend to be environment-specific and hence population-specific, yet such specificity seems inconsistent with the high genetic overlap among human populations. Both arguments are weaker than they seem. New complex traits can arise over a relatively short time through additions, deletions, or modifications to existing complex traits, and genetic overlap can be considerable even between species that are morphologically, behaviorally, and physiologically distinct.

There is thus no conceptual barrier to the existence of EEAs in post-Pleistocene times. Such a paradigm could shed light on such research topics as the visual word form area, reproductive strategy, predisposition to violence among young men, and personality traits. Eventually, a multi-EEA model may dominate evolutionary psychology, perhaps after an interim period of accommodation with the current model.


Frost, P. (2011). Human nature or human natures?

Saturday, June 18, 2011

More on French Canadians and Tay Sach's

French Canadian habitants playing at cards (Cornelius Krieghoff). With fewer British merchants than elsewhere, eastern Quebec was a land of opportunity for business-minded French Canadians. Did this selection affect the local gene pool?

When discussion turns to Tay Sach’s, people automatically think of the Jewish community. Yet this inherited illness reaches high levels in other human populations, particularly French Canadians.

Tay Sach’s has three unusual characteristics among French Canadians:

1. It is highly localized geographically, being concentrated in eastern Quebec. In Rimouski, the heterozygote frequency is 7.6%, versus 4.2% among Ashkenazi Jews and 0.3% among French Canadians in Montreal (De Braekeleer et al, 1992).

2. It is caused by two separate mutations: one that arose on the north shore of the St. Lawrence (Charlevoix and Saguenay-Lac Saint-Jean) and another that arose on the south shore (Bas Saint-Laurent) (Zlotogora, 1994).

3. It is relatively recent in origin, being absent in France. Neither mutation can be more than three centuries old and both probably postdate the British conquest of Quebec (1759).

These three characteristics argue for some kind of selective advantage, and not a random founder effect. Among Ashkenazi Jews, the selective advantage seems to be improved mental processing. Indeed, Tay Sach’s is one of four different genetic illnesses that are unusually common among Ashkenazim and that affect the same metabolic pathway in brain tissues (lysosomal storage). Homozygotes suffer neurological degeneration, mental retardation, and other neural problems. Heterozygotes, however, may be better at mentally demanding occupations (Cochran et al., 2006; Frost 2007; Murray, 2007; Zlotogora, 1994).

Interestingly, Tay Sach’s co-occurs in eastern Quebec with another hereditary illness that lies in the same metabolic pathway, i.e., lysosomal storage.

The mucolipidoses are composed of four distinct clinical conditions (designated type I–IV) that result from the accumulation of lipid and carbohydrate molecules due to specific lysosomal enzyme defects. (...) In the absence of this step, lysosomal enzymes are incorrectly routed into the extracellular space. This disorder is rare, with an estimated incidence of 1 in 640 000 births, although it may be higher in Saguenay-Lac-St Jean, a French Canadian isolate. (Ekstrand & Sankar, 2009, p. 603)

Are lysosomal storage illnesses common in eastern Quebec for the same reason that they are common among Ashkenazi Jews? At first thought, the idea may seem absurd. Weren’t French Canadians historically a nation of farmers? And didn’t British merchants fill all of the mentally demanding occupations?

In reality, things were not so simple. There was always a French-Canadian middle class, particularly wherever British merchants were few and far between. They were especially rare in those parts of eastern Quebec that today have high rates of Tay Sach’s (Charlevoix, Saguenay-Lac Saint-Jean, Bas Saint-Laurent). This rarity came to the notice of Alexis de Tocqueville while passing through Bas Saint-Laurent in 1831:

In this portion of Canada, one does not hear English at all. The population is only French, and yet when one encounters an inn, or a merchant, the sign is in English. (De Tocqueville, 2003, p. 185).

This lack of English competition opened up an enviable niche for French Canadians—or rather for those with the right aptitudes, especially in numeracy, literacy, and bilingualism. Elsewhere, these niches were filled by British immigrants, particularly in Montreal, Quebec City, the Eastern Townships, the Ottawa valley, and the southern and eastern shorelines of the Gaspé Peninsula.

