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April 22, 2005



Copying Gene Expression Patterns

Method shows how precisely gene expression signals are copied in DNA replication

“A group of University of Washington researchers has devised a method that combines DNA sampling and mathematical modeling to find out how accurately methylation patterns are copied during DNA replication. That could pave the way for understanding the role methylation plays in normal gene expression and how it factors in the development of human disease.”


“Methylation typically passes from genes in a DNA strand to the same genes in a daughter strand created during DNA replication. The new technique allows researchers to examine how faithfully this "maintenance" methylation is carried out across generations and how consistently it occurs on the same gene sequence, said Brooks Miner, a UW research scientist in biology and a co-author of the paper.

But DNA molecules also can undergo what is called "de novo," or new, methylation in which a methyl group shows up on a DNA strand at a place where it did not appear before. That could change how that particular gene sequence is expressed.”

“In the past, researchers could look at only one strand of DNA at a time and so could not conduct a side-by-side comparison of where methylation was occurring. An earlier paper from the same research group, led by Charles Laird, a UW biology professor, introduced a molecular method to look at both DNA strands together and observe methylation differences between them.”

Posted by fly at 09:03 AM | | TrackBack


Williams Syndrome Brain Images

Brain imaging study explains Williams syndrome language gifts:

“Findings: A team of neuroscientists led by UCLA researchers used a novel magnetic resonance imaging (MRI) technique to create the first detailed images showing how Williams syndrome affects the cerebral cortex. The study finds sharply defined cortical thickening and complexity in the area of the brain important to language.

Impact: The isolated, thickened cortical region in language areas is remarkable because patients with Williams syndrome show marked strengths in language and related abilities. The ability to map these abnormalities in living patients demonstrates how genes control development of the human cortex, and also aids clinical prognosis and understanding of the syndrome's underlying genetic trigger.

Background: Williams Syndrome is a genetic disorder characterized by heart defects, abnormalities in the outer layer of the brain, or cerebral cortex, and mild to moderate mental retardation. In addition, people with Williams syndrome often demonstrate high proficiency in language skills, social drive and musical ability. The syndrome affects 1 in 20,000 individuals.”

Posted by fly at 08:30 AM | | TrackBack

April 21, 2005



Swedish Nazi Ice Cream Madness

Racist nazi ice cream causes uproar in Sweden! Read all about it! Pictures inside!

The Nazi ice cream from hell:

naziicecream.jpg


And the money quote:

"Soon the Ice cream giant was slammed for "racist" ads as the Center Against Racism issued a press release denouncing the new ice-cream. "*

* This is a tax-payer funded organization.

More shocking pictures inside!

Swedish Ice Cream giant GB has now yielded, and has offered up an alternative, non-offensive ice-cream:

kice.jpg

*"kokoskon" = "cocotop"

...meanwhile, critics of the Center against racism have fallen silent, as new shocking evidence is discovered in German archives:


hice.jpg


PS.

There were no Sweden-related posts on the front page - just had to be rectified.

DS

Posted by dobeln at 11:30 PM | | TrackBack

April 20, 2005



Benedict XVI & evolution

There has been some talk about the new Pope and evolutionary theory. I certainly haven't read In the Beginning...: A Catholic Understanding of the Story of Creation and the Fall, a book that is a collection of five of Ratzinger's homilies from the early 1980s, but the online references seem to suggest plain vanilla theistic evolutionism, not the fleshy hopeful monster that is Intelligent Design (you can use Amazon's "search inside" feature to read much of the text. There are some portions where Ratzinger's usage of terms, or, more properly the translation from German, resembles typical Intelligent Design cant. But, reading earlier portions of the homily in question makes me skeptical that he was speaking in a specific and precise fashion as opposed to a general assertion of the salience of Design in a Thomistic fashion. And of course, the homilies were composed over a decade before ID emerged). Nevertheless, this document, titled Human Persons Created in the Image of God has some material about evolution in it, and it states:


...The present text was approved in forma specifica, by the written ballots of the International Theological Commission. It was then submitted to Joseph Cardinal Ratzinger, the President of the Commission, who has give his permission for its publication.

