Thursday, March 30, 2006

Where The REAL Action Is In Evolutionary Biology

AUTHOR: Allen MacNeill

SOURCE: Original essay

COMMENTARY: That's up to you...

Throughout the controversy over "intelligent design," it has occurred to me several times that the underlying problem in the ID vs evolution debate has centered around what could be called the "adaptationist program." As Lewontin and Gould pointed out in their "spandrels" paper, much of evolutionary biology from Darwin on has been shot through with a kind of "adaptationist ideology", in which the only things of interest are adaptations resulting from selection. Will Provine has pointed out that this focus, in a sense, simply replaces the God of the Bible with a "god" of natural selection.

What the last three decades of evolutionary biology at the molecular level have showed us is that the vast majority of evolutionary change is non-adaptational. Jukes, Kimura, Ohta, and others have conclusively shown that most of what happens at the genome level (and much of what happens at the proteome level) is non-adaptive. This new paradigm for evolution – the neutral theory – has been entirely ignored by "intelligent design theorists" and for good reason. Since it clearly isn't adaptive, then for a "designer" to have intervened to produce and/or guide it would argue that the "designer" is a kind of metaphysical dadaist who delights in pointlessness. Hence the insistence on the part of many IDers that there is no such thing as "junk DNA", nor even non-adaptive DNA (such as pseudogenes, transposon-derived regions, cDNA from retroviruses, etc.)

The relevence of this to the current discussion is this: by teaching students that evolution is all about adaptation, we miss some of the most interesting developments in recent theory and research. These developments decisively argue against the ID position and bring evolutionary biology much closer to the "modern" paradigm of quantum mechanical physics, in which "pointlessness" and randomicity underlies all of macroscopic reality. To paraphrase J.B.S. Haldane, the genome is not only queerer than we imagine, it is queerer than we can imagine.

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Thursday, March 23, 2006

The Origin of the Specious

AUTHOR: Allen MacNeill

SOURCE: Original essay

COMMENTARY: That's up to you...

John Wilkins over at Evolving Thoughts has posted the following abstract, along with a brief discussion of its significance for evolutionary biology:

The Nature of Plant Species

Loren H. Rieseberg [1], Troy E. Wood [1] and Eric J. Baack [1]

Many botanists doubt the existence of plant species, viewing them as arbitrary constructs of the human mind, as opposed to discrete, objective entities that represent reproductively independent lineages or 'units of evolution'. However, the discreteness of plant species and their correspondence with reproductive communities have not been tested quantitatively, allowing zoologists to argue that botanists have been overly influenced by a few 'botanical horror stories', such as dandelions, blackberries and oaks. Here we analyse phenetic and/or crossing relationships in over 400 genera of plants and animals. We show that although discrete phenotypic clusters exist in most genera (> 80%), the correspondence of taxonomic species to these clusters is poor (< 60%) and no different between plants and animals. Lack of congruence is caused by polyploidy, asexual reproduction and over-differentiation by taxonomists, but not by contemporary hybridization. Nonetheless, crossability data indicate that 70% of taxonomic species and 75% of phenotypic clusters in plants correspond to reproductively independent lineages (as measured by postmating isolation), and thus represent biologically real entities. Contrary to conventional wisdom, plant species are more likely than animal species to represent reproductively independent lineages.

Nature 440, 524-527 (23 March 2006) | doi:10.1038/nature04402; Received 26 July 2005

[1] Department of Biology, Indiana University, Bloomington, Indiana 47405, USA. Correspondence and requests for materials should be addressed to: Loren H. Rieseberg (Email:

He pointed out that this would mean that botanists would seem to have a clearer definition of what a species is than most zoologists. However, the paper cited above notwithstanding, I think I would have to disagree with that assertion.

For over a century, evolutionary biologists have been wrestling with the concepts of species and speciation, trying to determine which (if any) of the various species concepts are most useful, and which mechanism of speciation is the most important in nature. But all of this has been predicated on the assumption that species actually exist outside of the human imagination. Is it possible that all of this has been an exercise in futility, a kind of "origin of the specious?"

Consider the fact that nearly all of the people whose opinions on the subject of species and speciation have themselves studied animals almost exclusively, especially Charles Darwin, Theodosious Dobzhansky, and Ernst Mayr. Not really surprising: after all, we're all animals and most interested in ourselves. Furthermore, the most widely applied definition of a species, the so-called "biological species concept" was most forcefully advocated by Ernst Mayr in Systematics and the Origin of Species.

Which leads to the following question:

• Is there something peculiar about animals that predisposes people who study them to frame the question of what a species is in such a way as to get the biological species concept as the answer?

In a word, yes: Lynn Margulis at the University of Massachusetts has argued forcefully for the following radical interpretation of the "origin of species":

• There are no such thing as "species" among the most numerous and diverse organisms on Earth: the prokaryotes (commonly referred to as "bacteria") either don't have species at all in any commonly accepted sense, or they are all one huge "species."

• Horizontal gene transfer (i.e. gene transfer from organism to organism without sex, reproduction, and therefore "descent") hopelessly muddies the phylogenies of whole kingdoms of organisms (including many animals, and possibly including ourselves).

• In particular, the Protoctists (i.e. unicellular eukaryotes, also referred to as Protists) have such diverse and bizarre sexual and reproductive behaviors as to be all but unclassifiable (some have as many as eight "sexes"!)

