john hawks weblog

paleoanthropology, genetics and evolution

Why are organisms modular?

Wed, 2005-09-21 13:38 -- John Hawks

Modularity is a property of biological organization: organisms are composed of subunits that perform different functions. At the cellular level, the cell is composed of organelles that have different functions in protein assembly, metabolism, growth, and homeostasis. This organization is reflected at the level of DNA, which consists of sequences organized into functional subunits: coding regions, introns, promoter regions, multigene complexes, and ultimately chromosomes. It characterizes the anatomy of multicellular organisms, which are divided into organs such as hearts, lungs, ganglia, and eyes, or leaves, stems, flowers, and roots.

And modularity underlies the organization of the brain. Mammalian brains are divided into different parts --- neocortex, cerebellum, thalamus, etc. These parts contribute differently to different functions, as do the subcomponents of each of the parts. The neocortex is comprised of tissues that contribute to different tasks, such as Broca's area for speech and the

Brains do a lot of things that are analogous to computers, in terms of information processing. Indeed, the things that our brains are really good at are increasingly being done by computers, from adding and subtracting to face recognition. Our brains certainly have talents that are a challenge for computers, and vice versa. For one thing, our brains are well-motivated for the most part while computers have no motivation at all. But they are broadly similar in their ability to take in and manipulate information: a computer is more similar to our brains than, say, to our muscles.

But today's computers are not modular in the same way our brains are modular. Computers have different components, that is true --- they have memory chips and disk drives and power supplies and one or more central processing units (CPUs). But the great strength of computers is that the same CPU can be programmed to perform any algorithmic task. That's the principle of the universal Turing machine: a certain kind of simple device can --- by providing different instructions --- perform any transformation on data that we could think of. Indeed, if we had the right software we could cause today's computers to act like humans; they would just be really, really, really slow.

This provides a hint about why we would want the brain to be modular, rather than to provide different instructions to a single small but fast CPU. Differrent brain tissues can perform different functions at the same time, so that we can very quickly recognize someone's face, remember where we know her from, contort our faces to an pleasant expression of recognition, and say "Hello." Specializing each of these tasks into different tissues allows us to perform them much more quickly.

But that doesn't answer the question of how mental modularity evolved in the first place. After all, at the time that face recognition became important in primate evolution, our primate ancestors weren't doing all the things that we do now. Why couldn't they have simply evolved a single system that added new capabilities as it went along? This kind of mega-system would seem to be the natural consequence of evolution: tinkering slightly with a pre-existing function ought to be much easier than adding whole new modules from scratch.

Now, I should point out that we really don't have a lot of detail about how fine-grained the modularity of the brain actually is. It might very well be that a lot of what we do actually is cobbled together into a few mega-systems. But there is abundant evidence that a lot of cognition is actually very domain-specific: different neural circuits exist to perform discrete tasks.

A new paper by Nadav Kashtan and Uri Alon of the Weizmann Institute finds a reason why modularity might commonly evolve. Here's the abstract:

Biological networks have an inherent simplicity: they are modular with a design that can be separated into units that perform almost independently. Furthermore, they show reuse of recurring patterns termed network motifs. Little is known about the evolutionary origin of these properties. Current models of biological evolution typically produce networks that are highly nonmodular and lack understandable motifs. Here, we suggest a possible explanation for the origin of modularity and network motifs in biology. We use standard evolutionary algorithms to evolve networks. A key feature in this study is evolution under an environment (evolutionary goal) that changes in a modular fashion. That is, we repeatedly switch between several goals, each made of a different combination of subgoals. We find that such "modularly varying goals" lead to the spontaneous evolution of modular network structure and network motifs. The resulting networks rapidly evolve to satisfy each of the different goals. Such switching between related goals may represent biological evolution in a changing environment that requires different combinations of a set of basic biological functions. The present study may shed light on the evolutionary forces that promote structural simplicity in biological networks and offers ways to improve the evolutionary design of engineered systems (Kashtan and Alon 2005:13773).

The study simulated the evolutionary process by allowing different kinds of circuits to compete with each other. The circuits that best solved the range of problems in the "environment" were replicated into a new generation (i.e. "selection"), with a small likelihood of random changes (i.e. "mutations") to their function. They also performed a similar simulation using neural networks instead of circuits.

These experiments resulted in many different designs that satisfied the same computational goal. So the evolution in the different simulations was contingent: random factors led different simulations to different optimal solutions.

But this experiment added a novel component: sometimes the computational goals changed slightly over time. Each of the computational goals might involve several subtasks. One possibility is that these different subtasks might remain constant over time. But an additional possibility is that they might change slightly in importance relative to each other: in other words, the circuits might be presented with slightly different problems at some times than others.

Now, if this "environment" of problems to solve changed in a consistent direction over time, then we would expect the circuits likewise to evolve to solve the newer problems more efficiently.

But instead of changing the task from the beginning to the end of the simulations, Kashtan and Alon (2005) caused the tasks to oscillate over time. Sometimes one subtask might be more important, sometimes another, but there was no long-term directional change, just a steady variability in what kinds of tasks were important.

In this fluctuating environment, the circuits evolved to be modular. Changing different requirements at different times caused different subsystems to arise to solve each of these subtasks. These modular systems were slightly less efficient than the nonmodular systems that evolved to solve fixed tasks: they required additional logic gates to do the same job. But it took them a much shorter time to make the adjustment to solving slightly different problems.

You might think that this evolution was the result of the division of the computational goal into perceivable subtasks. But interestingly, when the environment encompassed goals that could logically be divided into subtasks but did not vary over time, the circuits did not evolve toward modular solutions. Here's an example:

A human engineer would easily notice the modularity in this problem and design a network that is made of two modules, one that analyzes the left side of the retina, and the other for the right side of the retina. In contrast, the structure of the evolved networks was not modular (Fig. 5b)(Qm = 0.15 0.02). As in the case of electronic circuits, fixed-goal evolution produces a nonmodular network even though the problem itself is readily decomposable into separate subgoals (Kashtan and Alon 2005:13776).

Nor was the effect simply the result of variation over time: when tasks were made to vary randomly, instead of by the emphasis of different subtasks, no modular structure resulted in the evolving circuits.

The authors discuss their results:

Why do modularly varying goals speed up evolution (in terms of the number of generations to reach perfect solution) when compared with evolution under a fixed goal? One reason that fixed-goal evolution is often slow is that the population becomes stuck in local fitness maxima. Because the fitness landscape changes each time that the goal changes, modularly varying goals can help move the population from these local traps. Over the course of many goal changes, modularly varying goals seem to guide the population toward a region of network space that contains fitness peaks for each of the goals in close proximity. This region seems to correspond to modular networks (ibid:13777).

The other element of the study is the demonstration that these kinds of modular circuits consist of similar structures repeated to comprise different modules. Such repeated elements are here called "network motifs". This is another characteristic of some biological organization, so it is very interesting:

In addition to their modular structure, the networks evolved under modularly varying goals display significant network motifs. The same motifs are reused throughout each network in different modules. Some of these motifs are also found in biological information processing networks. For example, feed-forward loops and bifans are found in transcription networks (7). Feed-forward loops, bifans, and diamonds are found in signal transduction and synaptic neuronal networks (7). In signal transduction networks (34) and the neuronal network of C. elegans (39), multilayered feed-forward patterns similar to those in Fig. 5c, are strong network motifs. An example is multilayered protein kinase cascades, in which families of kinases in each layer activate families of kinases in the next layer (34, 40, 41).

One possible explanation for the origin of the motifs in the olved networks is that modular networks are locally denser than nonmodular networks of the same size and connectivity. This local density tends to increase the number of subgraphs (42). To test this possibility, we evolved networks to reach the same modularity measure Q as the networks evolved under modularly varying goals, but with no information-processing goal (see Supporting Text). We find that these modular networks have no significant network motifs (Fig. 9). They show relatively abundant feedback loops that are antimotifs in the networks evolved under modularly varying goals. It therefore seems that the specific network motifs found in the evolved networks are not merely caused by local density, but may be useful building blocks for information processing (ibid:13777-13778).

The authors end with a discussion of how their results may apply to biological evolution, with specific biological examples, although not drawn from the brain.

References:

Kashtan N, Alon U. 2005. Spontaneous evolution of modularity and network motifs. Proc Nat Acad Sci USA 102:13773-13778.

Neandertal teeth: fast or slow?

Tue, 2005-09-20 15:44 -- John Hawks

National Geographic online is running a news story describing a new study of Neandertal dental development. The study is by Debbie Guatelli-Steinberg and collaborators and is supposed to be in PNAS early edition, but it isn't yet. When it gets there I'll post again. In the meantime:

The question of whether Neandertals, who died out some 35,000 years ago, shared the prolonged childhoods found in modern humans is a controversial one.

Other researchers who studied Neandertal tooth remains reported in 2004 that Neandertals became sexually mature adults by as young as 15 years of age (see "Neandertals Were Fully Developed by Age 15, Experts Say"). The 2004 study found Neandertal wisdom teeth grew 15 percent faster than those of modern humans.

Guatelli-Steinberg, though, says the earlier study did not take into account how variable modern populations are in their dental growth -- a criticism that was also raised at the time of the 2004 study's publication.

"We examined a much broader range of modern humans, from three different regions of the world," the anthropologist added. "When we did this we found that Neandertal [front teeth] formation spans are comparable to those of modern humans."

Personally, I think we have a long way to go in understanding the variation in growth rates in living people, before we can infer that Neandertals are very different from us in the sequence and timing of growth. That seems like it's going to be the conclusion of this work, so that sounds about right to me. This doesn't tell the whole story of Neandertal development, but it does help to establish a timeline. And teeth have a much bigger sample than the kinds of artificial growth-series of crania (from different times and places) that we are starting to see.

Intelligence in the age of the internet

Mon, 2005-09-19 21:45 -- John Hawks

CNET is running a series of articles on the kind of intelligence required for the world of changing technology. The first installment starts thusly:

Today, terabytes of easily accessed data, always-on Internet connectivity, and lightning-fast search engines are profoundly changing the way people gather information. But the age-old question remains: Is technology making us smarter? Or are we lazily reliant on computers, and, well, dumber than we used to be?

The article's answer is that different skills don't mean different reasoning and learning. Not unexpected, since business' focus in the wake of technological change is always training and retraining the same minds for different skillsets.

The main idea is how memory is less necessary when you have devices to keep track of things for you. I suppose if Sherlock Holmes' theory of mind is right, that means we should be able to fill up our minds with deeper thoughts:

"It's true we don't remember anything anymore, but we don't need to," said [Jeff] Hawkins, the co-founder of Palm Computing and author of a book called "On Intelligence."

"We might one day sit around and reminisce about having to remember phone numbers, but it's not a bad thing. It frees us up to think about other things. The brain has a limited capacity, if you give it high-level tools, it will work on high-level problems," he said.

Of course, this presupposes that the brain isn't full of cognitive adaptations that now lie fallow and useless in today's high-tech world. Or get filled with videogames and movies. I guess these fall under the Everything Bad Is Good for You theory.

I wonder what you would call a specialized cognitive adaptation that could be readily reprogrammed in different cultures for different purposes?

Mitochondrial DNA and "performance enhancement"

Mon, 2005-09-19 09:40 -- John Hawks

One of the articles by Douglas Wallace referenced in the previous post covering mtDNA selection is subtitled "On the road to therapeutics and performance enhancement."

One theme of the review article is the adaptive value of mtDNA variants to different human populations. He discusses in some detail the role of some of this variation in high latitude populations as a possible cold adaptation, with variants that decrease ATP production, but generate more heat as a side effect. These same variants are associated with greater longevity, less degenerative disease, but more disorders of energy metabolism.

But Wallace doesn't say a single word about the obvious inverse of these observations: if some populations have high-frequency variants that decrease ATP production, doesn't it follow that the other populations have variants that don't decrease it?