This point is made in a study of the life of John Guay (1828-1880), a leading French Canadian merchant in the Saguenay region. To enter this occupational niche required a special mental toolkit:

Success in trade was never easy because of the competition, the fragility of the markets, and the instability of business conditions. The ablest managed to live or survive. Others, the greatest number, closed shop after a few years. Only those possessing exceptional qualities would make a fortune. (Lapointe, 1996, p. 3)

But the payoff was huge. John Guay had ten children who survived to adulthood—twice the mean reproductive success of his French Canadian contemporaries. Lapointe (1996, p. 126) attributes Guay’s success in business to the mental outlook he displayed from an early age:

The evolution of market capitalism has given rise to rules that a businessman cannot evade. One cannot simply improvise as a merchant. It takes talent and of course capital. Spontaneous generation was very uncommon in 19th-century Quebec, indeed nonexistent in John Guay’s case. The family environment in which he grew up predisposed him to develop an interest and also aptitudes for the businesses of trade, forestry, and farming. His successful career henceforth proved that a French-Canadian merchant could ably penetrate the world of business; a world where, let us remember, English Canadians controlled most of the commercial and industrial activities.

The Beauce exception

One region in eastern Quebec, however, has always been solidly French Canadian and yet has low incidences of Tay Sach’s and mucoliposes. This is Beauce County, a region south of Quebec City that covers the Chaudière valley up to the American border. Furthermore, Beaucerons are stereotyped as being self-reliant, business-minded go-getters—the “Yankees” of Quebec.

Beauce County nonetheless differs demographically from the rest of eastern Quebec in one respect. Settlement began earlier there than elsewhere, well before the Conquest. There was thus a larger pool of people and hence more individuals who could fill the niches that opened up after the Conquest, as Quebec moved from a semi-feudal mercantilist society to a more market-driven economy. Selection thus had more leeway to favor individuals who had the necessary aptitudes while not suffering the costs that lysosomal storage illnesses impose on homozygotes.

Fast evolution?

All of this might seem hard to believe. How could such selection operate over a time span of less than two centuries? Yet that is what the data tell us. Neither of these Tay Sach’s mutations is present in France. They must have gone from zero to their current high prevalence in less than ten generations.


Cochran, G., J. Hardy, & H. Harpending. (2006). Natural history of Ashkenazi intelligence. Journal of Biosocial Science, 38, 659-693.

De Braekeleer, M., P. Hechtman, E. Andermann, & F. Kaplan. (1992). The French Canadian Tay-Sachs disease deletion mutation: identification of probable founders, Human Genetics, 89, 83-87.
De Tocqueville, A. (2003). Regards sur le Bas-Canada, Typo.

Ekstrand J. and R. Sankar (2009). Storage Disorders, in Lisak, R.P., D.D. Truong, W.M. Carroll, & R. Bhidayasiri (eds). International Neurology. A Clinical Approach, (pp. 600-608), Wiley-Blackwell: Oxford

Frost, P. (2007). Natural selection in proto-industrial Europe, Evo and Proud, November 16.

Lapointe, N. (1996). Le capitalisme marchand au Saguenay-Lac-Saint-Jean : John Guay (1828-1880), négociant et propriétaire foncier, Master’s thesis in regional studies for the Université du Québec à Chicoutimi, 153 p.

Murray, C. (2007). Jewish Genius. Commentary, April

Zlotogora, J. (1994). High frequencies of human genetic diseases: founder effect with genetic drift or selection? American Journal of Medical Genetics, 49, 10-13.

Saturday, June 11, 2011

Hue and luminosity of human skin: a visual cue?

The inferotemporal cortex is involved in both face perception and color perception. It may be in this region that the brain processes visual data on the hue and luminosity of human skin.

If you are a member of the International Society for Human Ethology, you can read my latest article: Hue and luminosity of human skin: a visual cue for gender recognition and other mental tasks.


Face recognition takes place within a distinct heritable module of the brain and includes the ability to distinguish between male and female human faces. To identify gender, this module targets a number of sexually dimorphic features, particularly the hue and luminosity of facial skin. Men look browner and ruddier in hue because melanin and blood are more present in their skin’s outer tissues. Women have a higher luminous contrast between their facial skin and their lips and eyes. Hue seems to provide a “fast channel” for gender recognition. If the observer is too far away or the lighting too dim, the brain switches to the “slow channel” and targets luminosity. In addition to assisting gender recognition, the skin’s hue and luminosity may also alter the observer’s mental state in a number of areas, ranging from sexual attraction to emotional distancing.


