Alexander the Great’s conquests, and later the Roman Empire’s expansion, transformed the cultural landscape by merging different peoples into a syncretic Greco-Roman culture. Religion too became universal through the Hellenization of non-Greek deities and ultimately the emergence of a single universal faith. Within this same context, local markets dissolved into a larger market that brought supply and demand together throughout the Mediterranean, and even beyond.
These broadening horizons affected slave markets as well. Slaves were initially taken in war or carried off by pirates. With the suppression of piracy after the battle of Actium (31 BC) and the stabilization of the empire’s borders under the emperor Hadrian (117-138 AD), people turned to other sources: condemned criminals, children sold by indebted parents, foreigners purchased from outside the Empire (Westermann, 1955, pp. 84-85). The last source supplied nearly one eighth of all slaves, including some from sub-Saharan Africa by way of Egypt (Westermann, 1955, pp. 96, 135).
How many? Although it is known that some black Africans were present in the ancient Mediterranean world, the magnitude of their presence is hard to quantify. It is widely believed, notably by the historian Bernard Lewis, that they were relatively few in number until the creation of the Muslim world in the 7th century, when the black slave trade presumably took off (Lewis, 1990, p. 41). But there are reasons for believing that their numbers had grown considerably even before Islam, having increased slowly but steadily throughout the early Christian era. During that era, 4% of people buried in Corinth seem to have been black African (Angel, 1972). In the Egyptian scenes of the Ashburnham Pentateuch (6th century AD), almost a quarter of the faces are black. Finally, early Christian literature often mentions Ethiopians, as black Africans were called in Greek and Latin. Many of these mentions indicate personal familiarity.
Meanwhile, pagan, Christian, and Jewish writings increasingly associated dark skin with slavery. In the 1st century, the Roman author, Petronius, represents very light skin by Gauls and very dark skin by Ethiopian slaves (Satyricon 102). In the 2nd century, the Greek satirist, Lucian, wrote: “In the first place, is he not generous in his proportions and pleasing in his complexion, neither dark nor fair of skin; for the one befits a woman, and the other a slave (De parasito 41).
This mental association intensified during the early Christian era. It is especially attested by the tendency from the 3rd to 5th centuries to reinterpret the ‘Curse of Ham’ in the book of Genesis. This is the original version: when Ham saw his father Noah naked and drunk, Noah angrily condemned to slavery all of Ham’s descendents through Ham’s son, Canaan (Genesis 9: 22-27). Initially, the curse served to justify enslavement of the former inhabitants of the land of Israel, the Canaanites. Then, during the first centuries of the Christian era, it tended to target the brown- and black-skinned peoples of Africa—Ham’s supposed descendents. Finally, it came to hang solely over the black Africans, who were said to be descended from another of Ham’s sons, Chusi, but also more generally from Ham or even from Canaan.
Thus, in the 3rd century, St. Origen invoked the Curse of Ham to explain the servility of the “discolored” Egyptians:
Pharaoh easily reduced the Egyptian people to servitude, nor is it written that he did so by force. For the Egyptians are prone to a degenerate life and quickly sink to every slavery of the vices. Look at their origin: you will discover that their father Ham, who had laughed at his father’s nakedness, deserved a judgment of this kind, that his son Canaan should be a servant to his brothers, so that his condition of servitude would testify to the wickedness of his conduct. Not without reason, therefore, does the discolored posterity imitate the ignobility of the race. (Hom. in Genesim 16.1)
Dark skin is explicitly attributed to this curse in a 3rd or 4th century Samaritan exegesis: “When Kush saw the nakedness of his father, he was cursed and he wore darkness—he and all his descendents forever” (Goldenberg, 2003, p. 100). Similarly, according to a 4th century Christian account, attributed to St. Ephrem of Nisibis (Syria), Noah said: “Accursed be Canaan, and may God make his face black” (Lewis, 1990, p. 124). Another work attributed to St. Ephrem, The Cave of Treasures, also seems to link this curse to dark-skinned peoples:
For by means of singing, and lewd play, and the mad lasciviousness of the children of Cain, Satan had cast down the mighty men, the "sons of God," into fornication. And through the music of reed pipes and harps sin had multiplied among the former generations until, at length, God became wroth and made the Flood. And Canaan was cursed because he had dared to do this, and his seed became a servant of servants, that is to say, to the Egyptians, and the Cushites, and the Mûsâyê (Mysians), [and the Indians, and all the Ethiopians, whose skins are black]. And because Ham had dared to make a mock of his father he was called "vile" (or "lascivious") all the days of his life. (Ephrem, 1927, fol. 19a, 19b)
Two late versions (8th century) add: “and other blacks” or “and all those whose skin color is black” (Goldenberg, 2003, p. 173). These peoples are thus seen as having especially dark skin, i.e., darker than that of early Christians in the Greco-Roman world.
The Egyptians hold first place in this list, probably because they were the best known “people of color” at that time. Thus, the Greco-Roman world tended to see them as encompassing Ethiopians, i.e., black Africans, viewing the latter as Egyptians with even darker skin. This tendency to lump the two peoples together also appears in ancient rabbinic literature, which states that Egypt and Kush (Nubia and more generally sub-Saharan Africa) are the lands of “dark men” and that Egypt is “a place of ugly and dark people” (Goldenberg, 2003, p. 107-109, 117-118). According to the historian David Goldenberg (2003, p. 109): “Both the Jewish and the Greek etiologies show that in regard to skin color, the Kushites/Ethiopians were not considered in a separate category but were seen as part of a larger class of dark-skinned peoples.” It is in this broader sense that the word Egyptian seems to be used further on in The Cave of Treasures:
Now the seed of Canaan, as I have already said, are the Egyptians, and behold, they are scattered over the whole earth, and have been made servants of servants. And of what kind is this slavery of slavery? Behold, the Egyptians go round about all over the earth carrying loads on their backs (literally, necks). Now, men who are not fettered under the yoke of slavery, when despatched by their masters on journeys, do not march on their feet and carry loads, but they ride upon beasts in an honourable manner, like their masters. The seed of Ham are the Egyptians who carry loads, and they march on the roads with their backs and necks breaking under their loads, and they wander round to the doors of the children of their brethren. The seed of Ham was reduced, through the folly of Canaan, to suffer this penalty, that is, to become servants even to servants. (Ephrem, 1927, fol. 19b, 20a)
These “Egyptians” were probably black Africans. If so, this passage would testify, three centuries before Islam, to a sizeable diaspora of black slaves in the ancient world. In addition, these slaves were considered to be different from other slaves. This view is attested a century earlier when Origen wrote:
Thus, the divine laws provided that whoever has bought a Hebrew servant will not keep him indefinitely in servitude: he will serve six years and, the seventh, will go free. Nothing similar is decreed for the Egyptians: nowhere does the divine law have a provision for the freedom of the Egyptians, for they lost it willingly, and it abandons them to the eternal yoke of their fate and to perpetual servitude (Hom. in Genesim 16.1)
The Curse of Ham was similarly transformed in post-biblical Jewish literature. According to a 5th century text, Ham wished to keep his share of the inheritance intact and, to this end, tried to prevent his father from having another son. One day, seeing his father drunk and undressed, he seized the opportunity and castrated him. Noah awoke from his stupor and cursed Ham: “You have prevented me from doing something in the dark [i.e., sex], therefore your seed will be ugly and dark-skinned.” (Genesis Rabba 36:7). According to two Talmudic accounts from the 4th and 6th centuries, Ham violated a rule prohibiting sexual intercourse in Noah’s ark. Persuaded that the first child born after the flood would inherit the world, Ham defied the prohibition and copulated with his wife, whereupon his skin turned black (Tractate Sanhedrin 108b, Tractate Ta’an 1.6, 64d).
