Getting noticed

"A rapid and effective means for getting noticed in the crowd." Lady Gaga(?) in Stylist France.

I'm back to blogging after a 3-month absence. During my hiatus the magazine Stylist France interviewed me about head hair as a form of advertising. The resulting article appeared on October 11 under the headline "Forget the slogan T-shirt. To get yourself heard, nothing is more effective than a new hairstyle."

The full interview, in French with an English translation, is provided below:

French version:

Pouvez-vous expliquer succinctement le rôle de la sélection sexuelle dans l'apparition des cheveux blonds ?

La sélection sexuelle favorise la brillance et la nouveauté. Ce qui est brillant demeure plus longtemps en mémoire; ce qui est nouveau retient plus longtemps l'attention. Si on considère les couleurs des cheveux et des yeux, on constate une évolution vers la brillance, c'est-à-dire les cheveux noirs et les yeux bruns cèdent leur place à des couleurs vives, comme les cheveux roux ou blonds et les yeux verts ou bleus.

Quant à l'évolution vers la nouveauté, celle-ci se manifeste par la diversification de la palette des cheveux et des yeux. Au début, une nouvelle couleur émerge par la mutation, puis elle se répand jusqu'à ce qu'elle perde sa nouveauté ; à ce moment-là, la pression de la sélection sexuelle se réoriente pour favoriser une couleur moins fréquente. Ainsi, un équilibre s'établit entre les diverses couleurs.

Qu'est-ce qui permet d'affirmer que la sélection sexuelle est aussi importante voire plus importante que les rayons UV dans l'apparition des cheveux blonds ?

D'abord, les gènes contrôlant la couleur de la peau et celle des cheveux ne sont pas les mêmes. On peut avoir la peau très blanche, tout en possédant les cheveux foncés. De plus, la pression de sélection exercée par les rayons UV n'explique pas la diversification des allèles contrôlant la couleur des cheveux et des yeux. Enfin, on ne voit pas cette diversification chez les peoples indigènes habitant les mêmes latitudes de l'Asie du Nord et de l'Amérique du Nord.

Vous affirmez que ces traits distinguant les Européens sur le plan visuel résultent d'une pression de sélection qui vise surtout la femme. Pourquoi pas l'homme ?

Il y a eu une pénurie d'hommes chez les premiers Européens, en partie parce que la dépendance de la viande, comme partie dominante de l'alimentation, rendait la polygamie trop coûteuse pour les hommes, sauf pour les meilleurs chasseurs. De plus, comme on le constate toujours chez les peoples chasseurs du Nord, le taux de mortalité est plus élevé chez les hommes que chez les femmes. Résultat : un surplus de femmes. Celles-ci devaient se concurrencer pour les hommes disponibles.

Finalement, il semble y avoir un parallèle fort entre la supposée attraction, aujourd'hui, des hommes pour les femmes blondes (et les stéréotypes et exemples qui en ont découlé dans la pop culture) et le phénomène d'apparition des cheveux blonds il y a 11.000 ans.

Aujourd'hui, grâce aux études de l'ADN extraits des restes humains, on sait que les cheveux blonds existaient déjà il y a 18 000 ans. Le lieu d'origine semble être chez les peoples chasseurs des plaines de l'Europe de l'est et de la Sibérie de l'ouest pendant la dernière glaciation.

English version:

Can you succinctly explain the role of sexual selection in the appearance of blond hair?

Sexual selection favors brightness and novelty. Anything bright remains longer in memory; anything novel holds attention longer. If we consider hair and eye colors, we see an evolution toward brightness, i.e., black hair and brown eyes have ceded their place to bright colors, like red or blond hair and green or blue eyes.

As for evolution toward novelty, this has manifested itself in a diversification of the palette for the hair and the eyes. Initially, a new color emerges through mutation; then it spreads until it loses its novelty; at that moment, the pressure of sexual selection reorients itself to favor a less frequent color. Thus, an equilibrium becomes established between the various colors.

What makes you think that sexual selection is as important, indeed more important, than UV radiation in the appearance of blond hair?

First, the genes controlling skin color and hair color are not the same. One can have very white skin while having dark hair. In addition, the selection pressure of UV radiation does not explain the diversification of alleles controlling hair and eye color. Finally, this diversification is not seen among indigenous peoples inhabiting the same latitudes of northern Asia and North America.

You affirm that these traits that visually distinguish Europeans result from a selection pressure that is aimed especially at women. Why not men?

There was a shortage of men among the first Europeans, partly because dependence on meat, as a dominant part of the diet, made polygamy too costly for men, except for the best hunters. In addition, as is still seen among northern hunting peoples, the mortality rate is higher among men than among women. Result: a surplus of women. Those women had to compete for the available men.

Finally, there seems to be a strong parallel between the purported attraction, today, of men for blonde women (and the resulting stereotypes and examples in pop culture) and the phenomenon of the appearance of blond hair 11,000 years ago.

Today, thanks to studies of DNA extracted from human remains, we know that blond hair already existed 18,000 years ago. The place of origin seems to be among the hunting peoples of the plains of eastern Europe and western Siberia during the last ice age.

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On rereading my answers I realize I may have misunderstood the last question. The intent seems to be:  “Given that these evolutionary processes happened thousands of years ago, how can they explain the growing popularity of blond hair today?” This intent became clearer to me when I read the article, which focuses on blondness in pop culture, and its apparent surge in popularity since the 1970s. 

This trend appears in a study of Playboy playmates from 1954 to 2007. From a low of about 35% in the mid-1960s the proportion of blonde playmates rose to a high of 60% by the year 2000 (Anon 2008). A similar trend was found by Rich and Cash (1993).

Natural blondes are actually a lot scarcer among white Americans. In a sample of undergraduates the proportions were 68% brown, 27% blond, and 5% red (Rich and Cash 1993). Similar proportions appear in a British study: 68% brown, 25% blond, 1% red, and 6% black (Takeda et al., 2006).

Natural blond hair has since become less common in the United States and the United Kingdom. Are we seeing the novelty effect in action? Are blondes becoming sexier because fewer real ones are out there?

References

Anon. (2008). Bygone brunette beauty: Fashion in hair color, Gene Expression June 29

www.gnxp.com/blog/2008/06/bygone-brunette-beauty-fashion-in-hair.php

D'Almeida, P. and M. Giuliani. (2018). Qu'elle a bien pu vouloir dire avec cette coupe ? Stylist France, October 11, pp. 2-5.