True to its subtitle, the paper does include a section on "performance enhancement". It is a short section, which includes a conclusory paragraph for the paper as a whole, but here are the two relevant paragraphs:

It is now clear that not all mtDNA variation is deleterious. Indeed, about 25% of all ancient mtDNA variation appears to have caused functional mitochondrial changes and thus been adaptive. Those mtDNA variants that are adapted to warm climates have mtDNA variants that result in tightly coupled OXPHOS, thus maximizing ATP output and minimizing heat production. The presence of these mtDNAs permits maximum muscle performance but also predispose sedentary individuals that consume excess calories to multiple problems. They would be prone to be overweight and their mitochondria would generate excessive ROS, thus making them susceptile to a variety of degenerative diseases, cancer and premature aging. Partially uncoupled mitochondria generate more heat, but at the expense of ATP production. Individual's with these variants are better able to tolerate the cold, and are less prone to obesity. They also generate less ROS making then resistant to degenerative diseases and aging. Finally, the mitochondria are why we breathe. Hence, mitochondrial variation might be an important factor in individual predisposition to altitude sickness.

All of these factors and numerous others are areas that influence our daily lives. Consequently, some individuals may wish to change their energetic phenotype by changing their mtDNA genotype. If some people will undergo surgery to change their appearance, there will certainly be some who will submit to mtDNA alterations to change their life style, appearance, and physical performance. For example, changing a single mtDNA nucleotide of a high performance athlete to increase mitochondrial ATP production through altered OXPHOS coupling could increase performance by several percent and mean the difference between Olympic immortality versus obscurity. Since such a change would be undetectable by any reasonable standard screening procedure. Why wouldn't a competitive athlete take advantage of such an opportunity?

So Wallace tells us that there are population differences in mtDNA metabolism, that some variants common at low latitudes have higher ATP production than others, and that genetic engineering an individual to have one of these high-ATP producing mtDNA types might be a form of performance enhancement.

Am I the only one who senses something missing here? Is Wallace saying that the "difference between Olympic immortality versus obscurity" is already a result of mtDNA metabolic differences?

If Wallace is really saying that these low-latitude mtDNA variants may "increase performance by several percent", then isn't that the most explosive aspect of his paper?

And while I'm at it, why should it be that low-latitude populations have high-ATP-producing variants? As far as I can tell, it's a total mystery that isn't addressed in the least.

References:

Wallace DC. 2005a. The mitochondrial genome in human adaptive radiation and disease: On the road to therapeutics and performance enhancement. Gene 354:169-180. Full text (subscription)

Mitochondrial DNA adaptations in living human populations

Sun, 2005-09-18 16:15 -- John Hawks

I had read this paper by Ruiz-Pesini et al. (2004) before, but the particular combination of factors it suggests came together for me in a new way recently:

Effects of Purifying and Adaptive Selection on Regional Variation in Human mtDNA

A phylogenetic analysis of 1125 global human mitochondrial DNA (mtDNA) sequences permitted positioning of all nucleotide substitutions according to their order of occurrence. The relative frequency and amino acid conservation of internal branch replacement mutations was found to increase from tropical Africa to temperate Europe and arctic northeastern Siberia. Particularly highly conserved amino acid substitutions were found at the roots of multiple mtDNA lineages from higher latitudes. These same lineages correlate with increased propensity for energy deficiency diseases as well as longevity. Thus, specific mtDNA replacement mutations permitted our ancestors to adapt to more northern climates, and these same variants are influencing our health today.

Here are the final two paragraphs of the paper:

This combination of the increased predilection to energy deficiency diseases, but protection from neurodegenerative diseases and aging is consistent with the expectations for mtDNA coupling efficiency mutations. Uncoupling mutations would reduce ATP production, increasing the probability of energetic failure. However, they would also decrease mitochondrial ROS production by increasing the oxidation of the electron transport chain, thus reducing oxidative damage and apoptosis. This could decrease neuronal and other cell loss, thus increasing longevity.

Our observations support the hypothesis that certain ancient mtDNA variants permitted humans to adapt to colder climates, resulting in the regional enrichment of specific mtDNA lineages (haplogroups). Today these same variants result in differences in energy metabolism and altered mitochondrial oxidative damage, thus affecting health and longevity. Therefore, to understand individual predisposition to modern diseases, we must also understand our genetic past, the goal of the new discipline of evolutionary medicine (Ruiz-Pesini et al. 2004:226).

So in other words, populations in northern latitudes today are enriched for a number of mtDNA haplogroups that are likely adaptive to cold. Today, these haplogroups (as a class) are largely protective against degenerative diseases of aging, possibly because they reduce oxygen free radical production. But they are also more susceptible to disorders of energy metabolism, because they reduce ATP production.

Needless to say, this says some interesting things about the relationship of longevity and energy metabolism in recent human populations.

But at the moment, I'm thinking about Neandertals. They lived in a cold place, but their lifestyle suggests that energy metabolism was at a premium. At the same time, they had a much shorter maximum lifespan than living people. According to the model of mtDNA mutations outlined by Ruiz-Pesini et al. (2004), this would be a very odd combination: cold adaptation today is linked to longevity and lower energy metabolism; Neandertals required high metabolism but had lower longevity.

Those functional considerations alone suggest that Neandertals needed a highly specialized mtDNA type that would have been unlike those of living people.

But additionally, the increase in longevity and difference in lifestyle apparent in later Upper Paleolithic people gives a clear reason for the replacement of the Neandertal mtDNA type. These people lived longer, and they had markedly less energy expenditure than Neandertals did. Their dietary and cultural adaptations would have been much more similar to recent arctic peoples (and indeed, might well have been completely identical to the ancestors of recent arctic peoples).

Would this have been an exceptional event? I don't really think so, because Ruiz-Pesini et al. (2004) outline how similar cold-adaptive mutations occurred in different macrohaplogroups that today are all present at higher latitudes. The occurrence of potentially adaptive mtDNA mutations appears to have been quite a common event throughout human prehistory, because today's haplogroups appear to be separated by many mutations that are adaptive in different contexts.

The situation is reviewed in two papers by Douglas C. Wallace (2005a, 2005b). The thing that surprised me about these two reviews is that they embrace a positive selection hypothesis for mtDNA migration out of Africa. Consider:

This mtDNA history is remarkable for the striking discontinuities that exist in mtDNA diversity between climatic zones. Of the extensive mtDNA variation present in Africa only two mtDNA lineages (M and N) succeeded in colonizing all of Eurasia. Of the plethora of Asian mtDNA types that subsequently accumulated, only three haplogroups (A, C, and D) and much later G came to occupy the extreme northeastern Chukotka Peninsula of Siberia. This strikingly correlation between mtDNA lineages and latitude and climate led to the hypothesis that mutations in certain mtDNAs that decreased the coupling efficiency increased mitochondrial heat production and permitted people to survive the cold of the more northern latitudes (Ruiz-Pesini et al., 2004) (Wallace 2005a:173).

This passage is followed by a section to support it, of which I find several parts very suggestive (my emphasis):

This hypothesis is supported by the fact that missense mutations in mtDNA protein genes show regional specificity. Missense mutations are prevalent in the ATP6 gene in the arctic, in the cytb gene in Europe, and in the COI gene in Africa. Mutations in different ND genes also show regional correlation (Mishmar et al., 2003). Moreover, many of the ancient missense mutations change amino acids that are as highly evolutionarily conserved as are most known pathogenic mutations, yet have been retained in the human population for tens of thousands of years. Hence, they could not be pathogenic in the environment in which they reside, but rather must be adaptive and thus beneficial. Furthermore, an analysis of the missense mutations in cytb of complex III, for which the crystal structure is known, revealed that many of these missense mutations affected CoQ binding sites which would alter the Q-cycle, proton pumping, and thus OXPHOS coupling (Ruiz-Pesini et al., 2004).

Finally, when European mtDNA haplogroups were correlated with longevity and predisposition to Alzheimer Disease (AD) and Parkinson Disease (PD), it was found that mtDNAs harboring uncoupling variants were enriched in the elderly and deficient in AD and PD patients. This led to the conclusion that the uncoupling mutations must enhance the flow of electrons through the ETC keeping the ETC carriers oxidized. This, in turn, reduces the spurious transfer of electrons to O2 thus minimizing ROS production and reducing mitochondrial and cellular damage.

These same uncoupling mutations would also reduce the efficiency of ATP generation which could then exacerbate ATP deficiencies resulting from milder mtDNA mutations. This could account for the predilection of patients with Leber's Hereditary Optic Neuropathy (LHON) that harbor the milder mtDNA mutations to also have haplogroup J mtDNAs which harbor either the np 14798 or np 15257 cytb missense mutations. Thus ancient adaptive mtDNA variants are affecting individual predisposition to degenerative diseases and aging today.

This last one also would apply to milder slightly deleterious mutations of nuclear genomic loci that contribute to mitochondrial metabolism. One might even conclude that today's mitochondrial degenerative disorders may in part be a legacy of ancient adaptive mtDNA variants that no longer exist.

Now, if we seriously accept the hypothesis that human mtDNA variation is regionally adaptive, then we have to conclude that a lot of literature that assumes mtDNA neutrality is just wrong. For example:

  1. If mtDNA is neutral, then the dates of mtDNA lineage divergences may tell us about the initial migrations of some human populations. If mtDNA is adaptive to different regions, then the dates of lineage divergences tell us about the times that adaptive mutations occurred.
  2. If mtDNA is neutral, then it is surprising that archaic mtDNA variants are gone. If mtDNA is selected, then this is not at all surprising: the current global mtDNA variation is simply the product of the last globally adaptive mutation.
  3. If mtDNA is neutral, then it is reasonable to explain the lack of ancestral haplogroup L outside of Africa as the consequence of an out-of-Africa population bottleneck. But if mtDNA is selected, this distribution is explained as Wallace (2005b:376) suggests: many mtDNA lineages may have entered Eurasia, but only a few survived local selection.

Is it possible that there have been no globally adaptive mutations? If the present pattern of variation is fine-tuned to climate and diet, it seems very unlikely that the massive life history, brain, and energetic changes during Pleistocene human evolution had no effect whatsoever.

The present distribution of adaptive mtDNA variants suggests a scenario for the replacement of Neandertal mtDNA. Variants of human mtDNA that appear to be adaptive in Eurasia, and particularly in the northern parts of Eurasia, evolved recently upon an African background. The present variation of human mtDNA is comparatively recent, but it is ancient enough that some of today's variants were segregating within Africa over 100,000 years ago, and the haplogroup M dispersal from Africa appears to have occurred between 60 and 70 thousand years ago. Ultimately these gave rise to European haplogroups H, T, U, V, W, X, I, J, and K (Wallace 2005b), in the time period between 50,000 and 9,000 years ago.

We know that these variants were superior to indigenous European mtDNA variants because the Neandertal mtDNA is gone today. Yet, we must suspect that the Neandertal mtDNA would have been very well adapted to their cold climate and high energetic requirements. The advantages of the incoming African-derived mtDNA variants were great, but they would not have been free of disadvantages -- especially with respect to either cold (which has historically restricted non-European mtDNA haplogroups to the south) or energy metabolism (which currently restricts European mtDNA haplogroups to the north).

Thus, the replacement of Neandertal mtDNA could occur only upon the abandonment of Neandertal lifeways. Only a reduction in energy expenditure and exposure to cold could allow the spread of the African-derived mtDNA variants. Both these changes could be accomplished by a cultural transition, which additionally could increase dietary supply and thereby change selective constraints on energy efficiency.

In this context, it is very significant that the latest Neandertals adopted Upper Paleolithic tool industries and other cultural elements usually associated with modern humans. This cultural transition may have decreased the selective advantages of endogenous European mtDNA variants and allowed the substitution of newer European variants of African derivation. In other words, it may have been the very process of adopting new cultural and demographic patterns that resulted in the selection against old Neandertal mtDNA, even within the European Neandertal population.

So far, I have said nothing of what benefit the African-derived mtDNA variants may have provided. It seems likely that it was not related to cold (considering the Neandertals had plenty of time to become cold-adapted), energy (considering that the Neandertals appear to have had higher total energy expenditure than later people), or diet (since Upper Paleolithic people had broadly similar (if slightly different) diets to Neandertals).