Below is an interesting excision, but, I suggest you click through and skip down to paragraph 62 (they are numbered) and read the whole section "Science and the stewardship of knowledge." I don't agree with Benedict XVI on many things, but, I am also not one who dreads the possibility that somewhere out there dwell monstrous beings who not only disagree with me on important issues, but holds opinions I find highly objectionable. To be offended is to be human, to respond is only natural.

63. According to the widely accepted scientific account, the universe erupted 15 billion years ago in an explosion called the “Big Bang” and has been expanding and cooling ever since. Later there gradually emerged the conditions necessary for the formation of atoms, still later the condensation of galaxies and stars, and about 10 billion years later the formation of planets. In our own solar system and on earth (formed about 4.5 billion years ago), the conditions have been favorable to the emergence of life. While there is little consensus among scientists about how the origin of this first microscopic life is to be explained, there is general agreement among them that the first organism dwelt on this planet about 3.5-4 billion years ago. Since it has been demonstrated that all living organisms on earth are genetically related, it is virtually certain that all living organisms have descended from this first organism. Converging evidence from many studies in the physical and biological sciences furnishes mounting support for some theory of evolution to account for the development and diversification of life on earth, while controversy continues over the pace and mechanisms of evolution. While the story of human origins is complex and subject to revision, physical anthropology and molecular biology combine to make a convincing case for the origin of the human species in Africa about 150,000 years ago in a humanoid population of common genetic lineage. However it is to be explained, the decisive factor in human origins was a continually increasing brain size, culminating in that of homo sapiens. With the development of the human brain, the nature and rate of evolution were permanently altered: with the introduction of the uniquely human factors of consciousness, intentionality, freedom and creativity, biological evolution was recast as social and cultural evolution.

...

70. With respect to the immediate creation of the human soul, Catholic theology affirms that particular actions of God bring about effects that transcend the capacity of created causes acting according to their natures. The appeal to divine causality to account for genuinely causal as distinct from merely explanatory gaps does not insert divine agency to fill in the “gaps” in human scientific understanding (thus giving rise to the so-called "God of the gaps”). The structures of the world can be seen as open to non-disruptive divine action in directly causing events in the world. Catholic theology affirms that that the emergence of the first members of the human species (whether as individuals or in populations) represents an event that is not susceptible of a purely natural explanation and which can appropriately be attributed to divine intervention. Acting indirectly through causal chains operating from the beginning of cosmic history, God prepared the way for what Pope John Paul II has called “an ontological leap...the moment of transition to the spiritual.” While science can study these causal chains, it falls to theology to locate this account of the special creation of the human soul within the overarching plan of the triune God to share the communion of trinitarian life with human persons who are created out of nothing in the image and likeness of God, and who, in his name and according to his plan, exercise a creative stewardship and sovereignty over the physical universe.


Stripping away the theological verbiage much of the above commentary about human evolutionary origins in particular almost resembles a "Great Leap Forward" narrative.

Posted by razib at 08:52 PM | | TrackBack


Whole population genome analysis

Method devised for whole-population DNA analysis. Seems more like a press release by the founder of a new biotech company than anything else, but there is more at The Wellcome Trust's website. The projected company seems like it is looking to capitalize on the window of opportunity before the rise of truly personal genomics and leverage populational level differences data toward medical applications. Nevertheless, apropos of some discussions on this site, this method might have more purely intellectual relevance.

Posted by razib at 03:37 AM | | TrackBack

April 19, 2005



A golden error?

In the comment board Theresa asserted: "Another side note, lots of ethnic Norwegians have dark hair and dark eyes -- the blonde, blue-eyed folks are mainly in the inner valleys -- and over there in Sweden." I don't know if this is true, but, it did make me wonder.

My post Why evolution doesn't make sense ruminated over the difficulties that lay people have when they think about evolution. The macroevolutionary realities tend to overshadow the more operationally relevant microevolutionary details.