Rich, M.K., and T.F. Cash. (1993). The American image of beauty: Media representations of hair color for four decades. Sex Roles 29: 113-124.

Takeda, M.B., M.M. Helms, and N. Romanova. (2006). Hair color stereotyping and CEO selection in the United Kingdom. Journal of human behavior in the social environment 13: 85-99

A modern myth

 

Your blood group cannot reliably identify your ethnicity, your race ... or even your species (Wikicommons, Etan Tal).

 

What sort of ideas will guide our elites twenty years from now? You can find out by observing university students, especially those in the humanities and social sciences. One popular idea is that race doesn't exist, except as a social construct. Its proponents include Eula Biss, a contributor to the New York Times Magazine:

Whiteness is not a kinship or a culture. White people are no more closely related to one another, genetically, than we are to black people. [...] Which is why it is entirely possible to despise whiteness without disliking yourself. (Biss, 2015, h/t to Steve Sailer)

The last sentence needs little explanation. It's possible to like yourself a lot while despising your own people. Such individuals have existed since time immemorial. But what about the second sentence? One often hears it among the educated, even those who dislike genetics and biology. Where does it come from?

From a study by geneticist Richard Lewontin, in 1972. He looked at human genes with more than one variant, mostly blood groups but also serum proteins and red blood cell enzymes. His conclusion:

The results are quite remarkable. The mean proportion of the total species diversity that is contained within populations is 85.4%, with a maximum of 99.7% for the Xm gene, and a minimum of 63.6% for Duffy. Less than 15% of all human genetic diversity is accounted for by differences between human groups! Moreover, the difference between populations within a race accounts for an additional 8.3%, so that only 6.3% is accounted for by racial classification.

[...] It is clear that our perception of relatively large differences between human races and subgroups, as compared to the variation within these groups, is indeed a biased perception and that, based on randomly chosen genetic differences, human races and populations are remarkably similar to each other, with the largest part by far of human variation being accounted for by the differences between individuals. (Lewontin, 1972)

The problem here is the assumption that genetic variation within a human group is comparable to genetic variation between human groups. In fact, the two are qualitatively different. When a gene varies between two groups the cause is more likely a difference in natural selection, since the group boundary also tends to separate different natural environments (vegetation, climate, topography) or, more often, different cultural environments (diet, means of subsistence, sedentism vs. nomadism, gender roles, state monopoly of violence, etc.). Conversely, when a gene varies within a population, the cause is more likely a random factor without adaptive significance. That kind of variation is less easily flattened out by the steamroller of similar selection pressures.

This point isn't merely theoretical. In other animals, as Lewontin himself noted, we often see the same genetic overlap between races of one species. But we also see it between many species that are nonetheless anatomically and behaviorally distinct. Some two decades after Lewontin’s study, this apparent paradox became known when geneticists looked at how genes vary within and between dog breeds:

[...] genetic and biochemical methods ... have shown domestic dogs to be virtually identical in many respects to other members of the genus. [...] Greater mtDNA differences appeared within the single breeds of Doberman pinscher or poodle than between dogs and wolves. Eighteen breeds, which included dachshunds, dingoes, and Great Danes, shared a common haplotype and were no closer to wolves than poodles and bulldogs.

[...] there is less mtDNA difference between dogs, wolves, and coyotes than there is between the various ethnic groups of human beings, which are recognized as a single species. (Coppinger and Schneider, 1995)

Initially, this paradox was put down to the effects of artificial selection. Kennel clubs insist that each breed should conform to a limited set of criteria. All other criteria, particularly those not readily visible, end up being ignored. So artificial selection targets a relatively small number of genes and leaves the rest of the genome alone.

But is natural selection any different? When a group buds off from a population and moves into a new environment, its members too have to conform to a new set of selection pressures that act on a relatively small number of genes. So the new group will diverge anatomically and behaviorally from its parent population, and yet remain similar to it over most of the genome. This is either because most of the genes respond similarly to the new environment—as with those that do the same housekeeping tasks in a wide range of species—or because they respond weakly to natural selection in general. Many genes are little more than "junk DNA"—they change slowly over time, not through the effects of natural selection but through gradual accumulation of random mutations.

With the extension of population studies to nonhuman species, geneticists have often encountered this paradox: a gene will vary much less between two species than within each of them. This is notably the case with sibling species that have emerged since the last ice age, when many new and different environments came into being.

Thus, the genetic overlap between dog breeds also appears between many natural species. In the deer family, genetic variability is greater within some species than between some genera (Cronin, 1991). Some masked shrew populations are genetically closer to prairie shrews than they are to other masked shrews (Stewart et al., 1993). Only a minority of mallards cluster together on an mtDNA tree, the rest being scattered among black ducks (Avise et al., 1990). All six species of Darwin's ground finches form a genetically homogeneous genus with very little concordance between mtDNA, nuclear DNA, and morphology (Freeland and Boag, 1999). In terms of genetic distance, redpoll finches from the same species are not significantly closer to each other than they are to redpolls from different species (Seutin et al., 1995). The haplochromine cichlids of Lake Victoria are extremely difficult to identify as species when one looks at their nuclear or mitochondrial genes, despite being well differentiated anatomically and behaviorally (Klein et al., 1998). Neither mtDNA nor allozyme alleles can distinguish the various species of Lycaedis butterflies, despite clear differences in morphology (Nice and Shapiro, 1999). An extreme example is a dog tumor that has developed the ability to spread to other dogs through sexual contact. It looks and acts like an infectious microbe, yet its genes would show it to be a canid and, conceivably, some beagles may be genetically more similar to it than they are to Great Danes (Cochran, 2001; Yang, 1996).

We see this genetic overlap not only between sibling species, but even between some species that have long been separated, like humans and other primates. This is the case with ABO blood groups:

Remarkably, the A, B, and H antigens exist not only in humans but in many other primates [...], and the same two amino acids are responsible for A and B enzymatic specificity in all sequenced species. Thus, primates not only share their ABO blood group, but also the same genetic basis for the A/B polymorphism. O alleles, in contrast, result from loss-of-function alleles such as frame-shift mutations and appear to be species specific. (Segurel et al., 2012)

Just think. Lewontin used the same blood group polymorphisms for his study. While the O alleles are specific to each primate species, the A and B alleles show considerable overlap between primates that have been separated for millions of years. So it's not surprising that this polymorphism should vary much more within human races than between them, as Lewontin found. Little did he know that the same pattern can continue above the species level.