Instead, I would propose that the advantage of the African-derived mtDNA variants was in the one area (out of mtDNA-associated factors) where Neandertals and later humans significantly differ: longevity. It is not at all obvious that living longer is a better adaptation for humans as compared to the shorter lifespan of Neandertals. As a very recent adaptive change, it may have required fairly exceptional demographic conditions, such as large population sizes, a reliance on extensive trade networks, or other behavioral attributes of recent people. Only in such a cultural context can the survival of older individuals provide a fitness advantage to their younger kin.

I do not think that the mtDNA change was the most important one; it probably followed many other genomic changes in favor of longevity. This would be similar to the effect of mtDNA variants in the face of climate or dietary differences today: no population was likely restricted from inhabiting the arctic by the lack of favorable mtDNA variants, but the fast mutation rate of mtDNA ensured that populations living in the arctic quickly gained new adaptive variants for their cold climates. Likewise, other genetic changes that led to a longer lifespan would quickly have led to mtDNA variants adaptive to the new demographic reality. The global human mtDNA variability likely reflects such trailing adaptive mutations. This might imply that the transition to greater longevity or other aspects of modern human life history would have been accompanied by not one, but multiple adaptive sweeps of global mtDNA variation.

References:

Ruiz-Pesini E, Mishmar D, Brandon M, Procaccio V, Wallace DC. 2004. Effects of purifying and adaptive selection on regional variation in human mtDNA. Science 303:223-226. Full text (subscription)

Wallace DC. 2005a. The mitochondrial genome in human adaptive radiation and disease: On the road to therapeutics and performance enhancement. Gene 354:169-180. Full text (subscription)

Wallace DC. 2005b. A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: a dawn for evolutionary medicine. Annu Rev Genet (Online before print)

French team studies Narmada fossil

Sat, 2005-09-17 15:40 -- John Hawks

These days it's increasingly easy to keep track of what everybody else is doing. Consider this, from newKerala.com:

A French paleontology team is currently in Kolkata to study the only homo erectus skull found in India to find new insights into the over half million year old fossil, which has baffled Indian scientists for over 21 years.

The team joined by their Indian counterparts took a CT scan of the skull here, where it has been housed since it was first discovered by geologist Arun Sonakia in the village of Hathnora, near Bhopal in Madhya Pradesh in December 1982.

The scientists hope the CT scan data will allow then to complete the severely damaged and delicate skull by using advanced compute [sic] simulation.

Having gotten valuable insights into brain formation and structures like inner ear and sinuses, scientists could even be able to make complete 3D image of the specimen, which initially was mistaken for years as of a man known as the "Narmada Man".

...

"It is interesting for us and we want to compare it with discoveries of the same species in Europe ...we have discovered items during our excavations and we want to compare with fossil discovered in China, in Java and some fossil in Africa also," said Madam De Lumley, who is leading the French team.

This should make for some interesting work. It would be exciting if the EU starts putting some of this data on The Neanderthal Tools!

Flores interviews on NOVA scienceNOW

Fri, 2005-09-16 11:49 -- John Hawks

I hadn't run across it before, but PBS ran a segment on the Liang Bua fossils in April. There is a webpage where you can watch the TV segment. You can also "compare the brains" (warning: requires QuickTime).

Whose opinion do we want?

The PBS site has a question-and-answer session between viewers who submitted questions and Bert Roberts, one of the discovery team. The segment also has clips of interviews with Ralph Holloway and Teuku Jacob, for which PBS does not provide full text.

And, guess who else they brought in to talk about the discovery?

Jared Diamond.

Now, if you're a regular reader you may think I'm a Diamond-hater, but it's not true. I really like Jared Diamond. I used to think he was the best science writer, and this was back when I got Discover as a kid. So I grew up with Jared Diamond. It's just lately -- when he started writing about social anthropology and archaeology -- that I started having some doubts (here, here, and here).

Consider this quote from the transcript of the scienceNOW segment:

JARED DIAMOND: My bet is we did not have sex with them. And here's my reasoning. I would have predicted that they would have been really nasty, just like any humans would be really nasty.

Huh?

I honestly don't know what to make of that. From the context, it would appear that Diamond actually thinks they would have been hostile toward each other, but even that doesn't make any sense in the context of human history: being nasty has rarely stopped anyone from "doing the nasty".

Anybody can make wacky assumptions based on their own perception of reality about what early hominids were like. We all "know" about people, after all. But few of us actually stop to think about the difference between "human nature" and the "nature" of people we know. Diamond is one of those who (it seems) ought to know better.

Interestingly, the host Robert Krulwich, is really good at catching Diamond in contradictions. Like this one:

Krulwich: ... What do [Komodo dragons] weigh?

Diamond: Up to 500 pounds. But it's worse than that because while the modern Komodo dragons weigh up to 500 pounds, the archeological excavations that produced the dwarves also produced evidence of a super-size Komodo dragon.

Krulwich: Oh, so these dragons are getting smaller, too, over time?

Diamond: No, the dragons are different. Warm-blooded animals shrink on islands. Cold-blooded animals often expand on islands, to fill the niche left by lions and tigers that could not get out there. Cold-blooded animals have lower food requirements, and so a cold-blooded animal requires as much food as a warm-blooded animal one-seventh of its size.

Krulwich: Oh! So while the mammals are going down, the reptiles could be going up?

Diamond: It happened there on Flores. Flores has the Komodo dragon, the world's biggest lizard today. But in the past apparently it had a super Komodo dragon.

So, you're saying the dragons did get smaller over time? Now, of course there were bigger lizards on Flores in the past, and they might be gone because humans are now there. No problem, although they apparently lived alongside some hominids for 800,000 years without too many problems. I'm just not sure this is the best example to use for your "cold-blooded giant, warm-blooded dwarf" theory.

Could it be that you're trying to shoehorn all these species into a universal rule that they don't -- in this particular case -- fit very well? You could see why someone would be confused.

Travellers' tales

Has anybody else noticed the problem with the artist's conception? You know, the one with a grizzled-looking hobbit with the giant rat slung over his shoulder?

Flores artist's conception, alongside scienceNOW host Robert Krulwich and a pygmy (from PBS website)

Yes, you guessed it -- the fossil skeleton LB1 is a woman, but the reconstruction is clearly not a woman. If the shrunken and tactfully figleafed version above doesn't convince you, you can see a bigger version here.

Now, this wouldn't be such a bad thing by itself; I mean, if this really was an ancient human species, then there must have been men.

But we have no reason to think that the men were necessarily the same size as the women, so presenting a female skeleton in a male reconstruction is clearly misleading about the biology of this "species". And why not show a woman? Because they wouldn't have carried a spear with a giant rodent slung over their shoulder? What does that say about our assumptions about this "radically different" hominid species?

The answer is clear: presenting a very tiny man instead of a woman exaggerates the differences between them and us.

It's not just the artist's conception, or the 500-pound super-Komodos: everything about the presentation of this discovery has been tilted to emphasize how strange and nonhuman (perhaps even subhuman) it is.

Remember medieval travellers' tales? They featured things like the "barnacle goose", which was supposed to hatch from barnacles in trees. And people with no heads and faces on their chests. And furry ape-men.

Now some of these things turned out to have been based -- however distantly -- on fact, like giraffes and chimpanzees. But the myth and the reality were hopelessly tangled up.

That is already happening with these "hobbits." Of course, there are the obvious mythological elements -- such as the ebu gogo myth. But there are plenty of other exaggerations: in the transcript of the NOVA scienceNOW segment, every fantasy aspect is emphasized and exaggerated, from the very introduction:

ROBERT KRULWICH: You're not going to believe this, and I wouldn't blame you, 'cause if I told you this story that..."once upon a time, on a little island, somewhere way off in the sea, there lived a race of teeny people not known to science. They lived with elephants the size of ponies. They hunted dragons that spat poisonous saliva laced with botulism and anthrax..."

You'd say, "Come on."

Yes, in fact I would. Especially when we hear things like this:

ROBERT KRULWICH: And if that's true, brain scientists would have a whole new model for human intelligence, and that's huge.

A WHOLE NEW MODEL FOR INTELLIGENCE! INCREDIBLE!

KIRA WESTAWAY: The fact that it came out at 18,000 was pretty much a shock to everybody.

ROBERT KRULWICH: A shock because that means that these little people were alive during, well, modern times.

MICHAEL JOHN MORWOOD: We know that modern humans have been in that area for at least 50,000 years.

ROBERT KRULWICH: So, if you do the math, little people and big people shared this island for over 30,000 years!

THEY SHARED THE ISLAND FOR 30,000 YEARS! INCREDIBLE!

JARED DIAMOND: It's spit that contains botulism bacteria and anthrax and other things you wouldn't want to get infected by, really nasty bacteria.

BOTULISM AND ANTHRAX AND, um, OTHER THINGS, OH MY!

Please don't misunderstand my sarcasm. If the "hobbits" are really a new species, then they really are very unusual. If they actually had an advanced stone tool technology, and actually hunted down stegodon and Komodo dragons, that is pretty neat.

But we're a ways from actually deciding that these things are true.

For one thing, all these "stunning" facts are self-contradictory. If modern humans and "hobbits" shared Flores for 30,000 years, then isn't it parsimonious to assume that modern humans made the "advanced" tools and hunted down the stegodons? Evidence of these "advanced" tools at 80,000 years ago (which we don't, by the way, have) wouldn't even disprove this proposition, since there could easily have been modern humans on Flores that early.

I give credit to Diamond for figuring this contradiction out:

But on top of that, people talk about possible coexistence between the micropygmies and modern sapiens for 40,000 years. I don't believe it. My guess is that within 100 years of modern sapiens arriving on the island, the dwarves would have been exterminated.

But that creates a different problem: how did humans make it to New Ireland and Bougainville by 30,000 years ago, and Australia by 50,000 years ago, without managing to step on Flores on their way?

For another, all the speculation about the size and organization of the brain assumes that all hobbit brains were the same. Perhaps it's true, but assuming it is clearly building a big story on an insufficiency of data.

And this isn't even considering the possibility that the specimen is pathological. As you'll remember, my view of the bones persuaded me that they aren't normal. Now, I'm not working on the skeleton myself and I am quite willing to admit that I could be wrong. But there's a lot of hand-waving in these stories.

The million-dollar question

Aside from the clip from Teuku Jacob, the segment doesn't really address the question of pathology. There is some reason to think this is by design.

Consider: the interview with Diamond says this:

Krulwich: Which leaves us with this other question of, when scientists have now begun looking at endocasts of these brains, they say--well, at least this fellow Ralph [Holloway, an anthropologist at Columbia University] who we talked to -- he says, well, they don't look the same as human brains. There could be two reasons for that. They could be sick human brains, in which case they would look like sick human brains, or they could be something different.

This would make it look like they asked Holloway about pathology, and he said it might be or it might not be, which I think was his view in April when this aired. But the televised segment does not feature any actual quotes from Holloway about whether there might be pathology.

Then, there is the "Ask the Expert" section with Bert Roberts. Out of 22 questions, not a single one relates to pathology in any way.

The most about pathology they allowed to slip into the public domain is this quote from Jared Diamond's interview:

Diamond: Well, I would bet $10, or 10 to one odds, that they were a separate species and not some deformed, microcephalic [that is, having an abnormally small head] modern humans.

Krulwich: Why? Because you want it? Because it's a great tale? Or because there's just something in you that says, yeah, the data will deliver?

Diamond: The data already out there -- well, the skull does not resemble that of known microcephalics. They've got eight different specimens, or fragments of eight different specimens. The recent information on the brain indicates a very distinctive form of brain. The whole form of the skull is erectus-like, and it's not pathological-sapiens-like. So everything says yes erectus and no, not a weird sapiens.

The thing that concerns me most about the segment is that they clearly had a choice. They could have reported on the controversy over the pathology. I can understand why they might not do that: the people who think that the specimen is pathological haven't yet published their results; their claims haven't been evaluated by other scientists, etc.

But what they chose to do, instead of giving Jacob (or someone else, like Maciej Henneberg) a chance to present their view of the discovery, they chose to interview a prominent American science writer to contextualize it.

