Wednesday, December 31, 2008

Predictions for 2009

Human genomics

The Neanderthal genome will be fully sequenced. There will be no evidence of interbreeding with modern humans (although proponents of the multiregional model will remain unconvinced). By comparing this genome with ours, we may reconstruct the genome of archaic humans who lived almost a million years ago and who were ancestral to Neanderthals and modern humans.

Meanwhile, work will begin on sequencing the genome of early modern humans (10,000 – 40,000 years ago). This project should ultimately prove to be more interesting by showing us how much modern humans have evolved during their relatively short existence. We will probably find out that John Hawks erred on the low side in concluding that natural selection had changed 7% of the human genome over the past 40,000 years.

Darwin remembered

With the 150th anniversary of The Origin of Species, much will appear in 2009 about Charles Darwin and his life. We already know how he came up with his theory of evolution (Darwin salted away almost everything he wrote), although a few questions remain unanswered. What would he have done if he had lived longer? What did he have in mind for future projects?

Probably not much. He had said everything he wanted to say. The Origin of Species (1859) came out of a backlog that had built up in his mind during the previous twenty years. Then came The Descent of Man (1871), which used material left out of The Origin. Finally, The Expression of the Emotions in Man and Animals (1872) was largely a spin-off of The Descent. With this trilogy completed, he had little more to say. A younger Darwin might have addressed one of the dilemmas of evolution. How do selected characteristics perpetuate themselves? What keeps them from being blended away into non-existence with each generation of sexual reproduction? Darwin might have learned about another contemporary scientist, Gregor Mendel, and together the two of them might have proposed a particulate theory of genetics—more than thirty years before later evolutionists rediscovered Mendel’s work. The field of genetics would have developed much faster and, under Darwin’s guidance, may have avoided some of its later blind alleys (e.g., mutation pressure, saltationism, etc.).

Perhaps. But Darwin was unprepared for success. He had finally got to tell the world everything he had so long held back. And the world listened. From then on, a sense of emptiness took over, as if his remaining years were little more than an epilogue.

The Crisis?

The Second Great Depression will not begin in 2009. In any case, what scares me is not the prospect of a sudden drop in the standard of living. Rather, it’s that of a gradual decline to almost half its current value. That scenario is scarier and likelier. And it’s probably already started. For the past fifteen years, median wages have stagnated despite decent economic growth. What will happen when growth stays in the 0-2% range?

Wednesday, December 17, 2008

Neanderthals in my sinus?

About two years ago, Gregory Cochran teased GNXP readers with a suggestion that Neanderthals might still be living among us. There was a flurry of speculation. Sasquatches? Yeti? Scottish redheads? Finally, the answer has come out. Greg thinks there may be infectious organisms that originally developed from Neanderthal tumors several tens of millennia ago. These organisms might look like amoebae, but genetically they would be Neanderthals.

The general idea is that host cell line infections can occur (TVT, Tasmanian devil facial tumor, and a contagious leukemia in Syrian hamsters), can mutate into something that is nonlethal and/or chronic if selection favors that (TVT usually goes away with time), can infect related species (TVT can be experimentally transmitted to wolves, jackals, coyotes and red foxes), and might exist in humans today. There are human diseases that appear infectious for which the transmissible agent has not been identified - sarcoidosis, for example. So modern humans might suffer from infectious organisms directly derived from Neanderthals or other archaic humans. As far as I know, no one has yet thought of looking for Neanderthal-derived cells inside people. Since such cells would have the required genetic code for making human signal molecules, they might be particularly likely to employ baroque forms of host manipulation.

… there _could_ be Neanderthal-derived cell line infections, and this is really the only scenario I've been able to come up with that gives us live Neanderthals - hiding in your sinuses, or maybe your prostate. The only one so far. There are other known infectious diseases in which some metazoan has completely chucked complexity and gone back to being a germ: whirling disease in fish, for example.

Will it then be possible to resurrect Neanderthals à la Jurassic Park? Another GNXP commenter, Eric J. Johnson, poured cold water on the idea:

… the problem would be a lack of purifying selection on all the morphogen genes, not to mention all the neuron-specific genes, etc. The tumor doesn't need any of that stuff. How fast they would all turn to garbage, I don't know. Probably pretty fast.