Some have argued that this genetic overlap between humans and apes is only apparent. In other words, the same antigens have evolved independently in each species. Well, no. It seems that this polymorphism has survived one speciation event after another for millions of years:

That different species share the same two A/B alleles could be the result of convergent evolution in many lineages or of an ancestral polymorphism stably maintained for millions of years and inherited across (at least a subset of) species. The two possibilities have been debated for decades, with a consensus emerging that A is ancestral and the B allele has evolved independently at least six times in primates (in human, gorilla, orangutan, gibbon/siamang, macaque, and baboon), in particular, that the human A/B polymorphism arose more recently than the split with chimpanzee. We show instead that the remarkable distribution of ABO alleles across species reflects the persistence of an old ancestral polymorphism that originated at least 20 million years (My) ago and is shared identical by descent by humans and gibbons as well as among distantly related Old World monkeys. (Segurel et al., 2012)

Are blood groups a special case? Perhaps. But there seem to be quite a few trans-species polymorphisms, at least between humans and chimpanzees:

Instances in which natural selection maintains genetic variation in a population over millions of years are thought to be extremely rare. We conducted a genome-wide scan for long-lived balancing selection by looking for combinations of SNPs shared between humans and chimpanzees. In addition to the major histocompatibility complex, we identified 125 regions in which the same haplotypes are segregating in the two species, all but two of which are noncoding. In six cases, there is evidence for an ancestral polymorphism that persisted to the present in humans and chimpanzees. (Leffler et al., 2013)

Many of these appear to be "disease polymorphisms." If an epidemic sweeps through a community, it pays to have surface antigens that differ somewhat from your neighbor’s. The result is selection that inflates within-group variability, especially for the sort of structural proteins that are easy to collect and examine for studies on population genetics.

If such polymorphisms can remain intact despite millions of years of separation, how many more persist among human populations that have been separated for only tens of thousands of years?

In sum, if we are to believe blood groups and other genetic markers, it seems that Eula Biss may have more in common with certain apes than with the white folks she despises. Let’s hope she feels gratified.

When I discuss Richard Lewontin's study with antiracists, preferably those with some background in biology, they often agree that he misunderstood his findings. They nonetheless go on to say that their position has many other justifications, particularly moral ones. Fine. But it is above all Lewontin who gave antiracism a veneer of scientific objectivity. He still impresses people who are less impressed by academics who attack racism by attacking objectivity, like Stephen Jay Gould. "I criticize the myth that science itself is an objective enterprise, done properly only when scientists can shuck the constraints of their culture and view the world as it really is" (Gould, 1996, p. 53). It was in this spirit that he impugned the integrity of long-dead scholars who could not defend themselves—or point out that Gould himself was manipulating the data to suit his preconceived views (Frost, 2013).

When one takes Lewontin and Gould out of the picture, who is left? A lot of people, to be sure. Followers for the most part—those like Eula Biss who believe because everyone else in their milieu seems to believe, at least anyone with moral authority.

References 

Avise, J.C., C.D. Ankney, and W.S. Nelson. (1990). Mitochondrial gene trees and the evolutionary relationship of mallard and black ducks, Evolution, 44, 1109-1119.

http://www.jstor.org/stable/2409570?seq=1#page_scan_tab_contents 

Biss, E. (2015). White Debt, The New York Times Magazine, December 2

http://www.nytimes.com/2015/12/06/magazine/white-debt.html?_r=1

Cochran, G. (2001). Personal communication. 

Coppinger, R. and R. Schneider (1995). Evolution of working dogs. In J. Serpell (ed.), The Domestic Dog: Its Evolution, Behaviour and Interactions with People. Cambridge: Cambridge University Press, pp. 21-47.

https://books.google.ca/books?hl=fr&lr=&id=I8HU_3ycrrEC&oi=fnd&pg=PA21&dq=evolution+of+working+dogs&ots=BccrPzh5v3&sig=Cy-uz8gKk_epZRPTP58-k-1D9wg#v=onepage&q=evolution%20of%20working%20dogs&f=false 

Cronin, M. (1991). Mitochondrial-DNA phylogeny of deer (Cervidae), Journal of Mammalogy, 72, 533-566.

http://jmammal.oxfordjournals.org/content/72/3/553.abstract 

Freeland, J.R. and P.T. Boag. (1999).The mitochondrial and nuclear genetic homogeneity of the phenotypically diverse Darwin's ground finches, Evolution, 53, 1553-1563.

https://www.researchgate.net/profile/Peter_Boag/publication/233529125_The_mitochondrial_and_nuclear_genetic_homogeneity_of_the_phenotypically_diverse_Darwins_Ground_finches/links/0deec514a004f3a887000000.pdf 

Frost, P. (2013). Not getting the point, Evo and Proud, June 22

http://evoandproud.blogspot.ca/2013/06/not-getting-point.html  

Gould, S.J. (1996). The Mismeasure of Man, New York: W.W. Norton & Co.

http://www.amazon.com/The-Mismeasure-Man-Revised-Expanded/dp/0393314251 

Klein, J., A. Sato, S. Nagl, and C. O’hUigin. (1998). Molecular trans-species polymorphism, Annual Review of Ecology and Systematics, 29, 1-21.

http://www.jstor.org/stable/221700?seq=1#page_scan_tab_contents

Leffler, E.M., Z. Gao, S. Pfeifer, L. Ségurel, A. Auton, O. Venn, R. Bowden, R. Bontrop, J.D. Wall, G. Sella, P. Donnelly, G. McVean, and M. Przeworski. (2013). Multiple instances of ancient balancing selection shared between humans and chimpanzees, Science, 339 (6127), 1578-1582.

http://www.sciencemag.org/content/339/6127/1578.short  

Lewontin, R. (1972). The apportionment of human diversity, Evolutionary Biology, 6, 381-398.

http://www.philbio.org/wp-content/uploads/2010/11/Lewontin-The-Apportionment-of-Human-Diversity.pdf  

Nice, C.C. and A.M. Shapiro. (1999). Molecular and morphological divergence in the butterfly genus Lycaeides (Lepidoptera: Lycaenidae) in North America: evidence of recent speciation, Journal of Evolutionary Biology, 12, 936-950.