In the 6th century, a Christian philosopher from Alexandria, John Philoponus, named solely the black Africans as a people destined for slavery: “The Scythians and Ethiopians are distinguished from each other by black and white color, or by long and snubbed nose, or by slave and master, by ruler and ruled”; “The Ethiopian and Scythian … one is black, the other white; similarly slave and master” (Goldenberg, 2003, p. 135).
If at that time the Greco-Roman world already associated black skin with slavery, it is not because the slaves were almost all blacks but because the blacks were almost all slaves; this was the status of most foreigners. Indeed, it is precisely because black Africans formed a small visible minority that their servile status was easy to recognize (Goldenberg, 2003, pp. 135-136, 138). Furthermore, as Origen noted, they tended to retain this status longer, if not for life, thereby strengthening the mental association between dark skin and slavery.
It remains to be explained why this slave population became so numerically important even before the Islamic era. What was stimulating its growth? Perhaps supply and demand were reciprocally stimulating each other: since black Africans were less likely to lose their slave status, people increasingly came to see their tasks as “slave work” —unworthy of free people and treated accordingly. The supply thus favored its own demand by degrading the working conditions.
References
Angel, J.L. (1972). Review of Blacks in Antiquity, American Anthropologist, 74, 159-160.
Ephrem (1927). The Book of the Cave of Treasures, translated from the Syriac by E. A. Wallis Budge. London: The Religious Tract Society]
Goldenberg, D.M. (2003). The Curse of Ham. Race and Slavery in Early Judaism, Christianity, and Islam. Princeton: Princeton University Press.
Lewis, B. (1990). Race and Slavery in the Middle East. An Historical Enquiry. Oxford: Oxford University Press.
Westermann, W.L. (1955). The Slave Systems of Greek and Roman Antiquity. Philadelphia: Memoirs of the American Philosophical Society.
Friday, January 25, 2008
Friday, January 18, 2008
Skin color in early Christianity and Judaism
About 15 years ago, I received an e-mail from a specialist in Jewish studies, Dr. David Goldenberg, who had read an article of mine and wanted to know more about the subject. The article described how early Christians perceived Black Africans, or Ethiopians as they were then called, especially those who lived as a small visible minority in the Mediterranean world. I had come to this subject out of a desire to understand how differences in skin color were perceived in contexts that preceded the historical experiences of European colonialism and black slavery. This desire led me to such culture areas as the Mediterranean world of Late Antiquity, ancient India, and the contact zone between Melanesia and Polynesia. Ultimately, I wanted to isolate the patterns of perception and response that existed during the long period of human existence when, in any given society, skin color differed primarily between men and women.
David Goldenberg came to this subject from a very different angle. A number of African American authors were arguing that the Jews had invented anti-black racism, the “proof” being early rabbinical writings that had reinterpreted the Curse of Ham (originally pronounced on the Canaanites) as applying to the dark-skinned peoples of Africa. These writings certainly did exist. My article, however, showed that they were part of a larger Mediterranean tradition of attitudes to skin color that had originated as much with early Christians as with Jews.
For David, the situation was all the more worrisome because many Black Muslims were taking up the argument that “the Jews did it.” Ironically, this early Christian/Jewish ‘colorism’ had not disappeared from the Middle East with the rise of Islam; the Muslim world preserved it virtually intact, including the notion that God had condemned Black Africans to slavery and had blackened their skin as a mark of shame.
I provided him with more references, including other articles I had written. God knows what he thought of my other articles. Even fellow anthropologists think they’re weird—“But what does that have to do with racism?”
Some years after, in 2003, David Goldenberg came out with a book that pulls together all of his research: The Curse of Ham. Race and Slavery in Early Judaism, Christianity, and Islam. I have only just now started reading it and truly regret not having done so sooner. It provides a lot of material I was not aware of and is by far the most authoritative work on the subject. As such, it forms a companion piece to Bernard Lewis’ Race and Slavery in the Middle East.
Today, people routinely interpret antipathy to dark skin as being racially based. Dr. Goldenberg rises above this simplism, arguing that attitudes to skin color were much more fluid and less ethnically constructed in the ancient world. At that time, they were still largely aesthetic in nature and centered on the individual. It was only later, with the expansion of European societies into the non-European world, that these attitudes became almost wholly racialized and, as such, assumed a preponderant role in the modern worldview.
In short, what we call ‘racism’ did not develop historically from a blank slate. It arose from a transformation of earlier sentiments that were unrelated to race or ethnicity. This earlier pre-racial world is now half-forgotten, if not forgotten entirely.
As The Curse of Ham concludes on its last page:
Yet, what struck me as I read through hundreds of modern biblical commentaries and historical and cultural studies of ancient Judaism was how strongly the perspective of one’s own time and place shapes one’s view of another time and place. We today are heirs to centuries of anti-Black sentiment, which has greatly conditioned our perspective.
(Goldenberg, 2003, p. 200)
References
Frost, P. (1991). Attitudes towards Blacks in the early Christian era, The Second Century, 8(1), 1-11.
Goldenberg, D.M. (2003). The Curse of Ham. Race and Slavery in Early Judaism, Christianity, and Islam. Princeton: Princeton University Press.
Lewis, B. (1990). Race and Slavery in the Middle East. An Historical Enquiry. New York: Oxford University Press.
David Goldenberg came to this subject from a very different angle. A number of African American authors were arguing that the Jews had invented anti-black racism, the “proof” being early rabbinical writings that had reinterpreted the Curse of Ham (originally pronounced on the Canaanites) as applying to the dark-skinned peoples of Africa. These writings certainly did exist. My article, however, showed that they were part of a larger Mediterranean tradition of attitudes to skin color that had originated as much with early Christians as with Jews.
For David, the situation was all the more worrisome because many Black Muslims were taking up the argument that “the Jews did it.” Ironically, this early Christian/Jewish ‘colorism’ had not disappeared from the Middle East with the rise of Islam; the Muslim world preserved it virtually intact, including the notion that God had condemned Black Africans to slavery and had blackened their skin as a mark of shame.
I provided him with more references, including other articles I had written. God knows what he thought of my other articles. Even fellow anthropologists think they’re weird—“But what does that have to do with racism?”
Some years after, in 2003, David Goldenberg came out with a book that pulls together all of his research: The Curse of Ham. Race and Slavery in Early Judaism, Christianity, and Islam. I have only just now started reading it and truly regret not having done so sooner. It provides a lot of material I was not aware of and is by far the most authoritative work on the subject. As such, it forms a companion piece to Bernard Lewis’ Race and Slavery in the Middle East.
Today, people routinely interpret antipathy to dark skin as being racially based. Dr. Goldenberg rises above this simplism, arguing that attitudes to skin color were much more fluid and less ethnically constructed in the ancient world. At that time, they were still largely aesthetic in nature and centered on the individual. It was only later, with the expansion of European societies into the non-European world, that these attitudes became almost wholly racialized and, as such, assumed a preponderant role in the modern worldview.