That's a reasonable choice for their likely viewers, but it has two unfortunate side effects. First, it removes everything from the evidence, because Diamond hasn't seen it, and would be unqualified to comment on it if he had seen it (hence, the silly comments about the brain).

Second, it raises the issue of exactly what PBS wants here: do they want to discuss the science, or to sensationalize it?

Because among all the people interviewed for the segment, Jacob is the only biologist who has actually seen the bones! He might be completely wrong, but at least we can presume he knows more about this than Jared Diamond does! Yet this is the full extent of Jacob's remarks presented in the segment:

ROBERT KRULWICH: "Wait a second," said this well-respected Indonesian anthropologist. Teuko Jacob says, "I think she's one of us, our species, but with a rare disease."

TEUKO JACOB (Gadjah Mada University): Therefore there's a small brain, microencephaly.

ROBERT KRULWICH: Microencephaly can severely retard growth in modern people. So she's one of us with a growth disease?

TEUKO JACOB: I'm sure about it.

ROBERT KRULWICH: "Well, you're wrong," said the Australian team.

Oh, well then. Sorry for asking.

Now, I don't expect anyone to believe what I say or anyone else says about these fossils; you should read the science yourself, and read everything skeptically, no matter what the source. I'm not out there saying why I think the bones might be pathology; it's not my research.

But it seems to me that these fossils are being interpreted in a way that enhances a narrative instead of in a skeptical light. And that doesn't seem right to me; I don't think it advances our understanding of anything. Especially since following the narrative generates internal contradictions.

We're impoverished in the U.S. for televised science programming, and PBS is about as serious as it gets (which isn't saying much). So seeing this makes me concerned.

Acne and anthropology

Thu, 2005-09-15 12:15 -- John Hawks

The Freakonomics guys have a blog, and this week they are having guest posts from Seth Roberts, who has developed a new diet through self-experimentation. Usually I don't go for that kind of thing (and I don't endorse any diet), but he has an interesting anecdote today about science, acne, and experiment.

I point to it because it refers to biological anthropologists as the kind of scientists who are more "with it" than medical researchers:

A few months ago I saw a dermatologist about a different problem. I couldn't resist: What causes acne? I asked. Well, not diet, he said. I knew this was false. And, really, how could you say such a thing without testing hundreds of different diets -- at least? Which no one had. Several years ago I asked my friend Katharine Milton, a Berkeley anthropologist, whether the indigenous people she studies have acne. No, she said, unless they eat foreign food. The anthropologist was right, the doctor was wrong. The situation reminded me of something in an NIH-sponsored online medical encyclopedia: dental malocculsion, it said, "is most often hereditary." Whereas the work of Robert Corruccini, a professor of anthropology at Southern Illinois University, such as this, had convinced me that dental malocculsion is due to soft food.

I like to point out when we shine.

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Comparing astronomy to paleoanthropology

Wed, 2005-09-14 23:42 -- John Hawks

Both sciences study rare events that happened a long time ago. Both require interpretations of process, and rely on comparisons between different observed cases -- stars, supernovae, and the like for astronomy, fossils for paleoanthropology.

It would seem that observing astronomical objects and events ought to be freer -- anyone with a telescope can look up and see them, right? But of course, the very distant, very rare, and therefore very interesting events can't be observed with just any telescope; they require special instrumentation, fixed investment in large telescopes and processing computers, and arrangements to share time between different projects on said instruments.

It's sort of the same with humans lately. Anyone can sequence a gene these days, so evidence for human evolution is almost free to anyone. But the very rare, and therefore very interesting, human fossils are difficult to obtain, require specialized facilities and personnel to prepare, and of course require special arrangements to share access among researchers studying them.

So there are some broad similarities. But there are also differences. The comparison occurs to me because of a story from NASA today about the detection of a recent gamma ray burst.

MOST DISTANT EXPLOSION DETECTED, SMASHES PREVIOUS RECORD

Scientists using NASA's Swift satellite and several ground-based telescopes have detected the most distant explosion yet, a gamma-ray burst from the edge of the visible universe.

This powerful burst was detected September 4. It marks the death of a massive star and the birth of a black hole. It comes from an era soon after stars and galaxies first formed, about 500 million to 1 billion years after the Big Bang.

"We designed Swift to look for faint bursts coming from the edge of the Universe," said Swift principal investigator Dr. Neil Gehrels of NASA Goddard Space Flight Center in Greenbelt, Md. "Now we've got one and it's fascinating. For the first time we can learn about individual stars from near the beginning of time. There are surely many more out there," he added.

Here's the part that interested me the most:

Swift detected the burst and relayed its coordinates within minutes to scientists around the world. Reichart's team discovered the afterglow using the Southern Observatory for Astrophysical Research (SOAR) telescope atop Cerro Pachon, Chile. Over the next several nights, the UNC team used SOAR and the Gemini South telescope, also on Cerro Pachon, to calculate a redshift of greater than 6 using a light filtering technique. A team led by Nobuyuki Kawai of the Tokyo Institute of Technology used the Subaru Observatory on Mauna Kea, Hawaii, to confirm the distance and fine-tune the redshift measurement to 6.29, using a technique called spectroscopy.

So, after detecting the furthest gamma ray burst yet known, they immediately broadcast the news to colleagues around the world to make observations from other stations, depended on the special capabilities of other teams to supplement their observations and provide independent replicates, and integrated those observations into a single picture of the astronomical event.

Paleoanthropology is also collaborative in this way. Research teams are made up of people with many different specialties, and people from outside the team may be drawn in to address special aspects of anatomy, to apply special techniques, or to independently check conclusions. The process appears less public than in astronomy, and it has a much slower response time to new discoveries and events, but then it is also much more poorly funded. Even so, not just anybody is supposed to find out about new stuff, as witnessed by the recent premature announcement of the Kuiper belt objects in the face of internet cracking attacks.

The biggest difference I see between the fields is in the dissemination of results. New results in physics, including astronomical research, are disseminated through arXiv, on which new research preprints are freely available. This system encourages early comment on new research as well as openness about what conclusions are supported by data, and which are more speculative. As an ideal, it encourages a scientific hierarchy based on ideas rather than data access. This is because its entire existence is about communicating ideas more quickly to those equipped to evaluate them.

The arXiv does not replace traditional journal publication in physical sciences; instead, journal publication remains highly important for peer review, provision of an imprimatur of quality, and status. There are suggestions that arXiv should itself begin to incorporate peer review of high-traffic articles, as a step toward ensuring the long-lasting utility of certain papers. But even lacking this, the utility of the arXiv service is clear: ideas are available for scrutiny long before they appear in journals.

Without as strong a tradition of circulating results, paleoanthropology is at a comparable disadvantage when it comes to quality of science. We have a long history of retractions. This is not necessarily bad; indeed, I would say that our research results ultimately undergo a much higher degree of scrutiny than most in the physical sciences. It is the truly exceptional gamma ray burst that gains as much attention as a new hominid fossil. But this heightened scrutiny takes years, when the basic issues might be sketched out in weeks with a faster mode of communication.

Is it only a matter of time before paleoanthropology moves in this direction? That is difficult for me to say. There is no institutional incentive at present for people to share their research. The Paleoanthropology Society has already begun making dissertations available for download -- a sort of mini-arXiv for theses, with participation voluntary. Since 2003, there has been a section of arXiv devoted to quantitative biology, the intersection between mathematical sciences and biology. This includes research devoted to populations and evolution, and I have been following the submissions for some time. So the infrastructure for such a system is not far away -- it is well within the capabilities of a single university, department, or organization.

But without the social expectation of communicating results quickly, there is really no force that can drive people to change. Graduate students are enculturated into a cult of secrecy -- sometimes the hard way as someone else steals their results or yanks their access to specimens. Entire books are published with factually wrong information because no outside professionals read them in advance.And new ideas from cranks get just as much attention as new ideas from established scientists, because the press cycle gives too little time to distinguish the two.

The lesson I draw from astronomy is that these problems are not inherent to the study of rare events, expensive analysis, or historical phenomena. They are symptoms of a social disorder.

I increasingly find that openness works. I get far more insightful peer review on what I write for free here, than on anything I have ever submitted to a journal. And it's instantaneous. I don't write scholarly review articles here, and I don't give out any research results. There's no incentive for it, and there's a positive disincentive in the likelihood of a high-ranking journal turning down previously published material. But if an incentive were available -- with credit for a tenure record -- I would start.

"Bones" debuts on Fox

Tue, 2005-09-13 20:48 -- John Hawks

Tonight was the series debut of the TV show Bones, which is a CSI-alike focused on forensic anthropology instead of just forensic science. What that means, in a nutshell, is that the bodies are too far gone for the next-of-kin to identify.

CSI has had a few forensic anthropology plotlines; this show is going to be all anthropology all the time.

Bones is based on the novels of forensic anthropologist Kathy Reichs Reich's website is a Flash wonderland with information about her novels and work in forensic anthropology. Here's her background:

From teaching FBI agents at Quantico how to detect and recover human remains, to separating and identifying commingled body parts in her Montreal lab, as a forensic anthropologist Kathy Reichs has brought her own dramatic work experience to her mesmerizing forensic thrillers. She continues to work full time for the Office of the Chief Medical Examiner in North Carolina and for the Laboratoire de Sciences Judiciaires et de Medecine Legale for the province of Quebec. She is a Professor in the Department of Sociology and Anthropology at the University of North Carolina-Charlotte. She is one of only fifty forensic anthropologists certified by the American Board of Forensic Anthropology and is on the Board of Directors of the American Academy of Forensic Sciences.

Most recently she has traveled to Rwanda to testify at the UN Tribunal on Genocide. For her work with CILHI she has identified war dead from World War II and from all over Southeast Asia - she even examined the remains from the tomb of the Unknown Soldier. How does she bear this kind of work? "You get used to it," she has said. "I don't like to see maggots. But you put on your mask and your surgical scrub and your latex gloves and you go at it."

Here's what Reichs told CNN about the difference between fictional and real forensics:

Coroner's offices and laboratories, also, are generally more gritty and less pretty than those on TV -- as are those who work in them. Forensic anthropologist Kathy Reichs, for one, said she's "never gone to a crime scene wearing pumps and pantyhose" like her onscreen "CSI" facsimiles.

I must admit, I've never worn pumps to a crime scene either. In fact, I've never been to a crime scene, and I've only worked indirectly on a couple of forensic cases. I study only bones that are beyond the maggot stage.

Nevertheless, all my students know I follow CSI pretty closely. Although Dr. Sheldon Hawkes was fairly clearly not based on me.

So, is this new show going to be any good?

The show

Skeleton found in a lake in D.C.: I suppose it's Chandra Levy.

Forensic anthropologists can find evidence of bursitis, and it may suggest physical activity. On the other hand, they generally don't do it just after pulling a skeleton out of a lake, and "tennis player" is the kind of detail that, if you found it in a missing person report, you would think it consistent. It wouldn't be the kind of thing you'd put in your lab notes -- a defense attorney could easily challenge your identification if the victim turned out to be, say, a weightlifter.

If any graduate student out there gets treated like Zack does in this show, please consider a transfer. No self-respecting scientific institution would tell students "not to talk to Ph.D.s". (OK, maybe I can think of a couple, but I would tell those students to transfer, too.) And you probably have good grounds to sue if your Ph.D. supervisor writes a novel with a fictional account of your sex life.

Great lab set -- in the middle of a giant, open greenhouse. Just the place to isolate insects in human remains -- unless of course they actually were living in one of the nearby plants. I've got to stop thinking like a defense attorney.

Very cool holographic reconstruction program, which is of course totally fake. The main value of it is to show us a facial reconstruction without taking the time to actually do one. No, there is no software that can, at the click of a button, change a facial reconstruction from one race to another. And since the tissue depth markers on the skull have to be based on a tissue depth standard for some race to start with, you can see that the point of putting them on would be to allow a single facial reconstruction assuming one race.

Generally, the characters who have mystical computer skills are the most interesting, and that will probably be true of "Angela Montenegro", also. But the computer stuff is totally made up.

Confirmed! Yes, it's the fictionalized missing intern of "that senator".