http://onlinelibrary.wiley.com/doi/10.1046/j.1420-9101.1999.00111.x/full 

Sailer, S. (2015). White Debt, The Unz Review, December 5

http://www.unz.com/isteve/white-debt/  

Ségurel, L.,  E.E. Thompson, T. Flutre, J. Lovstad, A. Venkat, S.W. Margulis, J. Moyse, S. Ross, K. Gamble, G. Sella, C. Ober, and M. Przeworski. (2012). The ABO blood group is a trans-species polymorphism in primates, Proceedings of the National Academy of Sciences U.S.A., 109, 18493-18498

http://www.pnas.org/content/109/45/18493.abstract  

Seutin, G., L.M. Ratcliffe, and P.T. Boag. (1995). Mitochondrial DNA homogeneity in the phenotypically diverse redpoll finch complex (Aves: Carduelinae: Carduelis flammea-hornemanni), Evolution, 49, 962-973.

http://www.jstor.org/stable/2410418?seq=1#page_scan_tab_contents 

Stewart, D.T., A.J. Baker, and S.P. Hindocha. (1993). Genetic differentiation and population structure in Sorex Haydeni and S. Cinereus, Journal of Mammalogy, 74, 21-32.

http://jmammal.oxfordjournals.org/content/74/1/21.abstract 

Yang, T.J. (1996). Parasitic protist of metazoan origin, Evolutionary Theory, 11, 99-103.

Trans-species polymorphisms

A trans-species polymorphism. Some genetic polymorphisms are found in distantly related species, having persisted across multiple speciation events. (source)

It is widely known that considerable genetic overlap exists between human populations, even those that are geographically distant from each other and quite different physically. You probably learned in BIO101 that genetic variation is much greater within than between human populations.

It is less widely known that this high degree of genetic overlap also exists between many species that are nonetheless distinct morphologically, physiologically, and behaviorally (Frost, 2011). This is especially so with young sibling species. Such species differ only over a small fraction of the genome—at those genes where a certain variant is adaptive in one species but not in the other. Elsewhere, over most of the genome, the same variant works just fine in both species, either because the gene itself is of little or no value or because certain body functions are pretty much the same in a wide range of organisms.

With time, and reproductive isolation, two sibling species will gradually lose this genetic overlap, as a result of random mutations here and there over the entire genome. The two species will be less and less alike even at “junk genes” of little value.

Even so, some overlap will remain. It’s not just that we see the same gene in distantly related species. We also see the same gene with the same set of alleles—a trans-species polymorphism (Klein et al., 1998). A good example is the ABO blood group system. On the basis of that gene marker, I probably have more in common with certain apes than I do with some of my readers. Such polymorphisms have in fact persisted for millions of years across multiple speciation events.

Until recently, it was believed that trans-species polymorphisms were no more than an oddity. Now, it looks like they may be more common than previously thought: 

[…] we searched for trans-species polymorphisms between humans and chimpanzees using genome-wide resequencing data for 10 western chimpanzees from the PanMap project and 179 humans from the 1000 Genomes Pilot 1 data. […] In addition to the MHC region, we identified over 100 cases, a set significantly enriched for transmembrane glycoproteins, which are often involved in interactions with pathogens. To further rule out the possibility of deep coalescent events by chance, we examined patterns of variation in seven samples of Gorilla gorilla. We discovered 25 cases shared among all three species, which we verified by Sanger sequencing. In a subset, within species diversity levels were unusually high and the tree of haplotypes clustered by allelic type rather than by species, providing definitive evidence for trans-species polymorphisms. (Segurel et al, 2012)

At such genes, variation within species exceeds variation between species … and even between genera.

So just what, then, makes a species a species? The traditional answer is reproductive isolation, and the resulting accumulation of genetic differences over time. Yet this answer seems increasingly problematic. On the one hand, we have cases of living fossils that remain essentially the same over eons of time. Analysis of “junk DNA” would show a steady accumulation of genetic change over those eons, although nothing has changed in  appearance or behavior. A coelacanth today is still a coelacanth after millions and millions of years.

On the other hand, we have cases of sibling species that have emerged in recent times and have become quite different from each other both anatomically and behaviorally. Yet genetic analysis of such species often shows considerable genetic overlap. If we use any of the usual genetic markers (blood groups, enzymes, etc), individuals may not be assignable to a single species with reasonable certainty.

So if genes in general don’t matter, what exactly does? What matters is what matters. Genes for highly adaptive traits matter. Differences you can see matter. Therefore, reproductive isolation in itself is not what makes two populations different; it’s the different ways in which they adapt to different environments.

If a population splits in two with one group moving into one environment and the other moving into another, the two groups will nonetheless continue to look and act similarly as long as their respective environments remain similar (of course, if the two groups are human societies, one of them might create a radically different cultural environment). It is the difference in selection pressures, as a result of differing environments, that will drive them apart … and such differentiation will proceed even if reproductive isolation is still incomplete:

Judging from the number of studies devoted to it, the nature of a reproductive barrier is currently central to the interests of researchers working on speciation. It seems to us, however, that the process of adaptation to the environment is a much more important and interesting part of speciation. The erection of the reproductive barrier may mark the end of speciation, but it tells us little about the process that makes the species differ from one to another, the process that creates biological diversity. (Klein et al., 2007)

References

Frost, P. (2011). Human nature or human natures? Futures, 43, 740–748. http://dx.doi.org/10.1016/j.futures.2011.05.017

Klein, J., A. Sato, S. Nagl, and C. O’hUigin. (1998). Molecular trans-species polymorphism, Annual Review of Ecology and Systematics, 29, 1-21.

 

Klein, J., A. Sato, and N. Nikolaidis. (2007). MHC, TSP, and the origin of species: From immunogenetics to evolutionary genetics, Annual Review of Genetics, 41, 281-304

http://e-groups.unb.br/fm/lmpdc/arquivos/artigos/MARILEN%20QUEIROZ%20MHC%20evolutionary%20genetics.pdf

Segurel, L., E. Leffler, Z. Gao, S. Pfeifer, A. Auton, O. Venn, L. Stevison, A. Venkat, J. L. Kelley, J. Kidd, C. Bustamante, R. Bontrop, M. Hammer, J. Wall, P. Donnelly, G. McVean, & M. Przeworski. (2012). When ancestry runs deep: Trans-species polymorphisms in apes, Annual Meeting of the American Society of Human Genetics, November 6-10

http://www.ashg.org/2012meeting/abstracts/fulltext/f120121882.htm

What makes hair color "hot"?

The ‘hot’ hair color this year (source). While there seems to be a general trend to prefer average physical characteristics, this doesn’t seem to apply to hair color. People seek colors that are uncommon or even unnatural.