In short, what we call ‘racism’ did not develop historically from a blank slate. It arose from a transformation of earlier sentiments that were unrelated to race or ethnicity. This earlier pre-racial world is now half-forgotten, if not forgotten entirely.
As The Curse of Ham concludes on its last page:
Yet, what struck me as I read through hundreds of modern biblical commentaries and historical and cultural studies of ancient Judaism was how strongly the perspective of one’s own time and place shapes one’s view of another time and place. We today are heirs to centuries of anti-Black sentiment, which has greatly conditioned our perspective.
(Goldenberg, 2003, p. 200)
References
Frost, P. (1991). Attitudes towards Blacks in the early Christian era, The Second Century, 8(1), 1-11.
Goldenberg, D.M. (2003). The Curse of Ham. Race and Slavery in Early Judaism, Christianity, and Islam. Princeton: Princeton University Press.
Lewis, B. (1990). Race and Slavery in the Middle East. An Historical Enquiry. New York: Oxford University Press.
Friday, January 11, 2008
Why I have no answer
In my last two posts, I argued against two widespread truisms:
1. The human genome is 99.9% the same in all people.
2. If we look at the 0.1% that does vary, 85% of this variation exists only between individuals and not between populations.
Both truisms are at best superficially true. They don’t mean what many seem to think they mean. Moreover, they’ve been known to be misleading for some time; in the case of truism #1, from the moment it was first presented.
So Mr. Smarty Pants, how much do genes really differ within our species? And how much of this difference clusters into recognizable populations?
I don’t know. The problem is not simply lack of information. We’re dealing with a conceptual, even existential, problem. Genes differ in any number of ways—not only in the timing and magnitude of a particular trait, but also in countless qualitative aspects. If genes vary along a multitude of dimensions, how can we compress this multidimensional reality into one yardstick called “human difference”?
Let’s assume, as I suspect, that 10-15% of the human genome exhibits some variability. Can we say that humans differ by 10-15% from each other? I’m not so sure. For one thing, a lot of this variability is confined to remote, isolated populations that are close to extinction. Their variability is irrelevant to the overwhelming majority of humans.
For another thing, much of this variability has little or no selective value. How relevant are blood types to your daily existence? What about dormant DNA that might reactivate in one of your descendants?
Well, let’s stick to the 7% of the human genome that clearly varies because it has been selected differently in different environments (Hawks et al., 2007). How relevant are those selection pressures now? What’s the point of having a beard if you shave it off every day? And how important are hair and eye color? At one time, these color traits were under intense selection. Do they matter to us today? I suspect most people would say ‘no’ if asked. They would probably affirm that only ‘inner qualities’ matter, i.e., the soul, personality, intelligence, etc. Yet this viewpoint might change once they’re in a drugstore, especially the hair products section or the magazine counter …
Well, let’s stick to inner qualities. How do we weigh their relative importance? For instance, about 30 per cent of people have a gene variant that results in fewer dopamine receptors and, apparently, in stubborn behavior (Hall, 2008). How useful is this quality? For someone like Winston Churchill, it could have made the difference between losing and winning the war. For many elderly people, it might lead them to refuse ‘newfangled’ medication.
It’s hard to compare things that vary in value not only from one person to another but also from one situation to another. Ultimately, the single yardstick is survival and reproduction: does this trait help its bearer to survive and have children? If this is to be our yardstick, we must conclude that some people are ‘superior’ even though their behavior is widely deemed to be inferior, if not pathological. As anthropologist Henry Harpending points out:
Evolution is a double-edged sword. What evolution cares about is that I have more offspring. If you can do it by charming and manipulating, and I'm a hardworking farmer that's going to feed the kids ten years down the road, then you're going to win. Hit-and-run, irresponsible males are reproducing more. That isn't good for anyone except those males, but that's evolution. (Keim, 2007).
References
Hall, A. 2008. Why the British bulldog spirit is in the genes. Daily Mail, January 10.
Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution. Proceedings of the National Academy of Sciences (USA) early view.
Keim, B. 2007. Humans Evolving More Rapidly Than Ever, Say Scientists. Wired Science, December 10, 2007.
1. The human genome is 99.9% the same in all people.
2. If we look at the 0.1% that does vary, 85% of this variation exists only between individuals and not between populations.
Both truisms are at best superficially true. They don’t mean what many seem to think they mean. Moreover, they’ve been known to be misleading for some time; in the case of truism #1, from the moment it was first presented.
So Mr. Smarty Pants, how much do genes really differ within our species? And how much of this difference clusters into recognizable populations?
I don’t know. The problem is not simply lack of information. We’re dealing with a conceptual, even existential, problem. Genes differ in any number of ways—not only in the timing and magnitude of a particular trait, but also in countless qualitative aspects. If genes vary along a multitude of dimensions, how can we compress this multidimensional reality into one yardstick called “human difference”?
Let’s assume, as I suspect, that 10-15% of the human genome exhibits some variability. Can we say that humans differ by 10-15% from each other? I’m not so sure. For one thing, a lot of this variability is confined to remote, isolated populations that are close to extinction. Their variability is irrelevant to the overwhelming majority of humans.
For another thing, much of this variability has little or no selective value. How relevant are blood types to your daily existence? What about dormant DNA that might reactivate in one of your descendants?
Well, let’s stick to the 7% of the human genome that clearly varies because it has been selected differently in different environments (Hawks et al., 2007). How relevant are those selection pressures now? What’s the point of having a beard if you shave it off every day? And how important are hair and eye color? At one time, these color traits were under intense selection. Do they matter to us today? I suspect most people would say ‘no’ if asked. They would probably affirm that only ‘inner qualities’ matter, i.e., the soul, personality, intelligence, etc. Yet this viewpoint might change once they’re in a drugstore, especially the hair products section or the magazine counter …
Well, let’s stick to inner qualities. How do we weigh their relative importance? For instance, about 30 per cent of people have a gene variant that results in fewer dopamine receptors and, apparently, in stubborn behavior (Hall, 2008). How useful is this quality? For someone like Winston Churchill, it could have made the difference between losing and winning the war. For many elderly people, it might lead them to refuse ‘newfangled’ medication.
It’s hard to compare things that vary in value not only from one person to another but also from one situation to another. Ultimately, the single yardstick is survival and reproduction: does this trait help its bearer to survive and have children? If this is to be our yardstick, we must conclude that some people are ‘superior’ even though their behavior is widely deemed to be inferior, if not pathological. As anthropologist Henry Harpending points out:
Evolution is a double-edged sword. What evolution cares about is that I have more offspring. If you can do it by charming and manipulating, and I'm a hardworking farmer that's going to feed the kids ten years down the road, then you're going to win. Hit-and-run, irresponsible males are reproducing more. That isn't good for anyone except those males, but that's evolution. (Keim, 2007).
References
Hall, A. 2008. Why the British bulldog spirit is in the genes. Daily Mail, January 10.
Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution. Proceedings of the National Academy of Sciences (USA) early view.
Keim, B. 2007. Humans Evolving More Rapidly Than Ever, Say Scientists. Wired Science, December 10, 2007.