Wednesday, December 10, 2008

Gene-culture co-evolution and evolutionary psychology

How much do human populations differ from each other in real, functional terms? The question remains open, but an answer is starting to unfold. In 2007, a team led by anthropologist John Hawks found that natural selection seems to have modified at least 7% of the human genome over the last 40,000 years, i.e., during the period when modern humans spread out of Africa and peopled the other continents. In addition, as they moved into these different physical and cultural environments, the pace of genetic change seems to have speeded up, particularly after the advent of agriculture 10,000 years ago. The rate of change may then have been over a hundred times what it had been during most of human evolution (Hawks et al., 2007)

We do not fully know the nature of these recent genetic changes. John Hawks suggests they may reflect adaptations to new ecological and cultural settings, specifically to cold, to new diets (cereals, milk, etc.), to new epidemic diseases associated with the spread of agriculture (smallpox, malaria, yellow fever, typhus, cholera), and to new forms of “communication, social interactions, and creativity.”

There thus seem to have been multiple EEAs in relatively recent times, and not simply one situated in the Pleistocene. Some of them would correspond to the different physical environments that modern humans moved into as they spread out of Africa 40 to 50 thousand years. Most however, seem to have arisen in the past 10 thousand years and correspond to different cultural environments.

John Hawks is certainly not the first one to suggest that culture has been a key part of the human adaptive landscape. Usually referred to as ‘gene-culture co-evolution’, this paradigm has had many proponents, notably Pierre van den Berghe, Charles Lumsden, and E.O. Wilson. It has nonetheless remained marginal, even among evolutionary psychologists. This is partly because of the influence of John Tooby and Leda Cosmides, whose influence was critical during the early years of evolutionary psychology:

It is no more plausible to believe that whole new mental organs could evolve since the Pleistocene—i.e., over historical time—than it is to believe that whole new physical organs such as eyes would evolve over brief spans. It is easily imaginable that such things as the population mean retinal sensitivity might modestly shift over historical time, and similarly minor modifications might have been made in various psychological mechanisms. However, major and intricate changes in innately specified information-processing procedures presentover brief spans of historical time. (Tooby & Cosmides, 1989)

In a more recent article, they have backed away from this position: “Although the hominid line is thought to have originated on edges of the African savannahs, the EEA is not a particular place or time.” Each biological adaptation has its own EEA, which is simply a composite of whatever selection pressures brought it into being (Tooby & Cosmides, 2005). There are thus potentially as many EEAs as there are adaptations. It follows, then, that some EEAs may have existed later in time than others.

How much later? Tooby and Cosmides considered complexity to be one limiting factor. The more complex the adaptation, the more genes it would involve, and the longer the time needed to coordinate the evolution of all those genes. Therefore, recent biological evolution has probably only involved simple traits, certainly nothing as complex as mental ones. Such traits could have arisen only through a faster process, notably cultural evolution.

The problem with this argument is that complex traits do not arise ex nihilo. They arise through modifications, deletions, or additions to existing traits. And such changes can occur through a single point mutation at a regulatory gene. As Harpending and Cochran (2002) point out:

Even if 40 or 50 thousand years were too short a time for the evolutionary development of a truly new and highly complex mental adaptation, which is by no means certain, it is certainly long enough for some groups to lose such an adaptation, for some groups to develop a highly exaggerated version of an adaptation, or for changes in the triggers or timing of that adaptation to evolve. That is what we see in domesticated dogs, for example, who have entirely lost certain key behavioral adaptations of wolves such as paternal investment. Other wolf behaviors have been exaggerated or distorted.

Gene-culture co-evolution also presents difficulties that are inherent to the paradigm itself:

1. The linkages between genes and culture tend to be remote, indirect, multiple, and complex. There are some straightforward ones, such as between lactose intolerance and consumption of dairy products, but such linkages are probably unrepresentative of gene-culture co-evolution.

2. With only a few minor exceptions, gene-culture co-evolution is specific to humans. Cross-species comparisons, so common in other fields of evolutionary study, are thus of little help (van den Berghe & Frost, 1986).

These difficulties are not insuperable. To some degree, they reflect an unconscious desire to study human evolution with the same conceptual tools that have been used to study the evolution of other species. Other tools will have to be developed, or simply borrowed from the social sciences of psychology, sociology, and anthropology. Thus, there are no real barriers to renewed use of this paradigm, particularly as we move beyond the single-EEA model and investigate this 7% of the human genome that has apparently changed over the past 40,000 years.


Harpending, H. & G. Cochran. (2002).
"In our genes", Proceedings of the National Academy of Sciences, 99(1), 10-12.

Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, & R.K. Moyzis. (2007).
Recent acceleration of human adaptive evolution. Proceedings of the National Academy of Sciences (USA), 104, 20753-20758.

Tooby, J. & L. Cosmides. (2005). Conceptual foundations of evolutionary psychology, in: D. M. Buss (Ed.) The Handbook of Evolutionary Psychology, Hoboken, NJ: Wiley, pp. 5-67.