Europeans have departed from the species norm of black hair and brown eyes by evolving a wide range of bright hair and eye colors. What is the selective advantage of these new hues? Or are they merely a side effect of something else?

I’ve argued that these new colors were selected for … their newness and colorfulness. To be precise, their selective advantage lay in their novelty and brightness. These eye-catching qualities enabled women to improve their mating prospects at a time when the operational sex ratio was skewed toward a female surplus and a male shortage.

This is the logic of advertising. Visual merchandising matters most in saturated, highly competitive markets that offer too many interesting choices (Lea-Greenwood, 1998; Oakley, 1990). Such a context rewards products that stand out because of their bright or novel look, as seen in colors for home interiors. This market has grown more competitive over the past half-century, and the novelty factor has correspondingly grown more important: preference for one paint color rises until satiated, then falls and yields to preference for another (Stansfield & Whitfield, 2005).

In the natural world, and under conditions of intense sexual selection, this same logic leads to a color polymorphism. A new color appears through mutation and spreads through the population until it is as common as the established color. This equilibrium will then last until another color variant appears. The total number of colors thus grows over time.

This aspect of sexual selection can be demonstrated under controlled conditions. In an American study, male participants were shown pictures of attractive brunettes and blondes and asked to choose, for each series, the woman they would most like to marry. One series had equal numbers of brunettes and blondes, a second series 1 brunette for every 5 blondes, and a third series 1 brunette for every 11 blondes. Result: the scarcer the brunettes were in a series, the likelier any one of them would be chosen (Thelen, 1983).

The same trend appears in popular culture. On American TV programs, women are four and a half times more likely than men to have red or auburn hair and five times more likely than men to have blonde hair. Conversely, men are four times more likely than women to have gray hair and 40% more likely than women to have black hair (Davis, 1990). A similar trend has been observed on Turkish TV programs:

Women were more likely than men to have red (5.3%) or blonde (15.6%) hair. In fact, no primary male characters in this sample had red or blonde hair at all, but female characters did. (Ikizler, 2007, p. 39)

This sex difference undoubtedly reflects the use of artificial hair coloring, although female hair color is naturally more diverse than male hair color (a legacy of the female-directed nature of sexual selection in Europe). Interestingly, women are using hair dyes to give themselves less typical hues, rather than more typical ones. Such colors may be uncommon but naturally occurring, such as platinum blonde and red. Or they may not exist at all in nature, such as green, purple, and magenta.

This year, the leading hair colors are forecasted to be “red, burgundy, strawberry blonde, copper brown and auburn shades.” Among celebrities, the hottest colors will include “bright reds, vibrant blues and pastel pinks” (Fall Hair Color Trends 2012).

References

Davis, M. D. (1990). Portrayals of women in prime-time network television: Some demographic characteristics. Sex Roles, 23(5/6), 325-332.

Fall Hair Color Trends 2012
http://researchanalyst.hubpages.com/hub/Hair-Color-Trends

Ikizler, A.S. (2007). Gender role representations in Turkish television programs, Submitted as a St. Mary's Project in Partial Fulfillment of the Graduation Requirements, St. Mary's College of Maryland for the Degree of Bachelor of Arts in Psychology
http://www.smcm.edu/psyc/_assets/documents/SMP/Showcase/0607-AIkizler.pdf

Lea-Greenwood G. (1998). Visual merchandising: a neglected area in UK fashion marketing? International Journal of Retail & Distribution Management, 26, 324-329.

Oakley M. (ed.) (1990). Design management. A handbook of issues and methods. Oxford: Basil Blackwell.

Stansfield J., & T.W.A. Whitfield. (2005). Can future colour trends be predicted on the basis of past colour trends? An empirical investigation. Color Research and Application, 30(3), 235-242.

Thelen, T.H. (1983). Minority type human mate preference. Social Biology, 30, 162-180.

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.

References

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
http://isteve.blogspot.com2011/05/old-blue-eyes.html

The puzzle of European hair and eye color

I’ve been fascinated by a puzzle of modern human evolution: the diverse palette of hair and eye colors that has developed in some populations (Frost, 2006; Frost 2008). Hair may be black, brown, flaxen, golden, or red, and eyes may be brown, blue, gray, hazel, or green. Both polymorphisms are largely confined to Europeans, especially those from the north and east.

This is an evolutionary puzzle for several reasons:

1. Hair color and eye color diversified through two separate processes that involved several gene loci (principally at MC1R for hair color and at OCA2-HERC2 for eye color).

2. Both processes occurred within the same geographic area.

3. Both processes occurred within a relatively narrow time frame, i.e., after the arrival of modern humans in Europe c. 35,000 years ago. Current estimates place this evolutionary change quite late in time, perhaps during the last ice age (25,000 - 10,000 BP).

For some anthropologists, this palette of hair and eye colors is a side effect of the lighter skin of Europeans. This lighter skin is, in turn, due to relaxation of selection for dark skin at non-tropical latitudes and a resulting accumulation of ‘loss of function’ alleles that affect not only skin color but also hair and eye color.

Yet relaxation of selection could not have produced so many new alleles over so little time. If selection is relaxed at loci for hair and eye color, close to a million years must elapse to produce the hair- and eye-color variability that Europeans now display, including ~ 80,000 years for the current prevalence of red hair alone (Harding et al., 2000; Templeton, 2002). This is much longer than the c. 35,000 years that modern humans have been in Europe. Moreover, the presumed initial cause—the whitening of European skin—seems to have occurred long after the arrival date of 35,000 BP (Norton & Hammer, 2007). As a Science journalist commented: “the implication is that our European ancestors were brown-skinned for tens of thousands of years” (Gibbons, 2007).

The puzzle is not resolved if Europeans turned white because of positive selection for lighter skin, as opposed to relaxation of selection for darker skin. Such a scenario would not have caused hair and eye color to diversify. In fact, most of the new alleles have little or no relationship with skin color. Only red hair and blue eyes are visibly associated with lighter skin.

There must have been positive selection for diversity of hair and eye color in and of itself. And this selection must have been very strong, given the relatively narrow time frame.

I have suggested that the likeliest explanation is sexual selection (Frost, 2006; Frost, 2008). This kind of explanation is consistent with several general facts:

1. Sexual selection typically creates brightly colored traits.

2. Such traits tend to be on or close to the face, because this part of the body attracts the most visual attention.

3. Intense sexual selection can produce color polymorphisms.

But why would sexual selection have been stronger among northern and eastern Europeans than among other human populations? To answer this question, we must understand why sexual selection should have differed in intensity among ancestral modern humans. In general, the differences were latitudinal, i.e., sexual selection differed primarily along a north-south axis.