Friday, January 4, 2008
The 85% truism
How much of the genome varies within our species? The question remained unanswered in my last post. Hawks et al (2007) have recently estimated that at least 7% of our genome has changed over the last 40,000 years—a period that has seen humans move into diverse environments with different selection pressures. Yet this is a minimal estimate that excludes much variation that may or may not be due to natural selection. The real figure could be higher. Much higher.
How is this genetic variation distributed among humans? Is it evenly scattered? Or does it form geographic clusters? Intuitively, the second answer seems more correct: This variation should be very unevenly distributed if it is due to humans settling in diverse environments with different selection pressures. It should occur primarily at the transition from one ecological zone to another or from one cultural zone to another (e.g., from agriculturalists to hunter-gatherers).
Yet this is not what we see in the data. If we look at genetic markers (blood types, serum proteins, enzymes, etc.), we consistently find far more variation within human populations than between them. And this is true not only for large ‘continental’ groups but also for smaller local populations. In a landmark paper, Richard Lewontin (1972, p. 397) concluded that 85% of human genetic variation exists only between individuals and not between populations:
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.
This finding is true. Like many findings, however, it does not necessarily mean what we think it means. This became apparent when geneticists looked at genetic markers in other animals, such as dogs:
… 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. These data make wolves resemble another breed of dog.
… 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 & Schneider, 1995)
One could object that humans have created dog breeds using a limited set of criteria that reflect a limited set of genes. Therefore, all other criteria, especially those not visible to the eye, should vary independently of breed. The category ‘breed’ is thus an artificial construct that human selection, and not natural selection, has imposed on canine genetic variability.
This objection is not wholly true. Many breeds, such as dingoes, originated in prehistory long before kennel clubs. More to the point, if one argues that human selection acts on a limited set of genes, the implication is that natural selection acts on the entire genome. It doesn’t. Natural selection also acts on a limited set of genes, often a larger set than the one used by dog breeders, but still much smaller than the entire genome.
This point can be illustrated with non-canine examples. Considerable genetic overlap exists not only between breeds of dogs but also between many anatomically and behaviorally distinct 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 seem to form a genetically homogeneous genus with very little concordance between mtDNA, nuclear DNA, and morphology (Freeland & Boag, 1999). In terms of genetic distance, redpoll finches from the same species are not significantly closer to each other than redpolls from different species (Seutin et al., 1995). Among the haplochromine cichlids of Lake Victoria, it is extremely difficult to find interspecies differences in either nuclear or mitochondrial genes, even though these fishes are well differentiated morphologically 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 & Shapiro, 1999). An extreme example is a dog tumor that has developed the ability to spread to other dogs through sexual contact: canine transmissible venereal sarcoma (CTVS). 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).
Does this seem paradoxical? Let’s review how organisms become different from each other through natural selection. This typically happens when a group buds off from its parent population and colonizes a new environment. The environment may be another ecosystem, another mode of subsistence or even, as with CTVS, another form of existence. As the group adapts to its new environment, it will begin to diverge anatomically and behaviorally from its parent population, in part because the environmental boundary hinders gene flow between them but more importantly because the pressures of natural selection are no longer the same. The two populations will evolve differently because what is useful in one environment may not be in the other. And vice versa.
Will these differences in selection affect the entire genome? No. For one thing, most genes have low selective value, some being little more than junk DNA. For another, many genes code for traits that are equally useful in a wide range of environments. The ‘building block’ proteins of human flesh and blood are largely identical to those of non-human primates and sometimes even non-primate mammals (King & Wilson, 1975).
Thus, only a fraction of the genome changes when one population differentiates from another in response to differences in natural selection. The rest remains unchanged, either because the genes have little selective value or because they handle adaptive problems that are common to both populations. Over most of the genome, then, variability is due not to adaptive differences created by different selection pressures but rather to non-adaptive variations that similar selection pressures have left in place.
Of course, once the two populations have become reproductively isolated, they will no longer accumulate the same non-adaptive variations and their entire genomes will drift steadily apart. But this takes time. Redpoll finches diverged into two species some 50,000 years ago and have distinct phenotypes, yet their mitochondrial DNA reveals a single undifferentiated gene pool (Seutin et al., 1995). It’s no surprise, then, that human populations exhibit so much genetic overlap. They began to move apart only 40,000 or so years ago (Pritchard et al., 1999).
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.
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.
Cronin, M. (1991). Mitochondrial-DNA phylogeny of deer (Cervidae). Journal of Mammalogy, 72, 533-566.
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.
Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution. Proceedings of the National Academy of Sciences (USA) early view.
King, M-C. and A.C. Wilson. (1975). Evolution at two levels in humans and chimpanzees. Science, 188, 107-116.
Klein, J., A. Sato, S. Nagl, and C. O’hUigin. (1998). Molecular trans-species polymorphism. Annual Review of Ecology and Systematics, 29, 1-21.
Lewontin, R.C. (1972). The apportionment of human diversity. Evolutionary Biology, 6, 381-398.
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.
Pritchard, J.K., M.T. Seielstad, A. Perez-Lezaun, and M.W. Feldman. (1999). Population growth of human Y chromosomes: A study of Y chromosome microsatellites.” Molecular Biology and Evolution, 16, 1791-1798.
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.
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.
Yang, T.J. (1996). Parasitic protist of metazoan origin, Evolutionary Theory, 11, 99-103.
How is this genetic variation distributed among humans? Is it evenly scattered? Or does it form geographic clusters? Intuitively, the second answer seems more correct: This variation should be very unevenly distributed if it is due to humans settling in diverse environments with different selection pressures. It should occur primarily at the transition from one ecological zone to another or from one cultural zone to another (e.g., from agriculturalists to hunter-gatherers).
Yet this is not what we see in the data. If we look at genetic markers (blood types, serum proteins, enzymes, etc.), we consistently find far more variation within human populations than between them. And this is true not only for large ‘continental’ groups but also for smaller local populations. In a landmark paper, Richard Lewontin (1972, p. 397) concluded that 85% of human genetic variation exists only between individuals and not between populations:
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.
This finding is true. Like many findings, however, it does not necessarily mean what we think it means. This became apparent when geneticists looked at genetic markers in other animals, such as dogs:
… 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. These data make wolves resemble another breed of dog.
… 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 & Schneider, 1995)
One could object that humans have created dog breeds using a limited set of criteria that reflect a limited set of genes. Therefore, all other criteria, especially those not visible to the eye, should vary independently of breed. The category ‘breed’ is thus an artificial construct that human selection, and not natural selection, has imposed on canine genetic variability.
This objection is not wholly true. Many breeds, such as dingoes, originated in prehistory long before kennel clubs. More to the point, if one argues that human selection acts on a limited set of genes, the implication is that natural selection acts on the entire genome. It doesn’t. Natural selection also acts on a limited set of genes, often a larger set than the one used by dog breeders, but still much smaller than the entire genome.
This point can be illustrated with non-canine examples. Considerable genetic overlap exists not only between breeds of dogs but also between many anatomically and behaviorally distinct 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 seem to form a genetically homogeneous genus with very little concordance between mtDNA, nuclear DNA, and morphology (Freeland & Boag, 1999). In terms of genetic distance, redpoll finches from the same species are not significantly closer to each other than redpolls from different species (Seutin et al., 1995). Among the haplochromine cichlids of Lake Victoria, it is extremely difficult to find interspecies differences in either nuclear or mitochondrial genes, even though these fishes are well differentiated morphologically 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 & Shapiro, 1999). An extreme example is a dog tumor that has developed the ability to spread to other dogs through sexual contact: canine transmissible venereal sarcoma (CTVS). 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).