• Nearly all fungi and many plants are generally indifferent to species boundaries. As sessile organisms, fungi and plants they can't be choosy about whom to mate with; whomever is nearby will do.

• This is particularly true for the fungi, who very rarely "go outside" - they live nearly their entire lives underground as widely distributed networks of tubular cells called hyphae.

• Orchids have been known to hybridize across not only species lines, but across genera and even families.

• Nearly all plants have the ability to reproduce asexually; indeed, some (like the dandelion) have given up sexual reproduction entirely and are therefore in essentially the same category as bacteria.

Pretty radical stuff, and a kind of "universal acid" for the biological species conceptfor anything except animals (but watch out for whiptail lizards). Lynn Margulisis admittedly a radical in this regard, but one with a solid track record. Her theory for the evolution of eukaryotes, called "serial endosymbiosis", was considered by many to be the ravings of a lunatic when she first proposed it in 1969. Now it is the most mainstream of orthodoxies.

So, how about it: are non-animal species "real"? Consider the following (From: Margulis, Lynn and Sagan, Dorion (2002). Acquiring Genomes: A Theory of the Origin of Species, Basic Books, New York, NY, pp. 54-55):

For the numbers of living species…we have only crude estimates that may be wildly incorrect. Animals, probably because people are good at distinguishing beetles, dominate. Over 10 million - perhaps as many as 30 million - are thought to exist. Some 500,000 plants, 100,000 fungi, and 250,000 protoctists are suggested to be lurking in the woods and waters of this world."

As for bacteria, although thousands have been named as species and no doubt thousands can be distinguished, the [biological] species concept doesn't apply. Although bacteria can be grouped on the basis of common features, these groups change so quickly that they are never fixed and recognizable like eukaryote species. Bacteria pass genes back and forth. All can simply reproduce, and thus at any given time have but a single parent. The intervention of sex…is a unidirectional affair. The genes pass from a donor to a recipient…but donors can change to recipients and vice versa in minutes. Furthermore the gene swapping is entirely optional…[I]ndeed bacteria are willing and able to "have sex" with naked DNA molecules that they absorb from the water in which they are bathed.

Life originated with bacteria; therefore we can say that the origin of life was concurrent with the origin of bacteria. But we agree with Professor Sorin Sonea and his colleague Lucien Mathieu, of the Université de Montreal, that bacteria do not have species at all (or, which amounts to the same thing, all of them together constitute one single cosmopolitan species). Speciation is a property only of nucleated organisms.

The Taxonomy of Some Common Trees

Okay, so perhaps taxonomists have been missing the forest for looking too closely at the trees? Consider these seemingly obvious tree species (if you live in the northeastern United States, you can see most of them by simply stepping outside and looking around):

SPECIES: Acer saccharum

• sugar maple
• rock maple
• hard maple

The currently accepted scientific name of sugar maple is Acer saccharum Marsh. Sugar maple is highly variable genetically and taxonomic controversy abounds. Some taxonomists recognize two to six varieties, but others recognize these entities as forms or subspecies. Several ecotypes or races, each exhibiting clinal variation, have also been delineated.

Florida maple (A. barbatum), chalk maple (A. leucoderme), and black maple (A. nigrum) hybridize and intergrade with sugar maple and are often included in the sugar maple complex. Some authorities recognize these taxa as subspecies of sugar maple, but most delineate them as discrete species. Sugar maple hybridizes with red maple (A. rubrum) in the field, and with bigleaf maple (A. macrophyllum) under laboratory conditions. Acer X senecaense Slavin is a hybrid derived from an A. leucoderme x sugar maple cross. A. skutchii is closely related to sugar maple and is treated as a subspecies by some taxonomists.

Tirmenstein, D. A. 1991. Acer saccharum In: U.S. Department of Agriculture(2002, September), Forest Service, Rocky Mountain Research Station, Fire Sciences Laboratory Fire Effects Information System:

SPECIES: Quercus alba

• white oak
• stave oak
• ridge white oak
• forked-leaf white oak
• fork-leaf oak

The currently accepted scientific name of white oak is Quercus alba L. It is a member of the order Fagales and has been placed within the white oak subgenus (Lepidobalanus). Three varieties of white oak are commonly recognized:
Quercus alba var. alba
Quercus alba var. repanda Michx.
Quercus alba var. latiloba Sarg.
Some authorities recognize these entities as forms rather than varieties.

White oak is highly variable genetically, and many forms and ecotypes have been described. According to Fowells, "no definite races have been defined, but within such a tremendously diverse habitat, climatic races undoubtedly exist." White oak readily hybridizes with many other species within the genus Quercus, including swamp white oak (Q. bicolor), bur oak (Q. macrocarpa), chinkapin oak (Q. muehlenbergi), dwarf chinkapin oak (Q. prinoides), overcup oak (Q. lyrata), swamp chestnut oak (Q. michauxii), sandpost oak (Q. margaretta), chestnut oak (Q. prinus), English oak (Q. robur), Durand oak (Q. durandii), and post oak (Q. stellata). Hybrids, their common names, and purported origins are listed below.
• Beadle oak……X beadlei Trel. (Quercus alba x michauxii)
• Bebb oak……..X bebbiana (Q. alba x Q. macrocarpa)
• Deam oak…….X deamii (Q. alba x Q. muehlenbergi)
• Faxon oak……X faxonii Trel. (Q. alba x Q. prinoides)
• Fernow oak…..X fernowii Trel. (Q. alba x Q. stellata)
• Jack oak……...X jackiana Schneid. (Q. alba x Q. montana)
• Saul oak……...X saulii Schneid. (Q. alba x Q. prinus)
Saul oak was formerly known as Q. alba f. ryderii but is now considered a heterozygous hybrid form of white oak.