Let us assume that Norwegians of the inland valleys do tend to be blonder than coastal Norwegians. Why could this be?

Here are some quick answers people might come up with.

Migration-clinal admixture: In her comment Theresa alluded to the fact that Swedes tend to be blonde. When physical anthropologists had a great concern about such topics a common data point brought up was that southern Sweden represented the modal frequency of the "blue eyed blonded" "Nordic" type. In fact, some texts asserted that only in southern Sweden did the intersection of blue eyes and blonde hair characterize the majority of the population. From this it is common sense to assume that blondism decreases as a function of distance from southern Sweden.

Modern paternal and maternal DNA markers suggest that it is possible that northern Europe was "repopulated" after the Last Glacial Maximimum by disparate populations that have been driven south into "refuges." Iberia, the eastern European borderlands and the Balkans are the primary candidates for the nodes from which the demographic expansion repopulated Europe. Luigi Cavalli-Sforza's magmum opus The History and Geography of Genes prefigured the findings of the later geneticists as he transformed various principal components of variation in his data sets into rich maps that illustrated clinal transitions issuing out of the southeast, southwest and east.

The details of this model are not relevant, rather, I would like to point out physical anthropologists have observed an increase in the frequency of dark hair as one moves to the west in the British Isles, the Welsh being darker than the English and the western Irish being less blonde than the eastern Irish. All this is to flesh out the possibilities that admixture and various migrational movements (blondes from the east intermarrying with dark haired people migrating up from Iberia) might account for the local phenomenon of inland folk being blonder in Norway.

Selection: Another hypothesis is that microevolutionary selective pressures have resulted in the differences between inlanders and costal dwellers. If one opens the can of worms that is social and sexual selection the possibilities are endless, rather, I will point to the more prosaic option: coastal dwellers did not need to synthesize as much Vitamin D because they could acquire that nutrient through fish oil. Therefore, the blondeness of the highlanders is a correlated response to the selection for fair skin, which facilitates endogenous synthesis of Viatmin D.

But these aren't the only options. #1 is something that the typical person might offer without any prompting or recourse to research. The exact details of #2 are more difficult to intuit from common sense, while the various possible epicycles that sexual and social selection imply are not even on the table in conventional disource.

And yet, as the title suggests, there is another option: Random Genetic Drift might be the cause of the higher frequency blondeness among the highland population. And this "Random Genetic Drift" might not be happenstance, that is, the highland populations simply random walked into a higher frequency of the blonde phenotype, rather, it might be an inevitable consequence of particular tendencies toward population substructure.

The thought is triggered by my reading of some of Cavalli-Sforza's original work in Italy. He foud that people who lived in the mountainous regions and away from the coasts had far more constricted marital networks. They were more inbred because their operational "deme," the rough & ready breeding population, was far smaller, and not only did they share many coancestors but they were subject to greater forces of drift. In fact, the correlation between topography and the average distance of birth between the spouses was larger striking. Lowland people were aided by good roads, gentle grades as well as the supplement of water transportation. Though the lowlanders (at this time) might not have been economically that much more advanced than their highland neighbors, they were part of a much more tightly integrated wider social and populational network. The marital connections and gene flow between the lowland villages was far greater than what one found among the highland villages.

Which brings us back to Norway. Qualitatively the model can be described as thus: lowland Norway is a large deme where Random Genetic Drift has had less power because of the high effective population size. In contrast, the highland demes are rather small, and so each has been buffeted by sampling error, Random Genetic Drift, to a far greater extent than the lowlanders. A crucial point is that the swings should cancel out so that the frequencies of alleles might not differ very much between the lowland deme and "the highlands," but because of the high degree of population substructure there are many populations where alternative alleles have been fixed. This is where blondeness comes it: it is traditionally characterized as a phenotype that is expressed when the alleles are present as homozygous. So, while in the lowland deme 50% of the alleles might be for "blondeness," only about 1/4 of the population is blonde because only 1/4 is homozygous for blonde alleles. In contrast, though the highlanders as an aggregate might be characterized by the same allelic frequencies as the lowerlands, say a 50-50 split between "blonde" and "brunette" alleles, the frequency of heterozygotes where the blonde allele is masked by a brunette allele is far lower, so the number of blondes is far higher because of the rise in homozygosity due to Random Genetic Drift.