Does this seem paradoxical? Let’s review how organisms become different from each other through natural selection. This typically happens when a group buds off from its parent population and colonizes a new environment. The environment may be another ecosystem, another mode of subsistence or even, as with CTVS, another form of existence. As the group adapts to its new environment, it will begin to diverge anatomically and behaviorally from its parent population, in part because the environmental boundary hinders gene flow between them but more importantly because the pressures of natural selection are no longer the same. The two populations will evolve differently because what is useful in one environment may not be in the other. And vice versa.
Will these differences in selection affect the entire genome? No. For one thing, most genes have low selective value, some being little more than junk DNA. For another, many genes code for traits that are equally useful in a wide range of environments. The ‘building block’ proteins of human flesh and blood are largely identical to those of non-human primates and sometimes even non-primate mammals (King & Wilson, 1975).
Thus, only a fraction of the genome changes when one population differentiates from another in response to differences in natural selection. The rest remains unchanged, either because the genes have little selective value or because they handle adaptive problems that are common to both populations. Over most of the genome, then, variability is due not to adaptive differences created by different selection pressures but rather to non-adaptive variations that similar selection pressures have left in place.
Of course, once the two populations have become reproductively isolated, they will no longer accumulate the same non-adaptive variations and their entire genomes will drift steadily apart. But this takes time. Redpoll finches diverged into two species some 50,000 years ago and have distinct phenotypes, yet their mitochondrial DNA reveals a single undifferentiated gene pool (Seutin et al., 1995). It’s no surprise, then, that human populations exhibit so much genetic overlap. They began to move apart only 40,000 or so years ago (Pritchard et al., 1999).
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.
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.
Cronin, M. (1991). Mitochondrial-DNA phylogeny of deer (Cervidae). Journal of Mammalogy, 72, 533-566.
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.
Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution. Proceedings of the National Academy of Sciences (USA) early view.
King, M-C. and A.C. Wilson. (1975). Evolution at two levels in humans and chimpanzees. Science, 188, 107-116.
Klein, J., A. Sato, S. Nagl, and C. O’hUigin. (1998). Molecular trans-species polymorphism. Annual Review of Ecology and Systematics, 29, 1-21.
Lewontin, R.C. (1972). The apportionment of human diversity. Evolutionary Biology, 6, 381-398.
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.
Pritchard, J.K., M.T. Seielstad, A. Perez-Lezaun, and M.W. Feldman. (1999). Population growth of human Y chromosomes: A study of Y chromosome microsatellites.” Molecular Biology and Evolution, 16, 1791-1798.
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.
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.
Yang, T.J. (1996). Parasitic protist of metazoan origin, Evolutionary Theory, 11, 99-103.
Friday, December 28, 2007
The 99.9% truism
There has been much comment on a recent finding that human evolution has accelerated over the past 40,000 years, i.e., the period during which our species has spread out of Africa and differentiated into the populations we see today (Hawks et al., 2007). There has been less comment on a related finding: at least 7% of the human genome has changed over the same 40,000 years.
This second finding seems to challenge a truism that has become widespread in academia and even in our political culture. In a speech earlier this year, Hillary Clinton cited genetic research showing that human populations are 99.9 percent the same and “that the differences in how we look -- in our skin color, our eye color, our height -- stem from just one-tenth of 1 percent of our genes.”
Isn’t there a contradiction here? How can human populations be 99.9% genetically identical if at least 7% of the genome has changed since they began moving apart some 40,000 years ago?
First, the 99.9% figure is not the number of genes that are the same. It’s the number of nucleotide sequences that are the same. A single gene is a long chain of nucleotides, often a very long one, and a single nucleotide mutation can significantly alter how the entire gene works. In theory, each and every human gene could differ by 0.1% from one population to another. And such a difference could make a big difference.
Second, the 99.9% estimate doesn’t capture higher-level nucleotide variation:
The technique originally used … could read the sequence of letters of a genetic code. But it couldn't detect repetitions of some parts of the code, which also occur. Differences in the number of these repetitions, called copy number variants, have since turned out to account for much of the variation in a species' DNA. Another type of variation recently found to be important is called insertion-deletion variants, snippets of code that are either extra or missing in some genomes compared to others. (World Science, 2007)
This higher-level variation has caused geneticist Craig Venter (of the Human Genome Project) to revise the 99.9% figure downward:
The findings reveal “human-to-human variation is more than seven-fold greater than earlier estimates, proving that we are in fact very unique individuals at the genetic level,” Venter said. The 99.9 figure might need to be lowered to about 99, he added. (World Science, 2007) (also see original article: Redon et al, 2006)
So our nucleotide sequences may be closer to being 1% different, and not 0.1%. And don’t be fooled by small numbers. Whether it’s 1% or 0.1% the difference is still big in absolute terms. As John Hawks points out: “one-tenth of 1 percent of 3 billion is a heck of a large number -- 3 million nucleotide differences between two random genomes.”
Finally, there is a third reason why we should not read too much into any of these estimates. When the 99.9% figure first came out in the 1970s, geneticists had also discovered that nucleotide sequences were 98.9% the same between humans and chimpanzees (King & Wilson, 1975). And yet, humans and chimps exhibit a wide range of anatomical and behavioral differences. How come?
There is of course the aforementioned ‘small percentage fallacy’: a tiny sliver of the genome still amounts to a lot of DNA. More importantly, humans and chimps seem to differ the most in ‘regulatory genes’ whose effects are many times greater than those of ‘structural genes’ (the ones that code for the building block proteins of body tissues). A single regulatory gene has such a disproportionate impact because it can control the expression of many other genes.
These less numerous regulatory genes have gained importance as organisms have grown more and more complex. This has especially been so during human evolution. Whereas humans and chimpanzees are almost identical in the proteins that form their tissues, they differ radically in the way their brains and bodies develop. This point is summarized by King and Wilson (1975, p. 115):
The genetic distance between humans and chimpanzees, based on electrophoretic comparison of proteins encoded by 44 loci is very small, corresponding to the genetic distance between sibling species of fruit flies or mammals. Results obtained with other biochemical methods are consistent with this conclusion. However, the substantial anatomical and behavioral differences between humans and chimpanzees have led to their classification in separate families. … A relatively small number of genetic changes in systems controlling the expression of genes may account for the major organismal differences between humans and chimpanzees.
Interestingly, King and Wilson see this paradox as applying not only to human-chimpanzee genetic differences, but also to genetic differences within our species:
This [human-chimpanzee] distance is 25 to 60 times greater than the genetic distance between human races. In fact, the genetic distance between Caucasian, Black African, and Japanese populations is less than or equal to that between morphologically and behaviorally identical populations of other species. (King & Wilson, 1975, p. 113)
Yet human races are not identical populations, anymore than humans and chimpanzees are sibling species. These measures of genetic distance are not comparable because the nature of genetic change can vary dramatically. In one case, there is simply tinkering with an existing body plan through mutations in structural genes. In another, there is radical developmental change through mutations in regulatory genes.