Introgressive populations are locally common throughout much of the range of white oak. Hybrid swarms derived from complex mixtures of parental forms are particularly common on disturbed sites, at the margins of white oak's range, and where several oak species occur sympatrically.

Tirmenstein, D. A. 1991. Quercus alba In: U.S. Department of Agriculture(2002, September), Forest Service, Rocky Mountain Research Station, Fire Sciences Laboratory Fire Effects Information System:

SPECIES: Salix nigra

• black willow
• swamp willow
• southwestern black willow
• Gulf black willow
• scythe-leaved willow

The currently accepted scientific name of black willow is Salix nigra Marsh. Recognized varieties are S. nigra var. nigra Marsh., S. nigra var. altissima Sarg., S. nigra var. falcata (Pursh.) Torr., and S. nigra var. lindheimeri.

Salix nigra, S. gooddingii Ball, and S. amygdaloides Anderss. are closely related taxa commonly referred to as the black willows. The three species are not easily distinguished morphologically, and in fact, some authorities consider S. gooddingii to be S. nigra var. vallicola Dudley or S. n. var. venulosa (Anderss.) Bebb. S. amygdaloides is sometimes considered to be S. nigra var. amygdaloides Anderss. For our purposes, however, these varieties will be considered as separate species. S. nigra hybridizes with S. amygdaloides (S. X glatfelteri Schneider); S. alba (S. X hankensonii Dode); and S. lucida (S. X schneider Boivin).

Tesky, Julie L. 1992. Salix nigra In: U.S. Department of Agriculture(2002, September), Forest Service, Rocky Mountain Research Station, Fire Sciences Laboratory Fire Effects Information System:

The Taxonomy of Roses

Ah, but according to Gertrude Stein, "a rose is a rose is a rose", right? Well, check these out:

Relationships Among Some Species of Roses
(From: Ma, Y., Crane, C. F., and Byrne, D.H. (1997). Relationships among some Rosa species, Caryologia, vol. 50, n. 3-4, pp. 317-326):

The genus Rosa is widely distributed and taxonomically difficult. The great majority of its 200 species hall into the ten sections of subgenus Rosa; the three other subgenera contain one to three species each. Morphological and ecological variation with subgenus Rosa is almost continuous because of wide adaptation, wide limits of crossability and hybrid fertility, and frequent human intervention in bybridization and dispersal. Polyploidy is frequent in sections Pimpinellifoliae, Gallicanae, Cinnamoneae, and Caninae of subgenus Rosa and essentially absent elsewhere among the wild species. Karyotype analysis is a traditional first step in the comparison of genomes among related species that are to be included in a breeding program.

Think that's bad? Consider this "war of the roses":

Chromosomes in Relation to Sterility in Roses
(From: Pal, B. P, (1972). The Rose in India, 2nd Ed. Maggs Bros, Ltd, New Delhi, RI)

The basic number of chromosomes in roses is 7, and several important species of Asian origin, which have contributed significantly to the development of such famous groups as the Hybrid Perpetual and the Hybrid Teas, are diploids, having 14 chromosomes (7 maternal and 7 paternal). These include moschata, gigantea, multiflora, wichuraiana and chinensis. A number of Western species with which these Asian diploids crossed to yield several modern groups of roses are tetraploids, with 28 chromosomes. These, which had their chromosome number doubled during the course of their evolution, whose record we do not have, include gallica, foetida and their derivatives such as damascena and centifolia.

One of the more important crosses involving these species of diverse geographical distribution was that between gallica and a variety combining in it the genes of chinensis and gigantea. The hybrid arising directly from this cross was a triploid, having 21 chromosomes, 14 from the European parent and 7 from the Asian. This imbalance made it sterile and restricted its utility; but plants with 28 chromosomes arose spontaneously from it. They were fertile and gave rise to the Hybrid Perpetuals with the further incorporation of some damascena genes.

A triploid origin has also been shown for the Hybrid Teas, which followed and replaced to a large extent the Hybrid Perpetual. The Hybrid Teas were derived from a cross between the tetraploid Hybrid Perpetuals and a diploid variety of the Tea roses which combines in it the genes of three Asian (moschata, chinensis and gigantea) and one European (damascena) species. As in the case of the Perpetuals, tetraploid varieties were spontaneously obtained from the original triploid hybrid; this restored the fertility of the plant, making it possible to obtain many different combinations of genes in its progeny.

The condition of triploidy resulting from the crossing of diploid and tetraploid parents, associated as it was with hybrid sterility, delayed the release of gene combinations which were destined to develop into our modern groups of roses. Not all triploid hybrids, however, had to wait for a change to the tetraploid level before their usefulness could be appreciated…There are also examples where a cross involving a diploid and a tetraploid skipped the expected condition of triploidy and gave rise to the tetraploid state directly through an abnormal behavior of the diploid parent, which passes its entire complement of chromosomes to its sex cells in place of only half the number, which is the normal practice.

Ouch! Those roses don't seem to give a damn about chromosome number, polyploidy, and all of those other things that are so often developmentally fatal to most animals. But, you say, this mess is mostly the result of humans messing about with the chromosomes of the original rose. Let's look at some roses that haven't been so corrupted by bourgeois gardeners. Say, some good, proletarian Russian roses...