Why is the smart professional anthropologist following the FBI dude like an insecure puppy? I guess it's a way to dramatize why she is not acting like a forensic anthropologist.

Oh, well, yeah, when she pulls a judo move on a senator's aide, she's not your average forensic anthropologist. I guess she's not too worried about being suitable as an expert witness.

Now Gretchen wants to know why I don't have a glowing wall of bones. I want to know how they get them to stay in there articulated at strange angles. It does cut the need for labels on the drawers if you can see bone silhouettes on all of them.

Not too much science since the first fifteen minutes. Yes, they can find stab wounds, and cutmarks on finger bones would be consistent with fingerprint removal. Fetal ear bones? Not impossible.

"For someone who hates psychology, she sure has a lot of it." Yeah. Like "Crossing Jordan". Not exactly the kind of thing that secures your career at the "Jeffersonian" Institution.

I'm pretty sure the FBI dude ("Seeley", David Boreanaz) would have an easier time trusting the "squints" (have you ever heard a scientist called that?) if he wasn't surrounded by psycho ones.

Now she's breaking into a house. Now she shot a guy in his own house, without a warrant. Now she's getting her stalker to do first aid on the guy she shot.

I'm thinking in the real world she would be out of a posh Jeffersonian job and into a mental ward.

Would I watch it again?

Yeah, it's not bad. It could use multiple plotlines like CSI; that would make it easier to live with weird never-gonna-happen elements and would cut the need for some of the fake drama.

And I find Temperance's colleagues at the lab to be some of the most potentially interesting characters. Although the storyline for Zack looks pretty predictable. Zack, rebel from your "I'm not really a virgin, far from it," dialogue!

Aside from that, they have the best lines, too ("How many warnings did you give before you sniped them?"). Give these supporting characters something to do!

I only hope Temperance doesn't go all "Crossing Jordan". The "missing parents" are a bad, bad sign. Maybe her boss at the Jeffersonian could just put her on unpaid medical leave and we could see how Montenegro would do in her place. And it's not like Brennan's the only forensic anthropologist south of Montreal (yes, she really said that). Hmmm..."Crossing Jordan" brought in Jack Klugman, maybe "Bones" could have guest roles for Angela Lansbury as a novelist/forensic mentor.

Did I just say I wanted more Angela Lansbury on television? Yeah, but not full-on Jessica Fletcher, more like a cool almost-"Manchurian Candidate" Lansbury. You've got to imagine how tough a Ph.D. advisor would have to be to put up with self-destructive Temperance. Psychological-control abilities would be a plus.

Gretchen says Peter Falk, and yeah, that would be good too. Or he could be a villain. That would be awesome.

If they are serious about having all this tension between Seeley and Temperance, they ought to consider something more like the Bruce Willis--Cybill Shepherd relationship in "Moonlighting". Cybill could be frustrated and angry with Bruce without acting like a spoiled child. So far, Temperance is looking like a stereotypical teenager, like she was emotionally stunted when her parents went missing. Boreanaz would have much more to work with if Temperance actually acted like a smart professional instead of constantly saying she is one (complete with saying she has a "high IQ"! Who says that?).

The biggest problem with the pilot is that there were no lingering clues. CSI always has clues that they discover early in the episode that they don't resolve until the end. "Bones" had nothing -- the instant she finds something, we hear what it is and what it means. That means there is no suspense at the end. Instead, the lame action tries to make suspense (why exactly did a smart senator's aide think that burning his house down was going to help?).

Granted, the pilot has a lot of extra work introducing characters. We'll see how it looks the next few weeks. Hopefully they'll send Temperance to some kind of sensitivity training.

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Why it's good to be Zilhão

Tue, 2005-09-13 00:52 -- John Hawks

Because being at the end of the alphabet gets you the last word.

Last weekend was the new Human Revolution conference at Cambridge: "Rethinking the Human Revolution: New Behavioural & Biological Perspectives on the Origins and Dispersal of Modern Humans".

The original "Human Revolution" conference was an important moment in the development and definition of the modern human origins problem. For one of the first times, archaeologists, paleontologists, and geneticists confronted the modern human origins problem with the specter of mtDNA variation hanging over them. The meeting was held in March, 1987 at Cambridge. The papers from the conference were split into two edited volumes. The major volume from the perspective of biology is The Human Revolution: Behavioral and Biological Perspectives on the Origins of Modern Humans, edited by Paul Mellars and Chris Stringer. This volume includes 17 papers on biological change (4 genetic), and 17 on archaeology and behavior (8 theoretical, 9 regional case studies).

Some of these papers constitute the best and most accessible published statements of the authors' theoretical frameworks -- especially some that have had a more limited role in the subsequent "Neandertal-modern human" debates.

I have spoken to several of the participants in that 1987 conference, who have diverse viewpoints on the interactions and effectiveness of the conference as a whole. At the least, it can be said that the event spurred the field toward the viewpoint that modern human origins was not merely a complex problem, but an actual stumbling block to any progress in understanding the evolution of human minds (comprising culture, language, sociality, and technology). There was certainly no consensus in the field then (any more than there is today) that archaic humans were substantially or completely replaced by "modern" humans. But once that logical extreme became a possibility, the behavioral, anatomical, and genetic records could not be interpreted without reference to this phylogenetic issue. If the mode of change was replacement, there would be no sense in interpreting the evolution of Neandertals as relevant to later people. Nor could it make sense to examine the pattern of behavioral change in Africa without reference to whether that pattern led to the replacement event.

So one view is that focusing on the problem actually intensified it. But this intensification has led to productive new research in African archaeology, in genetics, and in the chronology of Late Pleistocene Europe. In all three areas, the evidence has substantially changed during the past fifteen years. The phylogenetic problem remains a stumbling block, but in a very different way.

I'm not sure you would know any of this from the current "Revolution" conference. I have received several copies (thanks, readers!) of the extended abstracts of the current conference, which were embargoed before the conference and are not to be cited without permission. But I will give some of my impressions of the composition, based on the abstracts. I apologize for not being able to do the usual cite-and-critique; what I have to offer is a fairly general overview without specifics (except in one case). I have not been successful in finding any website associated with the conference; if anyone knows of one please let me know and I'll link it.

The new "Human Revolution" conference appears to have been much less biologically-oriented than the original. By my count, only twelve papers were primarily biological in focus, and of this number only four dealt in any substantial way with fossil evidence, three were molecular (2 mtDNA, 1 Y chromosome), one was linguistic, three dealt with social evolution and the brain, and one was devoted to species concepts.

Of course, several of the papers by working archaeologists had interesting things to say about the evolution of human behavior. There were twenty-nine such papers, ranging from site reports to theoretical synopses of the origin of culture. With more talks, the archaeological side appeared to have more diversity of viewpoints -- for example Francesco d'Errico is a notable contrarian to the hypothesis that behavioral modernity had a single origin in Africa, and he was included.

On the other hand, the geographical focus of the conference increased only marginally from the earlier Human Revolution meeting. The inclusion of more work in Africa is a valued addition, and reflects the increasing focus of the field on African MSA variability. But only two papers cover the world east of the Levant, none from South Asia or China. It seems to me that if "the human revolution" is really a valid pattern, that a simple test of its validity would be a truly global comparison.

A participant would have a better impression than I do, however, and if any report to me I'll be happy to relay their views.

The genetics have a certain "fiddling while Rome burns" flavor: the three papers are attempts to further refine the chronology of the "modern human dispersal", even as evidence from the vast majority of the genome now clearly indicates a substantially different picture of modern human origins. One imagines the work of the last Ptolemaic astronomers before they heard about Kepler's ellipses.

Considering the limited program, perhaps there were not available funds to bring in more speakers on fossil humans.

But at least there was Zilhão, who with the final abstract belies much of the preceding 70 pages. He has kindly given me permission to quote his abstract (with Erik Trinkaus) here. After laying out the "lines of reasoning" underlying the "Out of Africa with Complete Replacement" model, they respond thusly:

Recent research has exposed the empirical and logical flaws that cripple these arguments:

mtDNA is but a small fraction of the total human genome; when the nuclear genome is considered (hemoglobin beta locus or, recently, the patterns of polymorphism in the RRM2P4 pseudogene), there is ample evidence of the contribution of ancient non-African, hence by definition anatomically archaic, genetic lineages to extant humanity; that extant mtDNA lineages coalesce in Africa thus probably relates to differences in the size of the Pleistocene populations of the different continents;

the level of difference in the mtDNA of Neandertals and moderns is, by Primate standards, intra-specific, not inter-specific, and extant evidence of hybridization with viable, fertile offspring between close species, and even close genus, of monkeys and baboons precludes use of taxonomic arguments to assess past population dynamics;

the absence of Neandertal lineages in the sample of the five modern humans from ca.25 ka BP whose mtDNA has reportedly been obtained is in fact consistent, depending on a number of parameters, with levels of population admixture of up to 45%, i.e., approaching panmixia;

simulation studies concluding that levels of admixture greater than 0.1% would lead to observable percentages of Neandertal mtDNA lineages in extant Europeans use unrealistic models of population interaction and in fact simply arrive at conclusions that are already contained in the premises of the model used for the simulations;

if "fully symbolic sapiens behavior" is recognized in the archeological record by artifacts or features that carry a clear, exosomatic symbolic message, such as personal ornaments, then late Neandertals exhibited fully sapiens behavior; even if resulting from long-distance diffusion, the arrival of such innovations in southwestern France many millennia before any modern humans are documented in eastern Europe carries the implication that the process operated via the exchange networks of Neandertals, i.e., that we are dealing with the spread of a concept, and that is sufficient evidence for the existence of the cognitive capabilities required for its understanding and transmission;

the marked contrast apparent in the fossil record of the late twentieth century between the "early modern" and "classical Neandertal" trait-packages, suggesting population discontinuity, was an artifact of mistaking by "early modern" specimens that, in fact, were of much later age, most from the mid/late Holocene;

all the sufficiently complete, described specimens within ca.5000 years of contact currently known and directly dated (Oase and Muierii, Romania; Mladec, Czech Republic; Lagar Velho, Portugal) feature archaic/Neandertal traits that can only be explained by admixture between modern immigrants and local autochthonous populations.

One solution to a stumbling block is to assume it doesn't exist, that people who point it out are just being obstructionists, and that no right-thinking person could seriously hold such contrarian views. That attitude allows progress of a sort -- at least in theories -- and probably makes for a more pleasant post-conference reception. This is the "holding fingers in the ears and chanting 'la, la, la'" approach.

I for one welcome the stumbling blocks. They are the ways we learn things. They are sufficient now to teach us that the "human revolution" paradigm is wrong. Whatever the mode of biological change, it was more complex than replacement. Embrace the elephant in the room.

"Daily Show" investigates evolution/creation controversy

Mon, 2005-09-12 22:31 -- John Hawks

All week long, the Daily Show with Jon Stewart is devoting its comedy to "Evolution Schmevolution".

Tonight it's a visit to Dayton, Tennessee, the site of the Scopes Trial. There was also an interview with Chris Mooney, author of The Republican War on Science.

Tomorrow they will be at the Bronx Zoo, and will interview Kurt Vonnegut (not at the same time, I assume).

So far, the evolution part is relatively minor, driving the monologue and the on-location segment. The on-location stuff I always find to be mean-spirited, myself. But the monologue made me laugh -- especially the maladapted fire-breathing godzilla giraffe.

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Diagnosing science reporting

Sun, 2005-09-11 23:36 -- John Hawks

The Guardian is running a great editorial about why (and how) science reporting is bad:

OK, here's something weird. Every week in Bad Science we either victimise some barking pseudoscientific quack, or a big science story in a national newspaper. Now, tell me, why are these two groups even being mentioned in the same breath? Why is science in the media so often pointless, simplistic, boring, or just plain wrong? Like a proper little Darwin, I've been collecting specimens, making careful observations, and now I'm ready to present my theory.

It is my hypothesis that in their choice of stories, and the way they cover them, the media create a parody of science, for their own means. They then attack this parody as if they were critiquing science. This week we take the gloves off and do some serious typing.

Science stories usually fall into three families: wacky stories, scare stories and "breakthrough" stories.