Since the time that the ancestor of these two species lived, the chimpanzee lineage has evolved slowly relatively to the human lineage, in terms of anatomy and adaptive strategy. According to Simpson:
Pan is the terminus of a conservative lineage, retaining in a general way an anatomical and adaptive facies common to all recent hominoids except Homo. Homo is both anatomically and adaptively the most radically distinctive of all hominoids, divergent to a degree considered familial by all primatologists. (King & Wilson, 1975, p. 113)
This is the context in which the 99.9% statistic was initially presented to the academic community … way back in the 1970s. Even then, researchers thought it misleading and went to great pains to explain why it was misleading. Yet their caveats were to no avail. The 99.9% truism has taken on a life of its own, much like those stories we hear of alligators living in sewers or evil people sticking razor blades in Halloween apples. It seems to meet a deep-seated need to affirm our sameness and to give this affirmation a stamp of scientific approval.
But science it is not.
References
Anon. (2007). Finding said to show "race isn't real" scrapped http://www.world-science.net/othernews/070904_human-variation.htm
Elliott, P. (2007). Clinton tells grads only minor genetics make them different.
http://www.boston.com/news/nation/articles/2007/06/14/clinton_tells_grads_only_minor_genetics_make_them_different/
Hawks, J. (2007) Disagreeing with Hillary Clinton on human genetic differences.
http://johnhawks.net/weblog/topics/race/differences/clinton_2007_proportion_differences_speech.html
Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution. Proceedings of the National Academy of Sciences (USA) early view.
King, M-C. and A.C. Wilson. (1975). Evolution at two levels in humans and chimpanzees. Science, 188, 107-116.
Redon, R., S. Ishikawa, K.R. Fitch, L. Feuk, G.H. Perry, T.D. Andrews, H. Fiegler, M.H. Shapero, A.R. Carson, W. Chen, E.K. Cho, S. Dallaire, J.L. Freeman, J.R. González, M. Gratacòs, J. Huang, D. Kalaitzopoulos, D. Komura, J.R. MacDonald, C.R. Marshall, R. Mei, L. Montgomery, K. Nishimura, K. Okamura, F. Shen, M.J. Somerville, J. Tchinda, A. Valsesia, C. Woodwark, F. Yang, J. Zhang, T. Zerjal, J. Zhang, L. Armengol, D.F. Conrad, X. Estivill, C. Tyler-Smith, N.P. Carter, H. Aburatani, C. Lee, K.W. Jones, S.W. Scherer & M.E. Hurles. (2006). Global variation in copy number in the human genome. Nature, 444, 444-454.
This second finding seems to challenge a truism that has become widespread in academia and even in our political culture. In a speech earlier this year, Hillary Clinton cited genetic research showing that human populations are 99.9 percent the same and “that the differences in how we look -- in our skin color, our eye color, our height -- stem from just one-tenth of 1 percent of our genes.”
Isn’t there a contradiction here? How can human populations be 99.9% genetically identical if at least 7% of the genome has changed since they began moving apart some 40,000 years ago?
First, the 99.9% figure is not the number of genes that are the same. It’s the number of nucleotide sequences that are the same. A single gene is a long chain of nucleotides, often a very long one, and a single nucleotide mutation can significantly alter how the entire gene works. In theory, each and every human gene could differ by 0.1% from one population to another. And such a difference could make a big difference.
Second, the 99.9% estimate doesn’t capture higher-level nucleotide variation:
The technique originally used … could read the sequence of letters of a genetic code. But it couldn't detect repetitions of some parts of the code, which also occur. Differences in the number of these repetitions, called copy number variants, have since turned out to account for much of the variation in a species' DNA. Another type of variation recently found to be important is called insertion-deletion variants, snippets of code that are either extra or missing in some genomes compared to others. (World Science, 2007)
This higher-level variation has caused geneticist Craig Venter (of the Human Genome Project) to revise the 99.9% figure downward:
The findings reveal “human-to-human variation is more than seven-fold greater than earlier estimates, proving that we are in fact very unique individuals at the genetic level,” Venter said. The 99.9 figure might need to be lowered to about 99, he added. (World Science, 2007) (also see original article: Redon et al, 2006)
So our nucleotide sequences may be closer to being 1% different, and not 0.1%. And don’t be fooled by small numbers. Whether it’s 1% or 0.1% the difference is still big in absolute terms. As John Hawks points out: “one-tenth of 1 percent of 3 billion is a heck of a large number -- 3 million nucleotide differences between two random genomes.”
Finally, there is a third reason why we should not read too much into any of these estimates. When the 99.9% figure first came out in the 1970s, geneticists had also discovered that nucleotide sequences were 98.9% the same between humans and chimpanzees (King & Wilson, 1975). And yet, humans and chimps exhibit a wide range of anatomical and behavioral differences. How come?
There is of course the aforementioned ‘small percentage fallacy’: a tiny sliver of the genome still amounts to a lot of DNA. More importantly, humans and chimps seem to differ the most in ‘regulatory genes’ whose effects are many times greater than those of ‘structural genes’ (the ones that code for the building block proteins of body tissues). A single regulatory gene has such a disproportionate impact because it can control the expression of many other genes.
These less numerous regulatory genes have gained importance as organisms have grown more and more complex. This has especially been so during human evolution. Whereas humans and chimpanzees are almost identical in the proteins that form their tissues, they differ radically in the way their brains and bodies develop. This point is summarized by King and Wilson (1975, p. 115):
The genetic distance between humans and chimpanzees, based on electrophoretic comparison of proteins encoded by 44 loci is very small, corresponding to the genetic distance between sibling species of fruit flies or mammals. Results obtained with other biochemical methods are consistent with this conclusion. However, the substantial anatomical and behavioral differences between humans and chimpanzees have led to their classification in separate families. … A relatively small number of genetic changes in systems controlling the expression of genes may account for the major organismal differences between humans and chimpanzees.
Interestingly, King and Wilson see this paradox as applying not only to human-chimpanzee genetic differences, but also to genetic differences within our species:
This [human-chimpanzee] distance is 25 to 60 times greater than the genetic distance between human races. In fact, the genetic distance between Caucasian, Black African, and Japanese populations is less than or equal to that between morphologically and behaviorally identical populations of other species. (King & Wilson, 1975, p. 113)
Yet human races are not identical populations, anymore than humans and chimpanzees are sibling species. These measures of genetic distance are not comparable because the nature of genetic change can vary dramatically. In one case, there is simply tinkering with an existing body plan through mutations in structural genes. In another, there is radical developmental change through mutations in regulatory genes.
Since the time that the ancestor of these two species lived, the chimpanzee lineage has evolved slowly relatively to the human lineage, in terms of anatomy and adaptive strategy. According to Simpson:
Pan is the terminus of a conservative lineage, retaining in a general way an anatomical and adaptive facies common to all recent hominoids except Homo. Homo is both anatomically and adaptively the most radically distinctive of all hominoids, divergent to a degree considered familial by all primatologists. (King & Wilson, 1975, p. 113)
This is the context in which the 99.9% statistic was initially presented to the academic community … way back in the 1970s. Even then, researchers thought it misleading and went to great pains to explain why it was misleading. Yet their caveats were to no avail. The 99.9% truism has taken on a life of its own, much like those stories we hear of alligators living in sewers or evil people sticking razor blades in Halloween apples. It seems to meet a deep-seated need to affirm our sameness and to give this affirmation a stamp of scientific approval.
But science it is not.