The Present State of Taxonomy of the East European Roses
(From: Schanzer, L.A. (2001) Biological Series, vol. 106, part 2, pp. 1-2)

Critical overview of the taxonomic literature on the East European species of Rosa leads to the conclusion that this genus is still extremely inadequately studied as to species composition and relations. Quite a number of species, infra-, and superspecific taxa described so far do not make the taxonomy and nomenclature of the group any more clear. They moreover make any firm determination of most of the species perfectly impossible. Data available on chromosome numbers, interspecific crossings, and compatibility of West European species point to the necessity of such studies of East European species as well. The latter remain completely unstudied in these respects so far. On the other hand, sparse data on infrapopulational variability of Rosa suggest such studies to be important to understanding of many disputable questions of the Rosa taxonomy."

Conclusion: A rose by any other name would smell as sweet, but that doesn't help us with the classification of roses.

Perhaps Darwin's most important insight was his realization that species are not immutable, that they can intergrade over time in an "insensible series." But what Darwin didn't have the courage to come right out and say, and what most evolutionary biologists in general don't have the courage to propose, is that there are really no such thing as species at all, at least not in the way we have traditionally defined them. Darwin should have realized this: he made it clear that natural selection happens at the level of individuals, never at the level of species. Evolutionary biologists have agreed with him, but have not taken the obvious next step: to declare that individuals living organisms are the only things that exist in the natural world, and that species (including animal species) may quite literally be figments of the human imagination.

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Monday, March 13, 2006

Evolutionary Psychology and Historical Contingency

AUTHOR: Nicholas Wade

SOURCE: New York Times Magazine

COMMENTARY: Allen MacNeill

I usually like Nicholas Wade's columns, but this one leaves me feeling uncomfortable. Read it, and then we'll talk:
"The Twists and Turns of History, and of DNA"



Let's start with the very first paragraph:
East Asian and European cultures have long been very different, Richard E. Nisbett argued in his recent book "The Geography of Thought." East Asians tend to be more interdependent than the individualists of the West, which he attributed to the social constraints and central control handed down as part of the rice-farming techniques Asians have practiced for thousands of years.

Yes, I know, Ernst Mayr claimed that evolutionary biologists use "population thinking," but sweeping statements about whole groups of people are not generally what evolution is about. The most salient feature of natural populations of individual organisms is the fact that there are significant differences between those individuals. It is precisely such differences that provide the raw material for natural selection. As R. A. Fisher first pointed out, natural selection requires traits that display "continuous variation:" that is, a normal distribution of values for whatever trait is under consideration. For example, if beak size in finches is to undergo natural selection, there must a normal distribution of beak sizes from small to large, with a peak prevalence at some intermediate value.

So where does this leave us? Is "interdependence" the trait being selected for in the article under discussion? If so, I'm extremely skeptical. How would "interdependence" be mediated, at the level of biological processes that could be related to changes in allele frequencies or modifications of developmental pathways? These, after all, are the mechanisms that must be modified for biological evolution to occur, and especially if a biological adaptation is to evolve via natural selection.

True, the article does go on to suggest that there is empirical evidence that selection is happening:
Humans have continued to evolve throughout prehistory and perhaps to the present day, according to a new analysis of the genome reported last week by Jonathan Pritchard, a population geneticist at the University of Chicago.

Fine, so far: what Pritchard & Co. have found are segments of DNA (i.e. "genes") whose frequencies in different populations have changed in ways that are consistent with what one would expect as the result of natural selection. But then comes the punchline:
So human nature may have evolved as well.

It's like that famous Sidney Harris cartoon: "And then a miracle happens..." The logical step from changes in allele frequencies in the human genome to changes in "human nature" is one for which no empirical evidence is presented, and for which such evidence may be impossible to obtain.

Why is this important? Wade goes on to note:
Evolutionary changes in the genome could help explain cultural traits that last over many generations as societies adapted to different local pressures. Trying to explain cultural traits is, of course, a sensitive issue. The descriptions of national character common in the works of 19th-century historians were based on little more than prejudice. Together with unfounded notions of racial superiority they lent support to disastrous policies.

What disasterous policies? Well, those of the Nazis during World War II, for starters. Ascribing "general characteristics" to "societies" is precisely what the Nazis did. Jews as a group were venal, grasping, self-interested, conniving, dishonest, etc. etc. No matter that individual Jews might express such traits to varying degrees; what mattered in Nazi racial policy was the "biological" traits of whole groups of people.

Wade gives a nod to this caveat:
...the concept of national character could turn out to be not entirely baseless, at least when applied to societies shaped by specific evolutionary pressures.

Indeed. Is there any biological sense in calling "national character" an adaptation? Even the question seems laughable, and the answer is, of course, no. Evolutionary biologists can't actually agree on what constitutes an adaptation; if they could, no one would have read nor given any credence to Lewontin and Gould's famous "spandrels" paper. Evolutionary biologists with a proven track record, like Lynn Margulis (of "serial endosymbiosis" fame) have railed against the "pan-adaptationism" of most evolutionary biologists. Furthermore, the work of Jukes, Kimura, Ohta, and others have shown that the vast majority of DNA (and many of the proteins for which it codes) have evolved via "neutral" mechanisms that produce nothing like adaptations in the classical sense.