I don't know if this story is true, I don't know if the highlanders are blonder or more inbred than the lowlanders. Rather, I simply wanted to offer it as an explication of the power of simple genetic logic.

Addendum: My source for the clarification is Genetics of Populations by Philip Hedrick. I have made a few minor changes because of the limitations of HTML.

Kimur and Ohta's diffusion aproximation for a continous-time model for the mean time until fixation of allele A2 (in this case "blondeness") with an initial frequency q:

(1) - T(q) = - [4N(1-q) ln(1-q)]/q

As you can see, time until fixation is a function of population size, N, and the initial frequency. Let us assume that All-Father Odin created 200,000 Norwegians in Valhalla. Their frequency of alleles was A1 = 0.5 and A2 = 0.5. He divided them into two groups, the "lowland population" (L) and the "highland population" (H) of equal numbers, 100,000 each. Then, he settled the L group on the coasts. These villages and towns and farmsteads were connected by coastal roads and long-boats. They were functionally one population, one deme. In contrast, the H population was diffused amongst 100 valleys in equal portions, so you have H1...H100, each with an effective population of 1,000.1

Loki, trickster than he is, decides to put up walls between the L deme and all the H demes, as well as partitions between the H demes themselves. In other words, no migration. Also, Loki get's everyone drunk so that everyone mates with whoever they bump into at the local dance in a random fashion, so, no selection. Frey, feeling bad for them due to his Vanir soft heart decrees that they shall all birth perfect children, so, no mutation.

For population L, equation 1 suggests that the "mean time to fixation" for either allele will be about 280,000 generations. This doesn't mean it will necessarily take 280,000 generations, and offers no clue as to which one will really fix, but if you were All-Father Odin and turned time back and allowed the Norns to work their dice 280,000 would be the average time of fixation among the repeated iterations.

For the various H populations equation 1 suggests that fixation is going to happen on average in each population in about 2,800 generations. This makes sense, the N was 1/100th the size of L for each of them.

The probability of fixation for each allele is their initial frequency. In this case both have an equal shot, but, the substructure implies something special: after a long enough period L might fix, but "H" will likely not fix for a particular allele (it is not really one population aside from the ecological commonality), rather, each of the various H demes will fix, and the expected ratio A1 homozygotic demes to A2 homozygotic demes ratio should be 1:1.

Update: On second thought, I want to reiterate that I present the above argument for illustration's purpose primarily. If I was serious I suppose I would look to some sort of island model, but my interest in highlighting the topic was mostly to spur readers to explore the simple but often counter-intuitive concepts and algebra of population genetics. A high degree of fluency with the material requires good working knowledge of differential equations and linear algebra, but the basics are pretty accessible if you have high school algebra.

1 - Gods have perfect sampling sight, even with one eye. There isn't any "founder effect" at work here.

Posted by razib at 06:27 PM | | TrackBack


The Grand Old Man

123 years ago today, Charles Darwin died. So grip your glass with your opposable thumb and toast the man who revolutionized biology.

Heres to you, Chuck!

Posted by God Fearing Atheist at 05:20 PM | | TrackBack


Brains on Minds

Ronald Bailey, of Reason Magazine, reports on a 3-day conference with prominent neuroscientists and theologians called ”Our Minds and Us”. Concerned subjects are: Mind-brain duality, bioethics involved in understanding which structures of the brain are involved in things like violence and depression, and existential questions of "What is the self". Check it out.

Posted by scottm at 09:51 AM | | TrackBack

April 18, 2005



The Rise of Desktop Fimmaking

For all you Star Wars fans out there take a look at this fan-made trailer, Star Wars Revelations.

Posted by TangoMan at 11:09 PM | | TrackBack


Against type (but that's "OK")

Below the fold are pictures of Miss Norway 2005 and Miss Namibia 2005. The images are linked to "close ups" (you know you want to click!).