References
Anon. (2007). Finding said to show "race isn't real" scrapped http://www.world-science.net/othernews/070904_human-variation.htm
Elliott, P. (2007). Clinton tells grads only minor genetics make them different.
http://www.boston.com/news/nation/articles/2007/06/14/clinton_tells_grads_only_minor_genetics_make_them_different/
Hawks, J. (2007) Disagreeing with Hillary Clinton on human genetic differences.
http://johnhawks.net/weblog/topics/race/differences/clinton_2007_proportion_differences_speech.html
Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution. Proceedings of the National Academy of Sciences (USA) early view.
King, M-C. and A.C. Wilson. (1975). Evolution at two levels in humans and chimpanzees. Science, 188, 107-116.
Redon, R., S. Ishikawa, K.R. Fitch, L. Feuk, G.H. Perry, T.D. Andrews, H. Fiegler, M.H. Shapero, A.R. Carson, W. Chen, E.K. Cho, S. Dallaire, J.L. Freeman, J.R. González, M. Gratacòs, J. Huang, D. Kalaitzopoulos, D. Komura, J.R. MacDonald, C.R. Marshall, R. Mei, L. Montgomery, K. Nishimura, K. Okamura, F. Shen, M.J. Somerville, J. Tchinda, A. Valsesia, C. Woodwark, F. Yang, J. Zhang, T. Zerjal, J. Zhang, L. Armengol, D.F. Conrad, X. Estivill, C. Tyler-Smith, N.P. Carter, H. Aburatani, C. Lee, K.W. Jones, S.W. Scherer & M.E. Hurles. (2006). Global variation in copy number in the human genome. Nature, 444, 444-454.
Friday, December 21, 2007
Thoughts on the EEA
For the past twenty years, a key concept in evolutionary psychology has been the ‘environment of evolutionary adaptedness’ (EEA). This is the ancestral environment within which our species first evolved and whose selection pressures shaped our current psychology and behavior. Usually, writers situate this environment in the Pleistocene before Homo sapiens began to spread out of Africa some 50,000 years ago.
The EEA concept has increasingly come under fire in recent years, especially with the recent Hawks et al. study. It now appears that human genetic evolution did not stop 50,000 years ago. Nor has it since slowed down. In fact, it has accelerated by as much as a 100-fold. In light of these findings, can the EEA concept be salvaged? Should it?
Interestingly, its earliest proponents, John Tooby and Leda Cosmides, have always been reluctant to narrow it down to a specific place and time:
Although the hominid line is thought to have originated on edges of the African savannahs, the EEA is not a particular place or time. The EEA for a given adaptation is the statistical composite of the enduring selection pressures or cause-and-effect relationships that pushed the alleles underlying an adaptation systematically upward in frequency until they became species-typical or reached a frequency-dependent equilibrium (most adaptations are species-typical; see Hagen, Chapter 5, this volume). Because the coordinated fixation of alleles at different loci takes time, complex adaptations reflect enduring features of the ancestral world. (Tooby & Cosmides, 2005, p. 22)
According to Tooby and Cosmides, there are potentially as many EEAs as there are human adaptations. Therefore, some human characteristics may have originated in very old EEAs and others in more recent ones.
How recent? For Tooby and Cosmides, the limiting factor is complexity. The more complex the adaptation, the more genes it will involve, and the longer the evolutionary time to coordinate all those genes. Therefore, recent human evolution has probably only involved simple traits, certainly nothing as complex as behavior.
The problem with this argument is that complex traits do not arise ex nihilo. They arise from changes to existing traits that may be just slightly less complex. A point mutation can greatly alter the functioning of a trait that involves thousands upon thousands of genes. Keep in mind that genes vary considerably in their effects. At one extreme, a single ‘structural’ gene may code for one protein. At the other, a single ‘regulatory’ gene may control the output of numerous structural genes … or even numerous regulatory genes like itself. 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. A border collie's herding is recognizably derived from wolf behaviors, as is a terrier's aggressiveness, but this hardly means that collies, wolves, and terriers are all the same. Paternal investment may be particularly fragile and easily lost in mammals, because parental investment via internal gestation and lactation is engineered into females but not males.
In all fairness, when the EEA concept was first developed, few people were arguing that natural selection has modified human behavior over the last 50,000 years. In fact, the dominant view was the opposite: that natural selection has not shaped any specific human behavioral traits, not now, not over the past fifty thousand years, and not over the past fifty million. Not ever. The mind was a tabula rasa. Even sociobiologists, often castigated as biological determinists, commonly thought that people were simply predisposed to learn adaptively: “natural selection has produced in humans a general motivation to maximize one’s inclusive fitness—i.e., a domain-general psychological mechanism” (Buss, 1991, p. 463).
The EEA was part of a new paradigm, now called evolutionary psychology, to move away from the domain-general approach of sociobiology and to search for specific innate mechanisms within the human mind. Its earliest proponents saw the EEA not as a dogma, but as a guide—as a way of making people look at human nature from a broader evolutionary perspective, and not from the narrower one of modern industrial life.
The EEA concept has served us well. But it is now time to move on.
References
Buss, D.M. (1991). Evolutionary personality psychology. Annual Review of Psychology, 42, 459-491.
Harpending, H. and G. Cochran. 2002. "In our genes", Proceedings of the National Academy of Sciences 99(1):10-12.
Tooby, J. and L. Cosmides. (2005). Conceptual Foundations of Evolutionary Psychology. In David M. Buss (Ed.) The Handbook of Evolutionary Psychology. (pp. 5-67), Hoboken, NJ: Wiley.
The EEA concept has increasingly come under fire in recent years, especially with the recent Hawks et al. study. It now appears that human genetic evolution did not stop 50,000 years ago. Nor has it since slowed down. In fact, it has accelerated by as much as a 100-fold. In light of these findings, can the EEA concept be salvaged? Should it?
Interestingly, its earliest proponents, John Tooby and Leda Cosmides, have always been reluctant to narrow it down to a specific place and time:
Although the hominid line is thought to have originated on edges of the African savannahs, the EEA is not a particular place or time. The EEA for a given adaptation is the statistical composite of the enduring selection pressures or cause-and-effect relationships that pushed the alleles underlying an adaptation systematically upward in frequency until they became species-typical or reached a frequency-dependent equilibrium (most adaptations are species-typical; see Hagen, Chapter 5, this volume). Because the coordinated fixation of alleles at different loci takes time, complex adaptations reflect enduring features of the ancestral world. (Tooby & Cosmides, 2005, p. 22)
According to Tooby and Cosmides, there are potentially as many EEAs as there are human adaptations. Therefore, some human characteristics may have originated in very old EEAs and others in more recent ones.
How recent? For Tooby and Cosmides, the limiting factor is complexity. The more complex the adaptation, the more genes it will involve, and the longer the evolutionary time to coordinate all those genes. Therefore, recent human evolution has probably only involved simple traits, certainly nothing as complex as behavior.
The problem with this argument is that complex traits do not arise ex nihilo. They arise from changes to existing traits that may be just slightly less complex. A point mutation can greatly alter the functioning of a trait that involves thousands upon thousands of genes. Keep in mind that genes vary considerably in their effects. At one extreme, a single ‘structural’ gene may code for one protein. At the other, a single ‘regulatory’ gene may control the output of numerous structural genes … or even numerous regulatory genes like itself. 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. A border collie's herding is recognizably derived from wolf behaviors, as is a terrier's aggressiveness, but this hardly means that collies, wolves, and terriers are all the same. Paternal investment may be particularly fragile and easily lost in mammals, because parental investment via internal gestation and lactation is engineered into females but not males.