So, is there anything to this report beyond the recapitulation of long-ago discredited social prejudice? Let's see:
In a study of East Asians, Europeans and Africans, Dr. Pritchard and his colleagues found 700 regions of the genome where genes appear to have been reshaped by natural selection in recent times. In East Asians, the average date of these selection events is 6,600 years ago. Many of the reshaped genes are involved in taste, smell or digestion, suggesting that East Asians experienced some wrenching change in diet. Since the genetic changes occurred around the time that rice farming took hold, they may mark people's adaptation to a historical event, the beginning of the Neolithic revolution as societies switched from wild to cultivated foods.

In other words, the frequencies of certain regions of the genome have changed out of synch with other regions. The inference, therefore, is that the altered regions (e.g. "genes") have changed in frequency as the result of natural selection. So far, I have no problem with this. But look at what these genes/regions code for: physiological processes, virtually all of them mediated by enzymes or regulatory proteins of some kind (i.e. taste, smell, digestion, etc.) No problem: genes do, indeed, code for proteins, and therefore there is nothing particularly controversial about inferring that the non-conserved regions identified by Pritchard & Co. have evolved as the result of selection for altered diet, etc.

But can one then extrapolate from resultsand inferences like these to "national character?" Consider:
Some of the genes are active in the brain and, although their role is not known, may have affected behavior. So perhaps the brain gene changes seen by Dr. Pritchard in East Asians have some connection with the psychological traits described by Dr. Nisbett.

Now hold one, here: how do you get from changes in allele frequencies to changes in behavior? E. O. Wilson cautioned that we can't do this until the architecture of the brain can be broken down and its relationship to behavior studied in detail. Are we at that point? Hardly; cognitive psychologists can't even agree on how "thoughts" are related to behavior. Wade states this uncertainty clearly: "...their role is not known..." Exactly.

So can we make confident statements about changes in alleles being related to changes in "national character?" I don't think so, but clearly other folk do:
Some geneticists believe the variations they are seeing in the human genome are so recent that they may help explain historical processes. "Since it looks like there has been significant evolutionary change over historical time, we're going to have to rewrite every history book ever written," said Gregory Cochran, a population geneticist at the University of Utah. "The distribution of genes influencing relevant psychological traits must have been different in Rome than it is today," he added. "The past is not just another country but an entirely different kind of people."

Yeah, but do you rewrite the history books before or after you've shown the actual connections between the alleles and the relevent behaviors? And even when you do this (assuming you can), do you then extrapolate from that to "national character?" Not unless you believe that individual variations in "character" amount to virtually nothing.

But natural selection acts primarily at the level of individuals, or so the overwhelming majority of evolutionary biologists from Charles Darwin to G. C. Williams have asserted. Yes, Hamilton's "kin selection" seems to displace the focus of selection from individuals to their shared alleles, but in the real world it is still individual organisms that live and die, reproduce or fail to, and therefore remain the ultimate locus of action of natural selection.

But the article suggests that these recent findings might provide a kind of Seldonian theory of "psychohistory" by means of which we could understand and even predict the behavior of human groups (a la Isaac Asimov's Foundation series). In science fiction, that's fine, but we're talking about science here. The problem with historical processes is that they are stubbornly resistant to mathematicization. You can't formulate an equation that describes (much less predicts) something like the fall of the Roman Empire or the invention of gunpowder. In an earlier posting to this list, I pointed out that historical contingency is the root of the problem of macroevolutionary theory, in that historical events by definition can't be described nor predicted by mathematical models.

Isn't that exactly the unstated assumption what underlies statements like these? Seems so to me:
John McNeill [no relation, BTW], a historian at Georgetown University, said that "it should be no surprise to anyone that human nature is not a constant" and that selective pressures have probably been stronger in the last 10,000 years than at any other epoch in human evolution. Genetic information could therefore have a lot to contribute, although only a minority of historians might make use of it, he said.

The only way in which "genetic information" could contribute to an understanding of human history would be if:
1) there is a one-to-one correlation between genes and human behaviors,
2) there is a one-to-one correlation between sets of genes and "national characters",
3) individual differences within "societies" are swamped by the "national character" of such societies, and
4) the contingency that seems to affect historical processes can be shown to be entirely reducible to the foregoing.

Does anyone anywhere suggest that we are even remotely close to demonstrating any of these conditions? If so, I want to know where such results have been peer-reviewed and published. All I've seen so far is a lot of airy hypothesis spinning.

But wait, it gets weirder:
The political scientist Francis Fukuyama has distinguished between high-trust and low-trust societies, arguing that trust is a basis for prosperity. Since his 1995 book on the subject, researchers have found that oxytocin, a chemical active in the brain, increases the level of trust, at least in psychological experiments. Oxytocin levels are known to be under genetic control in other mammals like voles. It is easy to imagine that in societies where trust pays off, generation after generation, the more trusting individuals would have more progeny and the oxytocin-promoting genes would become more common in the population. If conditions should then change, and the society be engulfed by strife and civil warfare for generations, oxytocin levels might fall as the paranoid produced more progeny.

Notice that key phrase: It's easy to imagine... Indeed it is. Doing real science is hard work. So far, I don't see any evidence of it having been done, here. True, some people have done a lot of field work on human behavior:
Napoleon Chagnon for many decades studied the Yanomamo, a warlike people who live in the forests of Brazil and Venezuela. He found that men who had killed in battle had three times as many children as those who had not. Since personality is heritable, this would be a mechanism for Yanomamo nature to evolve and become fiercer than usual.