Tooby, J. & L. Cosmides. (1989). Evolutionary psychology and the generation of culture, Part I. Theoretical considerations, Ethology and Sociobiology, 10, 29-49.

van den Berghe, P.L., & Frost, P. (1986). Skin color preference, sexual dimorphism and sexual selection: A case of gene-culture co-evolution? Ethnic and Racial Studies, 9, 87-113.

Wednesday, December 3, 2008

More on father absence

I used to believe in a direct causal link between father absence and early sexual maturity in girls. The reasoning was that a daughter’s sexual development is accelerated when her biological father is replaced by a strange male (such as a stepfather). At the time, I saw this finding as a way to counter the argument that sociobiology denies human plasticity. It also offered hope that we could remedy a large number of social problems by ensuring father presence. Now I can’t help wondering whether all of this distorted my sense of judgment … and that of others.

One of the best studies on this subject is by Surbey (1990), who used a large sample (1,247 daughters) and measured several possible confounding factors: family size, birth order, weight, height, Quetelet Index, and socio-economic status (SES). On none of these measures did the father-absent daughters (16% of the sample) significantly differ from the father-present daughters. Nonetheless, they matured 4-5 months earlier than those who lived with both parents continuously and 7 months earlier than those who had experienced only an absent mother.

That sounds convincing. Yet how well was SES really controlled? The subjects were apparently university students, so they would have shared the SES of their mothers. But what about the SES of their absent fathers? What do we know about them? Typically nothing. And does SES fully capture all of the factors that distinguish father-absent daughters from father-present ones? Could it be that these two groups differ somewhat in their physiological make-up and, perhaps, in their genetic background?

These doubts led Mendle et al. (2006) to control for genetic background by examining the daughters of twin mothers. It turned out that the daughters did not differ in age of menarche if one mother was still living with the biological father and the other was not. Moreover, when the mother’s age of menarche was controlled among unrelated daughters, age of menarche no longer differed between daughters living with stepfathers and those living with biological fathers.

The presence of a step-uncle was as strongly predictive of early menarche as presence of a stepfather. It does not seem necessary for a child to experience the direct environmental influence of a stepfather to exhibit an accelerated age of menarche—as long as she is genetically related to someone who does have a stepfather. In a pair of twin mothers of which only one raises her children with a stepfather, the offspring of both twins are equally likely to display early age of menarche. It therefore appears that some genetic or shared environmental confound accounts for the earlier association found in female children living with stepfathers.

Mendle et al. (2006) raised another point. The correlation between father-absence and early menarche may be an artefact of population substructure:

The wholly Caucasian population of our Australian sample may explain our failure to replicate the strong father-absence association observed in more ethnically diverse American samples. Given that African American and Latina girls experience menarche on average 6 months prior to Caucasians (Herman-Giddens et al., 1997), it may be that the previously established associations between early menarche and lack of a traditional two-parent family structure are affected by racial differences in family structure. Correlates of early menarche may additionally be complicated by effects of poverty or socioeconomic status. For example, Obeidallah, Brennan, Brooks-Gunn, Kindlon, and Earls (2000) obtained a difference in age of menarche between Caucasian and Latina girls, but this effect disappeared after controlling for socio-economic status.

Why didn’t other studies control for ethnicity? Apparently because the authors felt that SES controls were sufficient. This may be true for Hispanic Americans but it is not for African Americans. Even among Hispanics, there may still be substructure effects. It is known that Hispanic SES correlates with European ancestry, so controlling for SES would bias this population toward individuals who are more genetically similar to European Americans.

All of this makes me wonder about all of the data that supposedly prove the adverse effects of single motherhood. Undoubtedly, there are adverse effects. But there are probably many “pseudo-effects” that would persist even if the biological father could be forced to stay around.

For what it’s worth, I spent part of my pre-adult life in a father-absent family (my father died of a cerebral hemorrhage). Yes, there were adverse effects, poverty in particular. Nonetheless, I think I would have ended up being substantially the same kind of person even if my father had continued to live.


Mendle, J., Turkheimer, E., D’Onofrio, B.M., Lynch, S.K., Emery, R.E., Slutske, W.S., Martin, N.G. (2006). Family structure and age at menarche: a children-of-twins approach. Developmental Psychology, 42, 533-542.

Nettle, D. (2008). Why do some dads get more involved than others? Evidence from a large British cohort. Evolution and Human Behavior, 29, 416-423.

Surbey, M.K. (1990). Family composition, stress, and the timing of human menarche. In T.E. Ziegler & F.B. Bercovitch (eds.) Socioendocrinology of Primate Reproduction, pp. 11-32, New York: Wiley-Liss Inc.