Update: People keep asking what is "unusual" about Miss Norway. I added another picture that makes the issue a bit more crisp. Read her profile in detail if you want to know what I suspect is atypical for a good Norwegian girl.

(Miss Norway)

Another picture of Miss Norway

(Miss Namibia)

(yes, I know Namibia has a white minority, 6% isn't much)

Posted by razib at 07:25 PM | | TrackBack


Scientifying the classics

Decoded at last: the 'classical holy grail' that may rewrite the history of the world. I don't know if it will rewrite the 'history of the world,' rather, the processes detailed in the piece might allow us to fill-in-some-of-the-blanks which dominate God's Book of History. 50 years ago reductionist physicists and mathematical model builders like Francis Crick and J.M. Smith created and revolutionized molecular and evolutionary biology respectively.1 Certainly they helped biology move beyond the "stamp collection" stereotype, in other words, they taught biologists to fish rather than simply waiting for someone else to reel in the catch. Most degree programs in biology require at least one year of calculus, chemistry and physics to serve as a basis for later methodological explorations. A generation ago E.O. Wilson expressed the ambition to reduce the social sciences to a branch of biology. His project failed more than not, and to some extent I suspect that the full execution of such a goal was doomed by the limitations imposed by our neurological hardware (the exploration of the life sciences is constrained by the realities imposed by those sciences). Nevertheless, I do think that the methods and mindset of the natural sciences can offer some illumination to scholarly fields which have become covered with the dust of unsolved problems. This does not mean that historians, to give one example, need to load up on a large number of irrelevant course work in the natural sciences in preparation for their career, rather, they need to be familiar with the methods which might allow them to extract more data from the mines of the past. Empirical, even positivist, oriented scholars should grasp on to these scientific tools to rebut the all too real challenge of those who would obfuscate the study of the past by spinning a web of Theory which leave the quest for "evidence" in discarded bins.

Via Jim Nutley via Pejmanesque.

Addendum: I have spent a great deal of time on this weblog publicizing the power of genetic science in aiding in the reconstruction of our demographic past. But, I do want to emphasize that its role is supplementary and supportive, on one locus do too many build their theories upon, betraying a lack of understanding of the subtle difficulties of interpretation of hard data and a common confounding of the history of a gene with the ancestry of an individual and the history of a population.

Related: Up from ignorance and Up from ignorance II.

1 - Most of you know Crick was trained as a physicist. Fewer likely know that J. M. Smith was trained as an engineer. Certainly R. A. Fisher (a first in mathematics) brought models to the fore in evolutionary biology, along with J.B.S. Haldane and Sewall Wright, but from my reading it seems that in general most biologists of the day neither understood nor cared a great deal for "the sums" as J. M. Smith would say. As late as the 1970s an editor of a zoological journal asked Smith why he did not "cancel out the ds" when he saw a derivative in the form of dy/dx (assuming it had to be an algebraic complexity that could be eliminated).

Posted by razib at 10:04 AM | | TrackBack


"Law and Behavioral Biology"

Regarding an article, Law and Behavioral Biology, in the March issue of the Columbia Law Review >>

Laws and public policy will often miss their mark until they incorporate an understanding of why, biologically, humans behave as they do, scholars from Vanderbilt and Yale universities argue in the March issue of Columbia Law Review.

“The legal system tends to assume that either people are purely rational actors or that their brains are blank slates on which culture and only culture is written. The reality is much more complicated and can only be appreciated with a deeper understanding of behavioral biology,” said Vanderbilt law professor and biologist Owen Jones. He co-authored the article with Timothy Goldsmith, Yale professor emeritus of molecular, cellular and developmental biology....

All laws at their foundation are designed to influence human behavior, from how we interact with one another, to how we relate to our own property and that of others, to how government agencies interact with each other and with citizens, Jones said.