They have some apt examples from non-paleoanthropology sciences, but it is easy to think of examples of each kind in paleoanthropology as well:

  • Wacky story: Metrosexual Neandertals, anyone? Generally, most stories about Neandertals fit in this category. People just love hearing the name. That's one reason the "Neandertal tuba" made such headway -- people are just used to hearing weird things about them. Unless it's the "first ever" something (like the "first ever" evidence Neandertals and modern humans overlapped), in which case it is usually billed as a "breakthrough".
  • Scare story: These are actually more rare in paleoanthropology -- it's hard to really be afraid that Neandertals are going to come get you. But I think all those "Pleistocene bottleneck" stories really fall into this category: humans were endangered in the past, and we could be endangered again if climate catastrophe X happens, whether it is another Toba supervolcano, another ice age, global warming, megavirus, or whatever. Lots of guilt stories in this vein also, like "we killed all the mammoths, and now we're killing the elephants." Pretty much any paleoanthropology that works by analogy to the present is filling the role of a scare story.
  • Breakthrough story: How many times have you heard it: "This discovery challenges all previous theories..."? Pretty much every new discovery fits in this category. Especially if it reveals how human evolution was a bush and not a ladder. Or if someone calls it "the last nail in the coffin" of something. That's never a good sign of honesty.

In the editorial's opinion, the main problem with science reporting is that it is too dumbed down:

Why? Because papers think you won't understand the "science bit", all stories involving science must be dumbed down, leaving pieces without enough content to stimulate the only people who are actually going to read them - that is, the people who know a bit about science. Compare this with the book review section, in any newspaper. The more obscure references to Russian novelists and French philosophers you can bang in, the better writer everyone thinks you are. Nobody dumbs down the finance pages. Imagine the fuss if I tried to stick the word "biophoton" on a science page without explaining what it meant. I can tell you, it would never get past the subs or the section editor. But use it on a complementary medicine page, incorrectly, and it sails through.

The editorial also discusses the problems of questionable authority figures, poor statistical understanding, and insufficient information. But the bottom line is one with which I whole-heartedly agree:

For many months I had a good spirited row with an eminent science journalist, who kept telling me that scientists needed to face up to the fact that they had to get better at communicating to a lay audience. She is a humanities graduate. "Since you describe yourself as a science communicator," I would invariably say, to the sound of derisory laughter: "isn't that your job?" But no, for there is a popular and grand idea about, that scientific ignorance is a useful tool: if even they can understand it, they think to themselves, the reader will. What kind of a communicator does that make you?

Write more. Write better.

Metrosexual Neandertals

Sun, 2005-09-11 15:26 -- John Hawks

Paleoanthropology defines the "slow news cycle". What else can explain The Independent (UK) picking up this six-month-old story about Gary Sawyer's and Blaine Maley's Neandertal "reconstruction" (via Anne Gilbert at Palanthsci)? Perhaps it's the compelling power of the AMNH press release?

I'm drawing attention to it because it contains the first public expression I can remember of the "sensitive Neandertal" theory:

Whereas Homo sapiens was able to pursue prey over very long distances, Neanderthals appear to have been markedly less able to do so and would probably therefore have had to have been more confrontational with their potential dinners.

As a consequence, Neanderthal males were probably away from their families for shorter periods than Homo sapiens - and it is likely that family structures and relationships between males and females may well have been markedly different.

"Markedly different" meaning more cohesive, stable and caring, evidently. The headline?

Official: Neanderthal Man was not a hairy oaf but a sensitive kinda guy

Carson would be so proud.

How does a paleoanthropologist react to this news?

"The reconstruction strengthens the case for regarding Neanderthals as representing a different species with their own survival strategies compared to those of Homo sapiens," said Professor Chris Stringer, head of the Human Origins Research Programme at London's Natural History Museum.

"The work shows how different strategies resulted from and reinforced different evolutionary paths," said Professor Stringer, author of a recent book on hominid prehistory, The Complete World of Human Evolution.

Hmmm. Either, (a) we are now ready to confirm that a caring man cannot be a member of the human species, or (b) no matter what feature somebody discovers, there will be somebody else to claim it puts Neandertals on a separate evolutionary path.

Maybe it's my Neandertal genes that make me act out when I see this kind of thing.

UPDATE (9/12/05): I have an e-mail from Chris Stringer letting me know that people are getting in touch with him about the post. Please leave the poor man alone -- he was clearly commenting generally on the reconstruction and not the headline! The humor in the story is the juxtaposition!

The "dark matter" of the cell

Sun, 2005-09-11 13:34 -- John Hawks

Last week's Nature got most of the media, with its papers on the chimpanzee genome. But last week's Science was actually the more important of the two -- a full issue devoted to the decidedly less sexy, but far more significant, topic of RNA function. Moreover, the articles in the issue say they are free (I can't confirm because I have a subscription).

I've been meaning to review some of the new work on microRNA (miRNA) gene regulation for awhile. This short introductory article gives a good introduction to why this is important stuff, and extends the story beyond miRNA to other kinds of noncoding RNA (ncRNA) sequences and their possible functionality.

Small noncoding microRNAs (miRNAs) have been found in such abundance that they have been christened the "dark matter" of the cell, a view reinforced by an analysis of the small RNAs found in Arabidopsis (pp. 1567 and 1525). The role of miRNAs and of their close cousins small interfering RNAs (siRNAs) in RNA silencing is discussed by Zamore and Haley (p. 1519), and illustrated in the poster pullout in this issue and in research showing that miRNAs can repress the initiation of translation (p. 1573) and, intriguingly, can also increase mRNA abundance (p. 1577). [See also this week's online Science of Aging Knowledge Environment (SAGE KE) and Signal Transduction Knowledge Environment (STKE)]. The phrase "dark matter" could well be ascribed to noncoding RNA in general. The discovery that much of the mammalian genome is transcribed, in some places without gaps (so-called transcriptional "forests"), shines a bright light on this embarrassing plentitude: an order of magnitude more transcripts than genes (pp. 1559, 1564, and 1529). Many of these noncoding RNAs (p. 1527) are conserved across species, yet their functions (if any) are largely unknown: A cell-based screen shows one, NRON, to be a regulator of the transcription factor NFAT (p. 1570). Of course, in some cases it is the act of transcription that is the regulatory event, as in the case of the transcriptional regulation of recombination (p. 1581). Finally, even the coding and base-paring capacity of RNA can be altered--by RNA editing, in which bases in the RNA are changed on the fly. Analysis of editing enzymes (p. 1534) reveals that the cell-signaling molecule IP6 is required for their editing activity (Riddihough 2005:1507).

On the subject of "What do introns do?", John Mattick provides a short review of noncoding RNA genomics that includes this:

It is also clear that the majority of the genomes of animals is indeed transcribed (12), which suggests that these genomes are either replete with largely useless transcription or that these noncoding RNA sequences are fulfilling a wide range of unexpected functions in eukaryotic biology. These sequences include introns (Fig. 1), which account for at least 30% of the human genome but have been largely overlooked because they have been assumed to be simply degraded after splicing. However, it has been shown that many miRNAs and all known small nucleolar RNAs in animals are sourced from introns (of both protein-coding and noncoding transcripts) (13), and it is simply not known what proportion of the transcribed introns are subsequently processed into smaller functional RNAs. It is possible, and logically plausible, that these sequences are also a major source of regulatory RNAs in complex organisms (20) (Mattick 2005:1528, citations in original).

If all you've ever heard of is mRNA and tRNA, the world has changed, my friend. A lot of that junk DNA you've heard about actually does stuff. Roll it over in your mind: "the majority ... is indeed transcribed"

A perspective by Jean-Michel Claverie hits another essential point:

A few months before the publication of the first drafts of the human genome sequence (1, 2), online bids predicting the number of human protein-coding genes ranged from 30,000 to 150,000 [see (3)]. To the surprise of many (4), initial bioinformatic analyses revealed no more than 35,000 human genes, an estimate that has steadily declined to the present 25,000 genes (5). On the other hand, the largest estimates based on the number of distinct polyadenylated transcript 3'-ends identified through the single-pass sequencing of cDNA libraries (6) [i.e., expressed sequence tags (ESTs)] have not followed a diminishing trend. On the contrary, more transcripts keep being discovered, many of which do not correspond to annotated genes [e.g., (7)], in particular when using the serial analysis of gene expression (SAGE) approach (8) (Claverie 2005:1529).

Estimates of the number of genes keep decreasing, while estimates of the number of protein transcripts keep increasing! The answer? These expressed sequence tags and other transcriptional products are recognized by their poly-A end sequences (that's a chain of adenines at the end of an RNA). You may remember from molecular biology that messenger RNA has these poly-A tags. But now we know that lots of non-protein-coding RNA also shares this polyadenation. The transcription identification project covered in this Science issue identified 181,000 transcripts in mice, comprising 62 percent of the mouse genome (FANTOM 2005). Much of this amount consists of noncoding RNA, and much consists of RNA sequences that partially overlap with protein-coding genes but do not include full reading frames.

These results provide a solution to the discrepancy between the number of (protein-coding) genes and the number of transcriptsÑnoncoding polyadenylated mRNA contributes to a large fraction of the 3'-EST sequences (and SAGE tags) subsequently clustered or remaining as singletons. Indeed, the noncoding Xist mRNA is abundantly represented in all EST projects. It is thus likely that sequences of noncoding transcripts have been accumulating in EST databases and have for the most part (including singleton and antisense ESTs) been erroneously interpreted as coming from the 3'-untranslated regions of protein-coding transcripts. Noncoding transcripts originating from intergenic regions, introns, or antisense strands have probably been right before our eyes for 8 years without having been discovered!

An interesting side note is that SNP databases were started by finding variants within these ESTs (e.g. Wang et al. 1997). This may mean that today's SNPs are a witches brew of sites in coding sequences, sequences that end up in noncoding RNA transcripts, functional but nonconserved regulatory RNA, and who knows what else. I wonder whether we know anything about their functional constrants as a set.

It will be a long time before anyone figures out what all this noncoding RNA does. Here's a hint:

In contrast, the promoter regions of ncRNAs are generally more conserved than the promoters of the protein-coding mRNA, not only between human and mouse but also down in the evolutionary scale to chicken (Fig. 3, B to F), and they contain binding sites for known transcription factors (18). We conclude that the large majority of ncRNAs that we analyzed display positional conservation across species. In considering function, one might conclude that the act of transcription from the particular location is either important or a consequence of genomic structure or sequence (for example, enhancers such as that of the globin locus can act as promoters), the transcript may function through some kind of sequence-specific interaction with the DNA sequence from which it is derived, or many noncoding RNAs have other targets but are evolving rapidly (19, 20) (FANTOM 2005:1562).

And another, suggesting that widespread transcription of the antisense strand of protein-coding genes may contribute to gene regulation:

Antisense transcription (transcription from the opposite strand to a protein-coding or sense strand) has been ascribed roles in gene regulation involving degradation of the corresponding sense transcripts (RNA interference), as well as gene silencing at the chromatin level. Global transcriptome analysis provides evidence that a large proportion of the genome can produce transcripts from both strands, and that antisense transcripts commonly link neighboring "genes" in complex loci into chains of linked transcriptional units. Expression profiling reveals frequent concordant regulation of sense/antisense pairs. We present experimental evidence that perturbation of an antisense RNA can alter the expression of sense messenger RNAs, suggesting that antisense transcription contributes to control of transcriptional outputs in mammals (RIKEN 2005:1564).

There's much more in there for people willing to wade through the acronyms and jargon. It's pretty clear that that path from DNA to protein has gotten a lot more complicated in the past few years, and we're uncovering the role of non-coding sequences in the genome.

References:

Claverie J-M. 2005. Fewer genes, more noncoding RNA. Science 309:1529-1530. Full text (free)

The FANTOM Consortium. 2005. The transcriptional landscape of the mammalian genome. Science 309:1559-1563. Full text (free)

Mattick JS. 2005. The functional genomics of noncoding RNA. Science 309:1527-1528. Full text (free)

Riddihough G. 2005. In the forests of RNA dark matter. Science 309:1507. Summary

RIKEN Genome Exploration Research Group et al. 2005. Antisense transcription in the mammalian transcriptome. Science 309:1564-1566. Full text (free)

Wang DG. et al. 1997. Large-scale identification, mapping, and genotyping of single-nucleotide polymorphisms in the human genome. Science 280:1077-1082.