But Chagnon's work shows quite explicitly that the patterns of behavior he has described can be explained by natural selection at the level of individuals. That's precisely what Chagnon's point was about unokais (the men who had killed other men in battle): their reproductive success could be directly linked to their behavior in a way that supported the concept of individual selection. That is, most individual Yanomami men are "fierce" because they are the offspring of individual men who were "fierce." "Fierceness," therefore, is a trait of individual Yanomami men, and only secondarily (and by analogy) of Yanomamo society.

All of the foregoing seems to me to be arguing that "societies" have "genomes," and that changes in those genomes can be directly linked to changes in those societies. In the following quote, a tendency to confuse the "genomes" of individuals and groups becomes glaringly obvious, at least to me:
Since the agricultural revolution, humans have to a large extent created their own environment. But that does not mean the genome has ceased to evolve. The genome can respond to cultural practices as well as to any other kind of change. Northern Europeans, for instance, are known to have responded genetically to the drinking of cow's milk, a practice that began in the Funnel Beaker Culture which thrived 6,000 to 5,000 years ago. They developed lactose tolerance, the unusual ability to digest lactose in adulthood. The gene, which shows up in Dr. Pritchard's test, is almost universal among people of Holland and Sweden who live in the region of the former Funnel Beaker culture.

But societies can't have genomes; only individuals do. There is a distressing tendency these days to equate the genome of individuals with the elements that are shared between individuals in "societies" (i.e. reproductively panmictic populations). When people make this equation, they are in effect reinventing Platonic idealism in its most pernicious form. The "national character" becomes the "ideal form" which is coded for by the "genome" of the society, and along the way all individual differences (the raw material upon which all selection depends) are brushed aside.

And finally, of course, the Jews are explicitly mentioned:
The most recent example of a society's possible genetic response to its circumstances is one advanced by Dr. Cochran and Henry Harpending, an anthropologist at the University of Utah. In an article last year they argued that the unusual pattern of genetic diseases found among Ashkenazi Jews (those of Central and Eastern Europe) was a response to the demands for increased intelligence imposed when Jews were largely confined to the intellectually demanding professions of money lending and tax farming. Though this period lasted only from 900 A.D. to about 1700, it was long enough, the two scientists argue, for natural selection to favor any variant gene that enhanced cognitive ability.

One theme in their argument is that the variant genes perform related roles, which is unlikely to happen by chance since mutations hit the genome randomly. A set of related mutations is often the mark of an evolutionary quick fix against some sudden threat, like malaria. But the variant genes common among the Ashkenazi do not protect against any known disease. In the Cochran and Harpending thesis, the genes were a response to the demanding social niche into which Ashkenazi Jews were forced and the nimbleness required to be useful to their unpredictable hosts.

And then comes the kicker:
No one has yet tested the Cochran-Harpending thesis, which remains just an interesting though well worked out conjecture. But one of its predictions is that the same genes should be targets of selection in any other population where there is a demand for greater cognitive skills. That demand might have well have arisen among the first settled societies where people had to deal with the quite novel concepts of surpluses, property, value and quantification. And indeed Dr. Pritchard's team detected strong selection among East Asians in the region of the gene that causes Gaucher's disease, one of the variant genes common among Ashkenazim.

That is, all we have here is a correlation between alleles, traits at the level of individuals, and a suggested correlation with "societal" traits. But as every good scientist knows, correlation is not proof of causation. On the contrary, valid arguments for causation always rely on analysis of mechanisms, and here the foregoing studies are completely mute. There are no actual mechanisms by which the correlations can be shown to have worked. Indeed, how exactly would one test the "Cochran-Harpending thesis" other than to collect more data supporting the suggested correlation?

I call myself an evolutionary psychologist, and must admit that I have suggested hypotheses such as those described in this article. But, when I have done so, I have tried to be careful to emphasize that what I have been doing is suggesting a hypothesis, not validating a theory. It may be that E. O. Wilson is correct and that we may have to wait until we can show the connections between alleles, neural circuitry, behaviors, and social patterns. If so, I'd rather wait than have our theories co-opted by yet another totalitarian regime bent on the "improvement" of our "national character."



Location Online: New York Times

Original posting/publication date timestamp:
Published: March 12, 2006

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Monday, March 06, 2006

A Theorist on Mass Extinction Is Honored

AUTHOR: Associated Press (news release)

SOURCE: New York Times

COMMENTARY: Allen MacNeill (following the article)

RENO, Nev., March 5 - A geologist who proposed the theory that a comet or asteroid smashed into the Earth and killed off the dinosaurs has won a top research award. The geologist, Walter Alvarez, of the University of California, Berkeley, is the 19th recipient of the Desert Research Institute's silver medallion and its $20,000 prize. He is to accept the award here on Monday.

Dr. Alvarez's nearly two-decade investigation produced an uncommon scientific drama of personal tenacity and ingenuity, said Stephen G. Wells, president of the institute.

"Until the impact theory was finally proven, Dr. Alvarez and his colleagues were regarded as heretics by the 'old guard' in the field of geology," Dr. Wells said.

The theory dates to the 1970's in Italy, where Dr. Alvarez and his colleagues found high levels of the element iridium, which is extremely rare on Earth, but common in comets and asteroids. They theorized that it must have come from the impact of a giant asteroid that sent smoke, dust and iridium into the sky, blocking the sun, lowering the Earth's temperature and eventually killing off plants and many species.