Latitudinal differences in the ratio of men to women on the mate market

In the tropical zone, a woman could gather or grow enough food for herself and her children with little assistance. Because the cost of providing for a second wife was very low (often negative, i.e., a net gain), a man’s optimal reproductive strategy was to have as many wives as possible. There were thus too many men competing for too few women.

The farther away ancestral humans were from the tropics, the more women needed food (meat) provided by men. This was especially so in winter, when opportunities for food gathering were scarce. The cost of providing for a second wife was thus high, making polygyny impossible for all but the ablest hunters.

Alongside this trend of increasing female dependence on male providers was another north-south trend: male mortality increased farther away from the tropics because of longer hunting distances and the resulting increased risk of death due to accidents, exposure, starvation, etc.

Continental Arctic: optimal conditions for sexual selection of women

These two trends culminated in the continental Arctic. Here, women had few opportunities for food gathering at any time of year. They and their children depended almost wholly on meat that men provided through hunting. Here too, hunting distance was at a maximum. Men hunted wandering herds of herbivores, mainly reindeer, over very long distances. The high rate of male mortality, combined with the low rate of polygyny, limited the number of males available for mating. Result: a corresponding surplus of unmated females and intense sexual selection of women.

Today, this kind of environment is confined to the northern fringes of Eurasia and North America, but during the last ice age (25,000 – 10,000 BP) it lay further south and covered more territory. This was especially so in Europe, where the Scandinavian icecap had pushed the steppe-tundra zone down to the plains stretching from southwestern France through northern Germany and into eastern Europe. These temperate latitudes permitted a high level of bioproductivity and a comparatively large human population—the ancestors of today’s Europeans.

Sexual selection and color traits

When sexual selection is weak, the adaptive equilibrium is dominated by selection for a dull, cryptic appearance that reduces detection by predators. As sexual selection grows stronger, the equilibrium shifts toward a more noticeable appearance that retains the attention of potential mates, typically by means of vivid and/or novel colors.

One outcome may be a polymorphism of brightly colored phenotypes, due to the pressure of selection shifting to scarcer and more novel hues whenever a color variant becomes too common. This frequency dependence has been shown in humans. Thelen (1983) presented male participants with slides showing attractive brunettes and blondes and asked them to choose, for each series, the woman they would most like to marry. One series had equal numbers of brunettes and blondes, a second 1 brunette for every 5 blondes, and a third 1 brunette for every 11 blondes. Result: the rarer the brunettes were in a series, the likelier any one brunette would be chosen.

Among ancestral Europeans, this selection pressure may have caused a proliferation of new hair and eye colors to the detriment of our species norm of black hair and brown eyes. The selection was partly for novel colors. A rare color engages visual attention for a longer time than does a more common color (Brockmole & Boot, 2009). It may be that color rarity stimulates a mental algorithm that scans the visual environment for new or unusual objects.

In addition to color novelty, there also seems to have been selection for color brightness. Hair is carrot-red but not burgundy red. Eyes are light blue but not navy blue. Maan and Cummings (2009) argue that brighter colors have a stronger impact because they deliver a stronger signal that is more readily learned and retained in memory.

In a mate market already saturated with high-quality females, these eye-catching characteristics—color novelty and color brightness—may have made the difference between success and failure in finding a mate.

Other evidence for unusually strong sexual selection of European women

Hair and eye color polymorphism coincide geographically with other unusual physical traits. There is, for instance, the extreme whitening of the skin, which we do not see in other human populations at similar latitudes and which may have been driven by male targeting of lighter skin as a female-specific characteristic.

There also seems to have been selection to accentuate female-specific traits. Women of European descent have wider hips, narrower waists, and thicker deposition of subcutaneous fat than do women of other geographic origins (Hrdlička, 1898; Meredith & Spurgeon, 1980; Nelson & Nelson, 1986). Even before birth, Euro-American fetuses show significantly more sexual dimorphism than do African-American fetuses (Choi & Trotter, 1970).

In the same vein, Liberton (2009) has found that face shape differentiated between Europeans and sub-Saharan Africans in part through a selective force that has acted primarily on women, and not on both sexes. This too would be consistent with the selection pressure that seems to have diversified European hair and eye color.

References

Brockmole, J.R. & W.R. Boot. (2009). Should I stay or should I go? Attentional disengagement from visually unique and unexpected items at fixation, Journal of Experimental Psychology, 35, 808-815.

Choi, S.C., & Trotter, M. A. (1970). Statistical study of the multivariate structure and race‑sex differences of American White and Negro fetal skeletons. American Journal of Physical Anthropology, 33, 307‑312.

Frost, P. (2008). Sexual selection and human geographic variation, Proceedings of the 2nd Annual Meeting of the NorthEastern Evolutionary Psychology Society, The Journal of Social, Evolutionary & Cultural Psychology, 2 (supp.), 49-65, www.jsecjournal.com/NEEPSfrost.pdf

Frost, P. (2006). European hair and eye color - A case of frequency-dependent sexual selection? Evolution and Human Behavior, 27, 85-103 http://www.sciencedirect.com/science/journal/10905138

Gibbons, A. (2007). American Association Of Physical Anthropologists Meeting: European Skin Turned Pale Only Recently, Gene Suggests. Science 20 April 2007: 316. no. 5823, p. 364 DOI: 10.1126/science.316.5823.364a http://www.sciencemag.org/cgi/content/summary/316/5823/364a

Harding, R.M., Healy, E., Ray, A.J., Ellis, N.S., Flanagan, N., Todd, C., Dixon, C., Sajantila, A., Jackson, I.J., Birch‑Machin, M.A., & Rees, J.L. (2000). Evidence for variable selective pressures at MC1R. American Journal of Human Genetics, 66, 1351‑1361.

Hrdlička, A. (1898). Physical differences between White and Colored children. American Anthropologist, 11, 347‑350.

Liberton, D.K., K.A. Matthes, R. Pereira, T. Frudakis, D.A. Puts, & M.D. Shriver. (2009). Patterns of correlation between genetic ancestry and facial features suggest selection on females is driving differentiation. Poster #326, The American Society of Human Genetics, 59th annual meeting, October 20-24, 2009. Honolulu, Hawaii.