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Diamond's Collapse in focus

Sat, 2005-09-10 22:50 -- John Hawks

The folks at Savage Minds are still whuppin' away on Jared Diamond's Guns, Germs and Steel, in posts About Yali, On cargo and cults - and Yali's question, Diamond's argument about the haves and have-nots, Malaria in Africa and Asia, and more.

Meanwhile, Mikey Brass at the Palanthsci Yahoo group put me onto this review in Reason magazine of Diamond's new book, Collapse: How Societies Choose to Fail or Succeed. It's a refreshing review in its extremely critical voice -- although in this case from the opposite side of the spectrum from anthropology.

Inside Collapse

Before going to the review, I want to give a bit of the flavor of Collapse's thesis to show why somebody might find it problematic.

Collapse is about the "collapses" of certain ancient societies. Like Guns, Germs and Steel, it is an attempt to make sense of disparate events by tying them under a common theme. The theme in Guns, Germs and Steel is geography: some societies developed more quickly because of favorable opportunities for domestication, diffusion of knowledge, and relative lack of disease.

In Collapse, the theme is bad decision-making. Some societies, when faced with ecological threats, either failed to recognize them or failed to take effective steps to prevent them. These societies collapsed, and if we aren't extremely careful, so will ours.

I haven't read Collapse yet, but Edge provides the text of a 2003 lecture by Diamond, titled "Why do some societies make disastrous decisions?" that reads as a precis of the book. I'm citing some parts of it because it gives a good impression of why a reasonable anthropologist might find reasons to disagree with Diamond's argument -- and disagree strongly at many points.

He starts the lecture with a conceit, which actually appears to constitute a theme:

As every teacher knows, though, if you have a good group of students, education is also about students imparting knowledge to their supposed teachers and challenging their assumptions. That's an experience that I've been through in the last couple of months, when for the first time in my academic career I gave a course to undergraduates, highly motivated UCLA undergraduates, on collapses of societies.

After this, the lecture has a definite tone: What will shock (sorry, challenge the assumptions) of UCLA undergraduates the most? First, there's this:

Surely the Easter Islanders, of all people, must have realized the consequences to them of destroying their own forest. It wasn't a subtle mistake.

After a less problematic account of the U.S. Forest Service, Diamond offers this nugget of wisdom:

The Classic Lowland Maya eventually succumbed to a drought around 800 A.D. There had been previous droughts in the Maya realm, but they could not draw on that prior experience, because although the Maya had some writing, it just preserved the conquests of kings and didn't record droughts. Maya droughts recur at intervals of 208 years, so the Maya in 800 A.D., when the big drought struck, did not and could not remember the drought of A.D. 592.

Of course, this has a modern-day parallel:

We, too, tend to forget things, and so for example Americans recently behave as if they've forgotten about the 1973 Gulf oil crisis. For a year or two after the crisis they avoided gas-guzzling vehicles, then quickly they forgot that knowledge, despite their having writing.

I suppose government regulations on maize economy would have solved the Maya's problems, too. Or maybe most American's weren't catastrophically affected by the oil crisis, so have no rational reason to fear its recurrence (which, speaking as someone who just bought a $50 tank of gas, it still could be a lot worse).

After this, Diamond warns us of the "disastrous consequences of reasoning by false analogy" (no, I can't make this stuff up):

An example of a society that suffered from disastrous consequences of reasoning by false analogy was the society of Norwegian Vikings who immigrated to Iceland beginning in the year AD 871. Their familiar homeland of Norway has heavy clay soils ground up by glaciers. Those soils are sufficiently heavy that, if the vegetation covering them is cut down, they are too heavy to be blown away. Unfortunately for the Viking colonists of Iceland, Icelandic soils are as light as talcum powder. They arose not through glacial grinding, but through winds carrying light ashes blown out in volcanic eruptions. The Vikings cleared the forests over those soils in order to create pasture for their animals. Unfortunately, the ash that was light enough for the wind to blow in was light enough for the wind to blow out again when the covering vegetation had been removed. Within a few generations of the Vikings' arriving in Iceland, half of Iceland's top soil had eroded into the ocean.

I guess after that mistake, the collapse of Icelandic society was inevitable.

Emerging as the real bad guys in Diamond's account are "irrational behaviors" like religion ...

Religious values are especially deeply held and hence frequent causes of disastrous behavior. For example, much of the deforestation of Easter Island had a religious motivation, to obtain logs to transport and erect the giant stone statues that were the basis of Easter Island religious cults.

... self-identity ...

In modern times a reason why Montanans have been so reluctant to solve the obvious problems now accumulating from mining, logging, and ranching in Montana is that these three industries were formerly the pillars of the Montana economy, and that they became bound up with the pioneer spirit and with Montanan self-identity.

... and "psychological denial":

For example, consider a narrow deep river valley below a high dam, such that if the dam burst, the resulting flood of water would drown people for a long distance downstream. When attitude pollsters ask people downstream of the dam how concerned they are about the dam's bursting, it's not surprising that fear of a dam burst is lowest far downstream, and increases among residents increasingly close to the dam. Surprisingly, though, when one gets within a few miles of the dam, where fear of the dam's breaking is highest, as you then get closer to the dam the concern falls off to zero! That is, the people living immediately under the dam who are certain to be drowned in a dam burst profess unconcern. That is because of psychological denial: the only way of preserving one's sanity while living immediately under the high dam is to deny the finite possibility that it could burst.

Denial? Could it be that people who decide to live under a dam are people who don't have an irrational fear of engineering disasters? Who do you think expresses a greater fear of flying: people who fly on business every week, or people who have never flown?

Of course, the irony of much of this is completely unrecognized by Diamond. Someone who disagrees with his priorities is "irrational," guilty of "short-term thinking" and in "psychological denial."

He doesn't report at the end on the reaction of his UCLA undergraduates.

The review

The Reason review is by author Ronald Bailey, who has written recent books bullish on biotech and bearish on global warming. You can imagine he is skeptical of Diamond's story:

Jared Diamond's new book, Collapse: How Societies Choose to Fail or Succeed, is neither "superb" (The New Statesman), "incisive" (The Washington Post), "magisterial" (BusinessWeek), nor "insightful and very important" (Boston Herald). It is, instead, a telling example of how a smart man can be terribly misled by a fixation on one big idea.

On the Maya, Bailey points out a contradiction between Diamond's argument and the archaeology, which -- although I am far from a Maya archaeologist -- is what I thought, also:

When Diamond discusses the "collapse" of the Mayan civilization in Central America around 900 A.D., he hauls out the standard Malthusian explanation: "It appears to me that one strand consisted of population growth outstripping available resources: a dilemma similar to one foreseen by Thomas Malthus in 1798." This population/resource imbalance led to civilization-destroying warfare, which Diamond declares is "not surprising when one reflects that at least 5,000,000 people...were crammed into an area smaller than the state of Colorado." Before nodding your head in sage agreement with this analysis, keep in mind that Colorado itself is today crammed with 4.5 million people whose standards of living are vastly more luxurious than those of 10th-century Mayan nobles and peasants.

Anthropologist Lisa Lucero of New Mexico State University at Las Cruces told USA Today that she disagrees with Diamond's analysis of the "collapse" of the Mayan civilization: "There's no evidence for massive violence and massive disease among the classic Maya." She believes the evidence indicates that the Mayans simply moved on because of widespread drought.

On the subject of wrong archaeological insights, Benny Peiser of Liverpool John Moores University has a paper that presents a fuller story of the Easter Island "collapse". Here's part of the abstract:

According to Diamond, the people of Easter Island destroyed their forest, degraded the island's topsoil, wiped out their plants and drove their animals to extinction. As a result of this selfinflicted [sic] environmental devastation, its complex society collapsed, descending into civil war, cannibalism and self-destruction. While his theory of ecocide has become almost paradigmatic in environmental circles, a dark and gory secret hangs over the premise of Easter Island's self-destruction: an actual genocide terminated Rapa Nui's indigenous populace and its culture. Diamond, however, ignores and fails to address the true reasons behind Rapa Nui's collapse. Why has he turned the victims of cultural and physical extermination into the perpetrators of their own demise? This paper is a first attempt to address this disquieting quandary. It describes the foundation of Diamond's environmental revisionism and explains why it does not hold up to scientific scrutiny.

The paper is freely available as a PDF. Other counter-arguments to Diamond's archaeology and social anthropology will likely emerge also.

The theme of Bailey's review is that Diamond ignores the ways that greater economic diversity, political freedom, and freedom of thought make societies stronger and more resistant to collapse. As he puts it:

As ecology teaches us, the simplest ecosystems are often the most fragile. Similarly, our modern globally interconnected economy that can draw upon a wide array of resources is far more stable and robust than either the fragile pre-modern or the marginally modern societies cited by Diamond.

This contrast is marked in Diamond's comparison of "overcrowded" Haiti and the neighboring, wealthier, Dominican Republic:

This simplistic analysis doesn't stand up to scrutiny. Diamond overlooks an even more "overpopulated" island right next door, Puerto Rico. Its population density is almost twice that of Haiti, at 1,120 people per square mile. By 1900 Puerto Rico's primary forests had been reduced to 1 percent of their original extent, and in 1953 its secondary forests covered only 6 percent of the island. Today 32 percent of Puerto Rico is forested, and the island's per capita GDP is $16,800 per year.

Why is Puerto Rico so much better off than its neighbors? In a word, institutions. Diamond vaguely recognizes the importance of social and political institutions, but his analysis doesn't go much deeper than arguing that Haitian dictators have been more rapacious than Dominican dictators. In fact, the last two centuries have shown that the more a country adheres to the rule of law, protects private property, reduces bureaucratic corruption, nurtures a free press, permits free markets, engages in trade, and allows democratic politics, the less likely it is to suffer from the Malthusian horrors of plagues, famines, and civil wars. What Haiti and Rwanda have in common is not just dense populations but shattered social and political institutions. What the United Kingdom, the Netherlands, and Puerto Rico have in common are not only dense populations, but adequately effective social and political institutions.

It's a good review, that puts the critical issues at the front and cuts broadly. I especially like the passage about farmers and parasites.

No doubt there is much that is good in Diamond's book. My impression, for example, is that he does stress the importance of political representation in decision-making and other aspects of freer societies that Bailey wants more attention to.

But the parts that are bad are just wrong. The peril of false analogy is that sometimes history doesn't repeat itself, because it really is different this time. Perhaps we're not living in such a lucky time, but even if not, I doubt we need another Jeremiad based on faulty social and archaeological arguments.

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Afar by NASA

Fri, 2005-09-09 21:40 -- John Hawks

NASA's Earth Observatory has made an overhead shot of the Afar Depression its image of the day (via MetaFilter):

In eastern Africa, in the Afar region of Ethiopia, a nearly barren rockscape marks the location of the meeting place of three separate pieces of the Earth's crust. This meeting place is known to geologists as the Afar Triple Junction; the central meeting place for the three pieces of Earth's crust is around Lake Abbe, just to the south of the area shown in this image from the Advanced Spaceborne Thermal Emission and Reflection Radiometer (ASTER) on NASA's Terra satellite. The three pieces of Earth's crust are each pulling away from that central point, though not all at the same speed.

Understatement-posing-as-segue of the day: "Besides its unusual geology, the Afar region is famous for its fossils."

Brain genes evolving at the origin of Homo?

Fri, 2005-09-09 14:54 -- John Hawks

Aside from the two papers finding very recent evolution in human brain-expressed genes, there is another paper (subscription required) in this week's science that documents an older genetic change in the brain. This paper is by Toshiyuki Hayakawa and colleagues from Ajit Varki's lab.

The lab studies sialic acid metabolism; sialic acids are part of the array of sugar chains (or "glycans") that adhere to the surfaces of cells, and are involved in cell signalling, among many other things. Thus, they are important in the metabolism of the brain (they are also involved in the malarial infection pathways discussed in this earlier post).