Dr. Alvarez's theory, first published in Science in 1980, had few supporters until scientists found evidence of a huge impact crater on the Yucatan Peninsula of Mexico in 1989. Later studies found evidence of debris from Mexico distributed by tsunamis that went as far as Arkansas.

The Desert Research Institute, established in 1959, is a nonprofit division of the University and Community College System of Nevada.


Walter Alvarez and his colleagues exemplify what is right with science (and, by comparison, what's wrong with "intelligent design"). They were looking for something (a way to test a theory about deposition of sediments using a "clock" based on infalling space dust) and entirely by accident discovered something else that turned out to be truly revolutionary. They did the difficult field research, published the results in a peer-reviewed journal, responded to their critics with more research and publications, and eventually carried the day. the IDers want the glory without any of the work, and are trying to "prove" a theory without even finding data to support it. That's intellectual masturbation, not revolutionary science.



Location Online: New York Times

Original posting/publication date timestamp:
Published: March 6, 2006

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The Reinvention Of The Self

AUTHOR: Jonah Lehrer

SOURCE: Seed Magazine

COMMENTARY: Allen MacNeill (following the excerpt)

It has been received dogma for about a century that our cognitive potential (i.e. our "intelligence") is essentially fixed at birth or shortly thereafter, and that whatever debate has swirled around this topic has had primarily to do with how much influence very early environmental conditions have on our "innate" intelligence. What Gould's work shows is that the primate brain is continuously remodeled throughout life, in response to shifting environment pressures:


Eight years after Gould defied the entrenched dogma of her science and proved that the primate brain is always creating new neurons, she has gone on to demonstrate an even more startling fact: The structure of our brain, from the details of our dendrites to the density of our hippocampus, is incredibly influenced by our surroundings. Put a primate under stressful conditions, and its brain begins to starve. It stops creating new cells. The cells it already has retreat inwards. The mind is disfigured.

The social implications of this research are staggering. If boring environments, stressful noises, and the primate’s particular slot in the dominance hierarchy all shape the architecture of the brain—and Gould’s team has shown that they do—then the playing field isn’t level. Poverty and stress aren’t just an idea: they are an anatomy. Some brains never even have a chance.


But it isn't all bad news; the process can go the other way, as well, making new pathways and connections:


Chronic stress, predictably enough, decreases neurogenesis. As Christian Mirescu, one of Gould’s post-docs, put it, “When a brain is worried, it’s just thinking about survival. It isn’t interested in investing in new cells for the future.”

On the other hand, enriched animal environments—enclosures that simulate the complexity of a natural habitat—lead to dramatic increases in both neurogenesis and the density of neuronal dendrites, the branches that connect one neuron to another. Complex surroundings create a complex brain.


To understand how revolutionary this finding is, consider the following statements about this process from the pre-eminent researcher in this field twenty years ago:


“All neurons of the rhesus monkey brain are generated during pre-natal and early post-natal life,” Rakic wrote in his 1985 paper, “Limits of Neurogenesis in Primates.” “Not a single” new neuron “was observed in the brain of any adult animal.” While Rakic admitted that his proof was limited, he persuasively defended the dogma. He even went so far as to construct a plausible evolutionary theory as to why neurons can’t divide: Rakic imagined that at some point in our distant past, primates had traded the ability to give birth to new neurons for the ability to retain plasticity in our old neurons. According to Rakic, the “social and cognitive” behavior of primates required the absence of neurogenesis. His paper, with its thorough demonstration of what everyone already believed, seemed like the final word on the matter. No one bothered to verify his findings.


And Gould's findings have political and economic implications:


Gould’s research inevitably conjures up comparisons to societal problems. And while Gould, like all rigorous bench scientists, prefers to focus on the strictly scientific aspects of her data—she is wary of having it twisted for political purposes—she is also acutely aware of the potential implications of her research.

“Poverty is stress,” she says, with more than a little passion in her voice. “One thing that always strikes me is that when you ask Americans why the poor are poor, they always say it’s because they don’t work hard enough, or don’t want to do better. They act like poverty is a character issue.”

Gould’s work implies that the symptoms of poverty are not simply states of mind; they actually warp the mind. Because neurons are designed to reflect their circumstances, not to rise above them, the monotonous stress of living in a slum literally limits the brain.


That the architecture of the brain actually changes over time should not come as a complete surprise. Neuroscientists have known for a while that synapses can change, for example as the result of antidepressant drugs:


For the last 40 years, medical science has operated on the understanding that depression is caused by a lack of serotonin, a neurotransmitter that plays a role in just about everything the mind does, thinks or feels. The theory is appealingly simple: sadness is simply a shortage of chemical happiness. The typical antidepressant—like Prozac or Zoloft—works by increasing the brain’s access to serotonin. If depression is a hunger for neurotransmitter, then these little pills fill us up.

Unfortunately, the serotonergic hypothesis is mostly wrong. After all, within hours of swallowing an antidepressant, the brain is flushed with excess serotonin. Yet nothing happens; the patient is no less depressed. Weeks pass drearily by. Finally, after a month or two of this agony, the torpor begins to lift.

But why the delay? If depression is simply a lack of serotonin, shouldn’t the effect of antidepressants be immediate?

The paradox of the Prozac lag has been the guiding question of Dr. Ronald Duman’s career....When Duman began studying the molecular basis of antidepressants back in the early 90s, the first thing he realized was that the serotonin hypothesis made no sense. A competing theory, which was supposed to explain the Prozaz lag, was that antidepressants increase the number of serotonin receptors. However, that theory was also disproved. “It quickly became clear that serotonin wasn’t the whole story,” Duman says. “Our working hypothesis at the time just wasn’t right.”