Maan, M.E. & M.E. Cummings. (2009). Sexual dimorphism and directional sexual selection on aposematic signals in a poison frog, Proceedings of the National Academy of Sciences (USA), 106, 19072-10977.

Meredith, H.V., & Spurgeon, J.H. (1980). Somatic comparisons at age 9 years for South Carolina White Girls and girls of other ethnic groups. Human Biology, 52, 401‑411.

Nelson, J.K., & Nelson, K.R. (1986). Skinfold profiles of Black and White boys and girls ages 11‑13. Human Biology, 58, 379‑390.

Norton, H.L. & Hammer, M.F. (2007). Sequence variation in the pigmentation candidate gene SLC24A5 and evidence for independent evolution of light skin in European and East Asian populations. Program of the 77th Annual Meeting of the American Association of Physical Anthropologists, p. 179.

Templeton, A.R. (2002). Out of Africa again and again. Nature, 416, 45-51.

Thelen, T.H. (1983). Minority type human mate preference. Social Biology, 30, 162-180.

More on the origins of male homosexuality

Are there other theories on the origins of male homosexuality? Yes, quite a few. These theories generally fall into two categories: those that explain the relatively small variance due to genetic factors (30-45%) and those that explain the larger variance due to some environmental factor. Conceivably, we could be looking at an interaction between the two, i.e., an environmental factor (a pathogen, prenatal trauma, or perhaps environmental estrogens) interacting with a genetic predisposition (partly feminized male brains, as postulated by Ed Miller).

This week, we will look at another theory. Like Miller, Zietsch et al. (2008) postulate a genetic predisposition maintained by a balanced polymorphism. Unlike Miller, they believe this predisposition somehow increases mating success, rather than offspring survival.

Using twin data, they found that heterosexuals tend to have more sexual partners over a lifetime if they have a homosexual twin than if they have a heterosexual twin. This increased mating success, however, was significant only when the heterosexual was female. The authors attribute these findings to a genetically influenced behavioral trait.

Our hypothesis is that a number of pleiotropic (more than one effect) genes predispose to homosexuality but also contribute to reproductive fitness in heterosexuals. In the case of males, there are a number of alleles that promote femininity: if only a few of these alleles are inherited, reproductive success is enhanced via increased levels of attractive but typically feminine traits such as kindness, sensitivity, empathy, and tenderness. However, if a large number of alleles are inherited, even the feminine characteristic of attraction to males is produced. In females, the converse explanation could be used—a low dose could lead to advantageous typically masculine characteristics such as sexual assertiveness or competitiveness, and a large dose could further lead to attraction to females. (Zietsch et al., 2008)

The authors attribute this hypothesis to Ed Miller, although Miller’s theory has more to do with increased offspring survival (due to increased paternal investment) than to increased success on the mate market.

Does this hypothesis explain the authors' findings? Does it predict that hetero women with gay or lesbian siblings have more lifetime sexual partners? No. First, it doesn’t explain why such an effect is confined to female heterosexuals. Nor is it clear why this hypothesis should account equally well for hetero women with gay brothers and for hetero women with lesbian sisters. The authors seem to be arguing that these women have more lifetime partners than do other women because they’re more feminine in some cases and more masculine in others.

Hmm … Could we be looking at a shared family environment effect? Parental attitudes toward homosexuality in offspring tend to correlate with parental attitudes toward promiscuity in offspring, especially in daughters. This correlation is especially high if we compare religious families with non-religious ones. If a mother and father accept expression of homosexuality in their children, they would probably also accept their daughters having more sexual partners. On these grounds alone, a gay or lesbian child is likelier to have a sister who has more sexual partners on average. But this correlation would not be a cause-and-effect one. It would flow from a common cause: parental permissiveness.

One could shoot back: “Homosexuals are not made by permissive parents. They’re born that way.” True, but the participants in this study were asked to self-identify as heterosexual or homosexual (on a scale of 1 to 6). Even if family environment doesn’t determine latent sexual orientation, this factor would probably influence one’s willingness to affirm it, both to oneself and to others.

References

Zietsch, B.P., Morley, K.I., Shekar, S.N., Verweij, J.H., Keller, M.C., Macgregor, S. Wright, M.J., Bailey, J.M., & Martin, N.G. (2008). Genetic factors predisposing to homosexuality may increase mating success in heterosexuals. Evolution & Human Behavior, 29, 424-433.

Origins of male homosexuality - The germ theory

How does male homosexuality originate? More to the point, how does it perpetuate itself? According to Ed Miller, it results from a balanced polymorphism—a delicate balancing act where too much feminization of the male brain causes attraction to one’s own sex and too little causes indifference to one’s own children. This week, I will present an alternate explanation: Greg Cochran’s germ theory.

Greg has never published his theory in a peer-reviewed journal, although it is briefly summarized in Cochran et al. (2000). In itself, this is no shortcoming. Most journals seem uninterested nowadays in real debate. But sometimes I wish he would at least pretend he was writing for a journal. He tends to be polemical, as if only political correctness—or sheer stupidity—could motivate his detractors.

His starting point is the same as Miller’s. Male homosexuality makes no sense as a reproductive strategy. It should die out for the same reason that the Shakers did (the Shakers were a Protestant sect dedicated to lifelong celibacy). This point might seem obvious. Or maybe not. The following is an exchange between a germ theory critic and Greg Cochran:

Critic: Is it not likely that human sexuality is in fact a bell curve, with "strict homosexual" on one end and "strict heterosexual" on the other end, and the majority of the people falling somewhere in between? (With the caveat that sexual preference and sexual practice are not necessarily the same thing).

Greg: No, it is not likely. Sheesh. That would make exactly as much sense as a bell curve of food preferences ranging from steak at the left to granite at the right, in which people in the middle liked steak and rocks equally well. Is an even split between a behavior that works and one that never does what you expect from biology? Do you expect half the geese to fly north for the winter? (source)

Since natural selection would tend to eliminate male homosexuality, it should be uncommon—like most genetic conditions that impair one’s ability to survive and reproduce.

First we have to say what ‘common’ means, in this context. Common means common compared to the noise in the system. So 1% is very common: no disease caused by random mutations is anywhere near that common. 1 in 10,000 is surprisingly common, but there are one or two mutation-caused diseases that are in that ballpark, like Duchenne’s muscular dystrophy. Turns out that the gene involved in muscular dystrophy is maybe 20 times longer than the typical gene — there are more opportunities for typos. So 1 in 7000 boys have Duchenne’s muscular dystrophy — that’s as common as a ‘system noise’ disease gets. (Cochran 2004?)