Here's the abstract:

Recent studies have shown multiple differences between humans and apes in sialic acid (Sia) biology, including Siglecs (Sia-recognizing-Ig-superfamily lectins). Comparisons with the chimpanzee genome indicate that human SIGLEC11 emerged through human-specific gene conversion by an adjacent pseudogene. Conversion involved 5' untranslated sequences and the Sia-recognition domain. This human protein shows reduced binding relative to the ancestral form but recognizes oligosialic acids, which are enriched in the brain. SIGLEC11 is expressed in human but not in chimpanzee brain microglia. Further studies will determine if this event was related to the evolution of Homo (Hayakawa et al. 2005:1163).

SIGLEC16 is a pseudogene -- an inactive copy of a gene -- shared by humans (hSIGLEC16) and chimpanzees (cSIGLEC16). It was generated by a gene duplication of the gene SIGLEC11 in some ancient primate, ancestral to both chimpanzees and humans, and possibly other extant species.

This means that human SIGLEC11 ought to look more like chimpanzee SIGLEC11 than either looks like human (or chimpanzee) SIGLEC16 -- the two homologous genes should be more similar.

But instead, human SIGLEC11 looks more like human SIGLEC16 than it looks like chimpanzee SIGLEC11. This is a case of gene conversion -- genetic material has been exchanged from the hSIGLEC16 inactive pseudogene into functional hSIGLEC11.

The converted allele appears to be fixed in living humans, so it likely happened a long time ago (i.e. more than a few hundred thousand years). The paper suggests that it "may be related to the evolution of genus Homo" (1163). Maybe so, although that's a pretty general statement. It would be helpful to know how long ago the conversion might have happened, but that will take a lot of study of flanking sequence and may still be difficult, depending on how the conversion happened. There's no evidence that this occurred at the origin of the genus, although the loss of human Neu5Gc occurred around 3 million years ago; if this is related to that genetic change, it wouldn't be too surprising if it happened shortly thereafter.

What does the new converted gene do? The chimpanzee form of the protein binds more closely to the Sia type Neu5Gc, which is missing from humans (part of that ancient malaria defense). The human form of the protein is expressed in microglia cells in the brain, and binds to oligosialic acids in the brain.

And that's about what's in the paper, hopefully in slightly clearer language.

It's been a long time since a paleoanthropologist could write a paper with only six references!

References:

Hayakawa T, Angata T, Lewis AL, Mikkelsen TS, Varki NM, Varki A. 2005. A human-specific gene in microglia. Science 309:1163.

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Recent human brain evolution and population differences

Thu, 2005-09-08 22:49 -- John Hawks

This week's Science carries two research articles from Bruce Lahn's lab documenting recent (and potentially ongoing) genetic changes in human brains.

I say "human brains" rather than "the human brain" quite deliberately: with these alleles, some people have them, and other people don't. And more noteworthy, some populations have them, and others don't.

I've had copies of these papers for a while; the story has now gone live (Google News) so I'll share some of my comments.

The genes

The genes are two that we have seen before: ASPM and Microcephalin. Both genes were subjects of papers by Lahn's students Patrick Evans and Jeffrey Anderson last year in Human Molecular Genetics (Evans et al. 2004a; Evans et al. 2004b). Both genes underwent repeated adaptive subtitutions in the primate lineages leading to humans: these changes in Microcephalin were concentrated in the ancient hominoid ancestors of humans and chimpanzees; ASPM fixed a new adaptive substitution on average every 300,000 or so years since the human-chimpanzee common ancestor. Disease-causing alleles of both genes are associated with forms of microcephaly. The normal functions of neither have been characterized, although their effects in microcephaly would indicate that one important function is in early neural growth and differentiation. Thus, it is reasonable to think that they may have been involved in the evolution of brain size and structure in humans and other primates.

The lab's strategy has been a simple one: find brain-expressed genes and see if they have been under selection in humans and primates (see also this interview with Lahn). An elegant expression of the simplicity of the project was the paper by Dorus and colleagues from late last year (Dorus et al. 2004), which found a high rate of selection in brain-expressed genes in the human (and hominoid) lineage compared to macaques (discussed in this earlier post). The meat of the lab's work so far has been papers like the two cited above (and others such as Choi and Lahn 2003) finding out how genes have changed leading to humans and other primates.

The current papers take the next logical step: Take the genes that have changed a lot during human evolution, and see whether they vary among people today. A functional difference between alleles in different people might reflect a difference in the structure or function of their brains. Microcephalin is covered by Evans et al. (2005); ASPM by Mekel-Bobrov et al. (2005).

The team sequenced each gene in around 90 "ethnically diverse" people. For each, they found considerable variation scattered across the genes, but one haplotype that occupied a large proportion (21% and 33% respectively) of the sequence samples. In each case, the proportion was so disproportionately large compared to other variants, that the haplotype almost certainly corresponded with a recently selected allele -- one that has expanded in numbers so quickly that it has not had time to recombine very much with other alleles. Conveniently (or confusingly), both papers name the selected alleles "haplogroup D", for "derived". The haplogroup is comprised of the original selected haplotype plus the small number of variants by recombination or mutation that have happened to it since it came under selection.

Recent selection

Both genes have an allele that has been recently selected. For both genes, this allele is still segregating in human populations. This means that if the allele is positively selected (i.e. on its way to fixation), it hasn't had time to get there yet. On the other hand, if the allele is subject to some kind of balancing selection (e.g. heterozygotes have an advantage relative to homozygotes), then it may or may not be at equilibrium yet in some populations; we just don't know.

But in either case, we can estimate how long the alleles have been selected, because selection caused these alleles to greatly increase in numbers. All of the variability encompassed by variant haplotypes that share a selected site must have accumulated since that selection began. The two papers each do this calculation, with some surprising results.

Haplogroup D for Microcephalin apparently came under selection around 37,000 years ago (confidence limit from 14,000 to 60,000 years ago). This is very, very recent compared to the overall coalescence age of all the haplotypes at the locus (1.7 million years). Some populations have this allele at 100 percent, while many others are above 70 or 80 percent. Selection on the allele must therefore have been pretty strong to cause this rapid increase in frequency. If the effect of the allele is additive or dominant, this selective advantage would be on the order of 2 or 3 percent -- an advantage in reproduction.

The story for ASPM is similar, but even more extreme. Here, the selected allele came under selection only 5800 years ago (!) (confidence between 500 and 14,100 years). Its proliferation has almost entirely occurred within the bounds of recorded history. And to come to its present high proportion in some populations of near 50 percent in such a short time, its selective advantage must have been very strong indeed -- on the order of 5 to 8 percent. In other words, for every twenty children of people without the selected D haplogroup, people with a copy of the allele averaged twenty-one, or slightly more.

Nobody currently knows what these alleles may have done. It seems likely that people with the allele have some sort of cognitive advantage, which ultimately translates into a reproductive benefit. This advantage is probably not associated with greater brain sizes, because the average brain size appears not to have changed appreciably during the past 30,000 years -- if anything, in fact it has gotten smaller, although this reduction in size is probably associated with reductions in body size over the same time period (Ruff et al. 1997). Figuring this out is going to take more work assessing the phenotypic characters of people have the alleles -- how do they score on tests, for example, and is there any apparent structural difference between their brains and non-allele carriers?

Population differences

The teams took one further step: they assayed over 1000 people in populations around the world to see where the selected alleles were more or less common.

Some populations have these alleles at high frequencies; other populations have them at lower frequencies or not at all. The genes are slightly different in their pattern: for example, the Microcephalin haplogroup D is virtually universal in New World populations; the recently-selected ASPM haplogroup D is almost completely absent there. The selected ASPM variant is most common in Europe and West Asia and less so in East Asia; Microcephalin haplogroup D is common across Eurasia from west to east. These differences may reflect time -- with the ASPM variant much more recently selected. Or they may reflect different selective gradients: perhaps the alleles are adaptive in some ecological contexts or genetic backgrounds but not others.

Both selected alleles are relatively rare in subsaharan Africa. Again, one of two explanations is possible: either they are advantageous but haven't had time to increase in frequency there yet, or their adaptive value is less in Africa than in other places where they are found.

Geneticists are increasingly finding genetic variants that affect behavior. Several of these variants are now known to vary in frequency in different human populations. These alleles are two; the 7r allele of the dopamine receptor D4 (DRD4) gene is another that influences ADD/ADHD susceptibility (Harpending and Cochran 2002). The selective structure underlying DRD4 variation may be frequency-dependent, with different alleles correlating with alternative behavioral strategies that pose greater or lesser advantages in some populations. It is not clear whether such a mechanism is true of ASPM and Microcephalin; the selected alleles have risen to such high frequencies in some populations that it seems they are not mere alternatives; they are unilaterally advantageous -- at least where they have become common already.

The question is whether there is anything keeping them from spreading through Africa. Is it possible that the ecology of Africa has led to a different level of selection on these alleles? Or have they just not had time since their origin to reach very far into Africa? At any rate, it is premature to say what their effects may be within different populations, particularly until something is known about the phenotypes of people who carry the alleles.

The fallout

I'm keeping a list of quotes related to the research, as more stories appear I'll continue to add. Here's the list so far:

Francis Collins in the San Jose Mercury News (an AP article):

That the genetic changes have anything to do with brain size or intelligence "is totally unproven and potentially dangerous territory to get into with such sketchy data," stressed Dr. Francis Collins, director of the National Human Genome Research Institute.

Mark Stoneking in Science:

"The case for selection acting on [the genes] is reasonably strong," says anthropologist Mark Stoneking of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. "However, there is absolutely nothing in either paper to relate the signature of selection to any brain-related phenotype."

David Goldstein in the New York Times -- my candidate for the "not even wrong" award:

Another geneticist, David Goldstein of Duke University, said the new results were interesting but that "it is a real stretch to argue for example that microcephalin is under selection and that that selection must be related to brain size or cognitive function."

The gene could have risen to prominence through a random process known as genetic drift, Dr. Goldstein said.

I have to say, someone who seriously thinks that these alleles are drift must not believe in natural selection under any circumstances. But possibly Goldstein was misquoted, or may not have seen the papers before making this comment.

John Hawks in New Scientist:

"Whatever advantage these genes give, some groups have it and some don't. This has to be the worst nightmare for people who believe strongly there are no differences in brain function between groups," says anthropologist John Hawks of the University of Wisconsin in Madison, US.

My favorite thus far, Bruce Lahn in New Scientist:

"It could be advantageous to be dumber," Lahn says. "I highly doubt it, but it's possible."

References:

Dorus S, Vallender EJ, Evans PD, Anderson JR, Gilbert SL, Mahowald M, Wyckoff GJ, Malcom CM, Lahn BT. 2004. Accelerated evolution of nervous system genes in the origin of Homo sapiens. Cell 119:1027-1040.

Evans PD, Anderson JR, Vallender EJ, Gilbert SL, Malcom CM, Dorus S, Lahn BT. 2004a. Adaptive evolution of ASPM, a major determinant of cerebral cortical size in humans. Hum Mol Genet 13:489-494.

Evans PJ, Anderson JR, Vallender EJ, Choi SS, Lahn BT. 2004b. Reconstructing the evolutionary history of microcephalin, a gene controlling human brain size. Hum Mol Genet 13:1139-1145.

Evans PJ, Gilbert SJ, Mekel-Bobrov N, Vallender EJ, Anderson JR, Vaez-Azizi LM, Tishkoff SA, Hudson RR, Lahn BT. 2005. Microcephalin, a gene regulating brain size, continues to evolve adaptively in humans. Science 309:1717-1720. Full text (subscription required)

Harpending HC, Cochran G. 2002. In our genes. Proc Nat Acad Sci USA 99:10-12.

Mekel-Bobrov N, Gilbert SL, Evans PD, Vallender EJ, Anderson JR, Hudson RR, Tishkoff SA, Lahn BT. 2005. Ongoing adaptive evolution of ASPM, a brain size determinant in Homo sapiens. Science 309:1720-1722. Full text (subscription required)

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