But if missing serotonin isn’t the underlying cause of depression, then how do antidepressants work? As millions will attest, Prozac does do something. Duman’s insight, which he began to test gradually, was that a range of antidepressants trigger a molecular pathway that has little, if anything, to do with serotonin. Instead, this chemical cascade leads to an increase in the production of a class of proteins known as trophic factors. Trophic factors make neurons grow. What water and sun do for trees, trophic factors do for brain cells. Depression was like an extended drought: It deprived neurons of the sustenance they need.

Duman’s discovery of a link between trophic factors and antidepressant treatments still left the essential question unanswered: What was causing depressed brains to stop producing trophins? Why was the brain hurting itself? It was at this point that Duman’s research intersected the work of Robert Sapolsky and Bruce McEwen (Gould’s advisor at Rockefeller), who were both studying the effects of stress on the mammalian brain. In an influential set of studies, Sapolsky and McEwen had shown that prolonged bouts of stress were devastating to neurons, especially in the hippocampus. In one particularly poignant experiment, male vervet monkeys bullied by their more dominant peers suffered serious and structural brain damage. Furthermore, this neural wound seemed to be caused by a decrease in the same trophic factors that Duman had been studying. From the perspective of the brain, stress and depression produced eerily similar symptoms. They shared a destructive anatomy.

Just as Duman was beginning to see the biochemical connections between trophins, stress, and depression, Gould was starting to document neurogenesis in the hippocampus of the primate brain. Reading Altman’s and Kaplan’s papers, Gould had realized that her neuron-counting wasn’t erroneous: She was just witnessing an ignored fact. The anomaly had been suppressed. But the final piece of the puzzle came when Gould heard about the work of Fernando Nottebohm, who was, coincidentally, also at Rockefeller. Nottebohm, in a series of beautiful studies on birds, had showed that neurogenesis was essential to birdsong. To sing their complex melodies, male birds needed new brain cells. In fact, up to 1% of the neurons in the bird’s song center were created anew, every day.


Perhaps the time lag of antidepressants was simply the time it took for new cells to be created....In December 2000, Duman’s lab published a paper in the Journal of Neuroscience demonstrating that antidepressants increased neurogenesis in the adult rat brain. In fact, the two most effective treatments they looked at—electroconvulsive therapy and fluoxetine, the chemical name for Prozac—increased neurogenesis in the hippocampus by 75% and 50%, respectively. Subsequent studies did this by increasing the exact same molecules, especially trophic factors, that are suppressed by stress.

Duman was surprised by his own data. Fluoxetine, after all, had been invented by accident. (It was originally studied as an antihistamine.) “The idea that Prozac triggers all these different trophic factors that ultimately lead to increased neurogenesis is just totally serendipitous,” Duman says. “Pure luck.”


Several major drug companies and a host of startups are now frantically trying to invent the next generation of antidepressants (a $12-billion-a-year business). Many expect these future drugs to selectively target the neurogenesis pathway. If these pills are successful, they will be definitive proof that antidepressants work by increasing neurogenesis. Depression is not simply the antagonist of happiness. Instead, despair might be caused by the loss of the brain’s essential plasticity. A person’s inability to change herself is what drags her down.


It would be difficult to overemphasize how revolutionary Gould's findings are to the fields of evolutionary psychology and psychology in general. That we had a limited ability to do this has been increasingly recognized over the past two decades, as neuroscientists discovered that new synapses could be formed, not just by altering the quantities of neurotransmitters released by existing synapses, but also by building new receptors or eliminating existing ones. However, until this new work by Gould and her colleagues, it was assumed that the underlying neural architecture of the brain was essentially predetermined by genetics, and that all the environment could do was to downgrade that architecture as a result of malnutrition, under-stimulation, and other environmental injuries and insults.

Now, however, it looks like the brain can be remodeled throughout life, with whole new neurons being added along with multiple synapses, thereby fundamentally altering the cognitive potential of individuals throughout life. In other words, the nervous system is much more plastic than heretofore suspected, and can therefore respond much more robustly to environmental changes, in both positive and negative directions.

This discovery has political ramifications, as well as scientific ones. Programs like Head Start and other early educational "interventions" have all been premised on the idea that such remediation only works if instituted very early in development, and even then probably have little effect. However, if the architecture of our brains is modifiable throughout life, it may be possible to successfully intervene at nearly any stage of cognitive development. Therefore, withholding such intervention as the result of economic or political exigencies becomes even more egregious than it is at present.

As far as evolutionary psychology is concerned, it would seem on reflection that discoveries like these make perfect evolutionary sense. Primates are known for our behavioral plasticity; it's our most obvious (and most valuable) adaptive trait. Finding out that this plasticity goes all the way down to the neural architecture itself shouldn't be that surprising. However, it does cast even more doubt on the "hard inheritance" stance of people like Herrnstein, Murray, et al, and even the "hard hereditarian" position of E. O. Wilson and other "genetic sociobiologists." If Gould's findings hold up, and even moreso if they are expanded, it seems as though the environmental plays an even more important role in altering primate behavior and "intelligence" than formerly thought.

And so the pendulum swings again...



Location Online: Seed Magazine

Original posting/publication date timestamp:
February 23, 2006 12:37 AM

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