Since male homosexuality is not rare, it cannot have a genetic cause, at least not principally. There may be a genetic predisposition (with around 30-45% heritability, according to twin studies), but this predisposition is interacting with something in the environment. And this something cannot be a recent environmental change, since male homosexuality has been around for a long time.

The only remaining cause would be some kind of infectious agent that selectively alters certain parts of the brain while leaving the rest intact. There are precedents for this sort of thing.

Do we know of diseases in which there are very specific targets—in which certain cell types are damaged or destroyed while neighboring cells are left intact? Sure. In some cases, a pathogen targets a particular cell type and has little effect on anything else. Human parvovirus (also known as fifth disease) hits erythroid precursor cells (the cells that manufacture red cells) and temporarily inhibits red cell production. In type-I diabetes, it seems likely that Coxsackie virus infections (in people with a genetic predisposition, in which HLA type plays a major role) trigger an autoimmune disease that gradually (over a year or so) destroys the islet cells which produce insulin. Other cells are not much affected. (Cochran 2004?)

Such pathogens may be more common than we think. The ones that get our attention—that make us go and see a doctor—are the ones that cause discomfort. But those ones may be a small minority of all pathogens, with most of the others flying under the radar. After all, it is in the pathogen’s own interest to be discrete and not cause too much havoc. It needs a healthy home to live in, until it can spread to another host.

Greg also argues that male homosexuality should be less common in smaller communities than in larger ones—where pathogenic transmission is likelier.

We can deduce a few things about the hypothetical agent causing homosexuality. First, it has a small, but not incredibly small, critical community size. That is the size of the clump of people required to keep the agent going. Some agents, ones in which infection results in permanent immunity, need a _large_ number of people, big enough that there are new infected people showing up by the time it circles the community. Measles for example requires almost half a million people in close proximity. An agent that causes a persistent infection can have a very small community size: I'd guess that Epstein-Barr has a CCS under 50.

Since some communities seem to have no homosexuality at all (Bushmen, some hunter-gatherer groups in Indonesia and the Philippines, pre-contact Polynesians) we can be sure that this hypothetical agent has a critical community size larger than that of Epstein-Barr. More like chickenpox, which has a CCS of about 300 people. Not that I'm saying it _is_ chickenpox, mind you. (Cochran 2005)

Finally, this pathogen may selectively alter sexual orientation for reasons that go beyond those of not harming the host too much. There are, in fact, a number of pathogens that alter the host’s behavior in order to enhance their chances of transmission. The protozoan Toxoplasma gondii causes infected rats to lose their fear of cats, thus enabling it to enter a cat body and complete its life cycle (Wikipedia – Toxoplasmosis). The parasitic worm Euhaplorchis californiensis forms cysts in the brains of infected killifish that cause the fish to swim near the surface of the water and make tight turns that show off their glinting sides, thus enabling the worm to enter a bird’s body (Zimmer, 2008).

As a child, I remember being told that a chicken is an egg’s way of making another egg. If Greg Cochran is right, a gay man is a vehicle that a pathogen has constructed for its own survival and reproduction. Everything else is human-centered delusion.

This is an interesting argument, but it has a few holes. First, some genetic conditions do reach incidences that are comparable to that of male homosexuality (about 3-5% of all men). Abnormal hemoglobin variants can reach high incidences in sub-Saharan Africans and other populations (8% in the case of Hb AS among African Americans). These variants are typically maintained through balancing selection where the heterozygote state provides some protection against malaria. Greg acknowledges that such selection exists but sees it as being confined to malaria protection. Yet balancing selection can exist for many other reasons. For example, one in 200 Hopi is albino, apparently because cultural selection offsets the environmental disadvantages of albinism (Hedrick, 2003).

Second, male homosexuality is frequently reported in small communities, including bands of Amerindian hunter-gatherers. Known as ‘berdaches’, these male homosexuals were described by early European explorers and appear to have existed in pre-contact times, as indicated by origin myths (Desy, 1978). One witness was John Tanner, a white captive who lived among the Ottawa of Ontario and then the Ojibwa of Manitoba until 1828:

Some time in the course of this winter, there came to our lodge one of the sons of the celebrated Ojibbeway chief, called Wesh-ko-bug, (the sweet)... This man was one of those who make themselves women, and are called women by the Indians. There are several of this sort among most, if not all the Indian tribes. They are commonly called A-go-kwa, a word which is expressive of their condition. This creature, called Ozaw-wen-dib, (the yellow head), was now near fifty years old, and had lived with many husbands. I do not know whether she had seen me, or only heard of me, but she soon let me know she had come a long distance to see me, and with the hope of living with me. She often offered herself to me, but not being discouraged with one refusal, she repeated her disgusting advances until I was almost driven from the lodge. (Desy, 1978)

Of course, neither point disproves the germ theory of male homosexuality. An infectious agent may indeed be the cause or one of several causes. If we consider the developmental pathway for heterosexual orientation, there is probably a ‘default’ sequence that leads to sexual interest in men and an ‘override’ sequence that leads to sexual interest in women. The second sequence may be disrupted for many reasons: a psychological trauma, a chemical insult, or an infectious agent in combination with a pre-existing genetic predisposition for incomplete masculinization. As one comment noted:

Some of the disruptive factors implicated by empirical evidence are excess prenatal testosterone exposure (a major factor), prenatal stress, and exotic factors such as disruptive chemical agents. Infections proposed by Cochran may also disrupt development, but I do not know of any evidence that supports this assertion as of yet. (Cochran 2005)

References


Cochran, G.M. (2005). Cause of Homosexuality: Gene or Virus? Cochran Interview. Thrasymachus Online.

Cochran, G.M. (2004?). An evolutionary look at human homosexuality. World of Greg Cochran.

Cochran, G.M., Ewald, P.W., & Cochran, K.D. (2000). Infectious causation of disease: an evolutionary perspective. Perspectives in Biology and Medicine, 43, 406-448.

Désy, P.P. (1978). L'homme-femme. (Les berdaches en Amérique du Nord), Libre — politique, anthropologie, philosophie, 78(3), 57-102.

Hedrick, P.W. (2003). Hopi Indians, “cultural” selection, and albinism. American Journal of Physical Anthropology, 121, 151-156.

Zimmer, C. (2008). The Parasite Files. Discover. Dec. 16.