Frost, P. (2011). Hue and luminosity of human skin: a visual cue for gender recognition and other mental tasks, Human Ethology Bulletin,

Friday, June 3, 2011

On the impossibility of blue eyes

Although blue eyes are more recessive than brown eyes, eye color does not follow a simple recessive/dominant mode of inheritance. There is a wide range of intermediate hues.

As discussed in my last post, one puzzle of human evolution is the diverse palette of European hair and eye colors. Although these two polymorphisms have largely developed at separate genes, they share a similar geographic range and similar conspicuous hues. They also appear on or near the face—the focus of human visual attention. Could a common selection pressure be responsible? And could it be sexual selection?

This topic came up a month ago on Steve Sailer’s blog, specifically the evolution of blue eyes. Greg Cochran pointed out that sexual selection could not be responsible because blue eyes are recessive:

First, an advantageous allele whose action is purely recessive is far more likely to be lost when new than a dominant allele with an equivalent advantage. Second, assuming that it is not lost and that the population mates randomly, it takes much longer to reach 50% frequency than a dominant allele. Third, if the population is spread out over space, the Fisher wave spreads far more slowly, something like 20 times more slowly.

Mutations are fairly common, but a potentially adaptive one—like an allele for blue eyes—is usually rare. In this case, the same rare allele must occur twice and come together in the same person before sexual selection can do its work. And this work would be lost in the next generation.

All of this assumes, of course, that blue eyes are recessive. Although eye color is polygenic, alleles at two STPs (rs12913832 and rs1129038) seem to account for most cases of blue eyes (Eiberg et al., 2008). In a Polish sample, 89% of the blue-eyed individuals had both copies of the ‘C’ allele at rs12913832 and no copies of the alternate ‘T’ allele (Branicki et al., 2009).

But the C allele is far from silent if only one copy is present, as seen in the same Polish sample. Among CT heterozygotes, 16% had blue or grey eyes, 10% green eyes, 47% hazel eyes, and only 27% brown eyes.

Although the C allele is relatively recessive for expression of blue eyes, it shows strong heterozygote effects for expression of green or hazel eyes:

Blue or grey-eyed individuals: 89% had both copies, 10% one copy, 9% no copies
Green-eyed individuals: 67% had both copies, 30% one copy, 2% no copies
Hazel-eyed individuals: 9% had both copies, 80% one copy, 11% no copies
Brown-eyed individuals: 0% had both copies, 84% one copy, 16% no copies

In short, the C allele is less dominant, but not truly recessive. Even in the heterozygous state, it usually produces hues that visibly diverge from the human norm of brown eyes.

Greg also forgets that evolution can reach an initially inaccessible state by passing through intermediate states. When the C allele first appeared, it produced only green or hazel eyes for sexual selection to act upon. As copies of this allele increased in the population, there was a corresponding increase in the probability of homozygotes that could produce blue eyes—which became a new target for sexual selection.

The selection here is not for a single color, be it blue, green, hazel, or brown, but rather for any colors that can catch attention by their novelty or brightness. The end result is more and more eye colors—a balanced polymorphism where sexual selection is always on the lookout for new and interesting hues. Needless to say, this outcome is possible only when the operational sex ratio is very lopsided, thus favoring the evolution of ‘eye candy’ among members of the sex in excess supply.


Branicki, W., U. Brudnik, and A. Wojas-Pelc. (2009). Interactions between HERC2, OCA2 and MC1R may influence human pigmentation phenotype, Annals of Human Genetics, 73,160–170.

Eiberg, H., J. Troelsen, M. Nielsen, A. Mikkelsen, J. Mengel-From, K.W. Kjaer, & L. Hansen. (2008). Blue eye color in humans may be caused by a perfectly associated founder mutation in a regulatory element located within the HERC2 gene inhibiting OCA2 expression, Human Genetics, 123, 177–187

Sailer, S. (2011). Old Blue Eyes, May 10