In all fairness, when the EEA concept was first developed, few people were arguing that natural selection has modified human behavior over the last 50,000 years. In fact, the dominant view was the opposite: that natural selection has not shaped any specific human behavioral traits, not now, not over the past fifty thousand years, and not over the past fifty million. Not ever. The mind was a tabula rasa. Even sociobiologists, often castigated as biological determinists, commonly thought that people were simply predisposed to learn adaptively: “natural selection has produced in humans a general motivation to maximize one’s inclusive fitness—i.e., a domain-general psychological mechanism” (Buss, 1991, p. 463).
The EEA was part of a new paradigm, now called evolutionary psychology, to move away from the domain-general approach of sociobiology and to search for specific innate mechanisms within the human mind. Its earliest proponents saw the EEA not as a dogma, but as a guide—as a way of making people look at human nature from a broader evolutionary perspective, and not from the narrower one of modern industrial life.
The EEA concept has served us well. But it is now time to move on.
References
Buss, D.M. (1991). Evolutionary personality psychology. Annual Review of Psychology, 42, 459-491.
Harpending, H. and G. Cochran. 2002. "In our genes", Proceedings of the National Academy of Sciences 99(1):10-12.
Tooby, J. and L. Cosmides. (2005). Conceptual Foundations of Evolutionary Psychology. In David M. Buss (Ed.) The Handbook of Evolutionary Psychology. (pp. 5-67), Hoboken, NJ: Wiley.
Friday, December 14, 2007
The rising curve
It was long thought that human genetic evolution pretty much ended with the advent of culture. As Paul Ehrlich (2000, p. 63) wrote:
So did cultural evolution make genetic evolution obsolete? Paul Ehrlich seemed to draw this conclusion … only to pull himself back. “There are many ways in which culture can alter selection pressures,” he says, noting that genes have co-evolved with changes to diet, farming practices, and shelter (Ehrlich, 2000, p. 64). Indeed, the same properties that make cultural evolution so fast have also been diversifying the adaptive landscape at an unparalleled rate. Whenever our species came up with a cultural innovation—a new technology, domestication of a plant or animal, or the advent of agriculture itself—our environment changed as fundamentally as if we had moved to a new ecosystem.
So which factor has mattered most in determining the pace of human genetic evolution? Has cultural evolution been resolving more and more adaptive problems that were formerly resolved by genetic evolution? Or has genetic evolution been resolving more and more adaptive problems because human environments have been diversifying more and more?
The second factor, apparently. A recent study has concluded that genetic evolution has actually accelerated over the past 40,000 years and even more over the past 10,000-15,000. This is partly because there are many more of us and partly because we are spread over an increasingly diverse range of natural and man-made environments. At least 7% of the human genome appears to have changed since the advent of Homo sapiens. And the rate of change has increased a 100-fold since the advent of agriculture (Hawks et al., 2007).
These are high numbers. As one of the study’s authors observes:
These figures, if anything, err on the low side. They do not capture recent selective pressures that are just emerging above noise in the data. Nor do they capture older selective pressures that have already pushed many alleles to fixation. The real figures won’t become known until we’ve retrieved the human genome that existed 40,000 years ago—something that is certainly within the realm of possibility.
All this underlines a point I made in an earlier post: human evolution is not a straight line. It’s a logarithmic curve with most of the evolutionary change in the recent past. If we met a Homo erectus face to face, or even a Neanderthal (who was probably just an arctic-adapted Homo erectus), we wouldn’t consider it to be human. It would look to us like an overgrown ape. Nor would its behavior reassure us otherwise.
References
Ehrlich, P.R. (2000). Human Natures. Genes, Cultures, and the Human Prospect. Penguin: New York.
Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution. Proceedings of the National Academy of Sciences (USA), 104(52), 20753-20758.
The evolution of that body of extragenetic information—cultural evolution—has been centrally important in making us the unique beasts we are. Cultural evolution rests on a foundation of genetic (or biological) evolution—especially that of our brains and tongues—but can proceed at what by comparison is a lightning pace. … cultural evolution can vastly outpace genetic evolution because it’s not constrained by generation time. Our genes are passed only from one generation to relatives in succeeding generations. In contrast, the units of culture—ideas, basically—are passed among both relatives and nonrelatives not only between generations (in both
directions) but also within generations.
So did cultural evolution make genetic evolution obsolete? Paul Ehrlich seemed to draw this conclusion … only to pull himself back. “There are many ways in which culture can alter selection pressures,” he says, noting that genes have co-evolved with changes to diet, farming practices, and shelter (Ehrlich, 2000, p. 64). Indeed, the same properties that make cultural evolution so fast have also been diversifying the adaptive landscape at an unparalleled rate. Whenever our species came up with a cultural innovation—a new technology, domestication of a plant or animal, or the advent of agriculture itself—our environment changed as fundamentally as if we had moved to a new ecosystem.
So which factor has mattered most in determining the pace of human genetic evolution? Has cultural evolution been resolving more and more adaptive problems that were formerly resolved by genetic evolution? Or has genetic evolution been resolving more and more adaptive problems because human environments have been diversifying more and more?
The second factor, apparently. A recent study has concluded that genetic evolution has actually accelerated over the past 40,000 years and even more over the past 10,000-15,000. This is partly because there are many more of us and partly because we are spread over an increasingly diverse range of natural and man-made environments. At least 7% of the human genome appears to have changed since the advent of Homo sapiens. And the rate of change has increased a 100-fold since the advent of agriculture (Hawks et al., 2007).
These are high numbers. As one of the study’s authors observes:
Personally, I can't believe that nobody noticed how extreme these estimates of recent selection really are. I guess that folks doing genomics just weren't as primed in evolutionary theory to perceive how weird the human estimates looked compared to what is measured in the wild on other species, or even over the span of human evolution!
In the earliest studies, when people were finding that 3 or 4 percent of a sample of genes had signs of recent selection, those numbers were already extremely high. They got even higher, as more and more powerful methods of detecting selection came online. Our current estimate is the highest yet, but even this very high number is perfectly consistent with theoretical predictions coming from human population numbers.
These figures, if anything, err on the low side. They do not capture recent selective pressures that are just emerging above noise in the data. Nor do they capture older selective pressures that have already pushed many alleles to fixation. The real figures won’t become known until we’ve retrieved the human genome that existed 40,000 years ago—something that is certainly within the realm of possibility.
All this underlines a point I made in an earlier post: human evolution is not a straight line. It’s a logarithmic curve with most of the evolutionary change in the recent past. If we met a Homo erectus face to face, or even a Neanderthal (who was probably just an arctic-adapted Homo erectus), we wouldn’t consider it to be human. It would look to us like an overgrown ape. Nor would its behavior reassure us otherwise.
References
Ehrlich, P.R. (2000). Human Natures. Genes, Cultures, and the Human Prospect. Penguin: New York.
Hawks, J., E.T. Wang, G.M. Cochran, H.C. Harpending, and R.K. Moyzis. (2007). Recent acceleration of human adaptive evolution. Proceedings of the National Academy of Sciences (USA), 104(52), 20753-20758.
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