When developing laws, legislators and legal scholars have traditionally relied heavily on the social sciences, such as economics, psychology and political science, often responding to the popular or political trends of their time. They have rarely looked to incorporate the latest findings from fields such as biology, neuroscience and cognitive psychology, which have grown exponentially in recent years and have shed brand new light on how the human brain is structured and how it influences behavior....

Jones argues that integrating law with behavioral biology, which examines the biological underpinnings of human behavior, could strengthen legal measures in a variety of areas. Such an approach might enhance understanding of why some penalties are more effective than others, how people make choices in areas such as environmental protection and retirement savings, and what the underlying causes of aggression are and how they help explain why young men are sometimes willing – even in the face of the severest penalties – to kill in reaction to threats to their status.

Posted by theresa at 08:26 AM | | TrackBack

April 17, 2005



FYI y' all

A reflection of my Northeast + Northwestern upbringings.... (I still say "soda" and tend to slur "horror" in a New York/New England sort of way)

Your Linguistic Profile:

50% General American English
30% Yankee
15% Upper Midwestern
5% Dixie
0% Midwestern
Posted by razib at 11:06 PM | | TrackBack


Randomized Strategies versus Evolutionary Branching (yes, this is "Social Work")

A preview of an article that is going to be in the June issue of American Naturalist, The Evolution of Phenotypic Polymorphism: Randomized Strategies versus Evolutionary Branching:


A population is polymorphic when its members fall into two or more categories, referred to as alternative phenotypes. There are many kinds of phenotypic polymorphisms, with specialization in reproduction, feeding, dispersal, or protection from predators. An individual's phenotype might be randomly assigned during development, genetically determined, or set by environmental cues. These three possibilities correspond to a mixed strategy of development, a genetic polymorphism, and a conditional strategy. Using the perspective of adaptive dynamics, I develop a unifying evolutionary theory of systems of determination of alternative phenotypes, focusing on the relative possibilities for random versus genetic determination. The approach is an extension of the analysis of evolutionary branching in adaptive dynamics. It compares the possibility that there will be evolutionary branching, leading to genetic polymorphism, with the possibility that a mixed strategy evolves. The comparison is based on the strength of selection for the different outcomes. An interpretation of the resulting criterion is that genetic polymorphism is favored over random determination of the phenotype if an individual's heritable genotype is an adaptively advantageous cue for development. I argue that it can be helpful to regard genetic polymorphism as a special case of phenotypic plasticity.

I have cut & pasted the discussion below....

Studying the evolution of phenotype determination in terms of the signs and relative magnitudes of the branching and randomization disruptivities, as illustrated in figure 1, has the advantage of bringing genetic and random determination into a single analysis. This was achieved by limiting consideration to situations close to a phenotypically monomorphic equilibrium. The approach can be regarded as an extension of the analysis of evolutionary branching in adaptive dynamics (Metz et al. 1996; Geritz et al. 1998), which gives a unified perspective on the evolution of genetic polymorphism. Such conceptual unification is helpful and important, but when alternative phenotypes have evolved away from a previously monomorphic state, there is in principle a new situation that may require a separate analysis. In addition, phenotypic polymorphism could come about in different ways, such as by modification of a previously existing polymorphism or by mutations of large effect or drastic changes in environments. Nevertheless, the individual-based simulations I performed showed that an analysis in terms of branching and randomization disruptivities can often succeed in predicting the evolutionary outcome.

One important feature of my analysis is that cases are split into those where a genotype can function as an advantageous cue for determination of alternative phenotypes and those where such a genetic cue instead would be disadvantageous compared to random determination, as well as the intermediate cases where genetic and random determination are neutral relative to each other. This kind of division has general validity and makes the point that genetic determination of the phenotype is conceptually parallel to environmental determination, for which issues of the accuracy and other statistical properties of environmental cues are fundamental. In fact, it could be helpful to regard genetic determination of alternative phenotypes as a special case of adaptive phenotypic plasticity.

It is common to think of alternative phenotypes as threshold traits or developmental switches (Roff 1996; Lynch and Walsh 1998; West-Eberhard 2003), where trait expression is switched when the value of an internal liability passes a threshold. The liability might be the concentration of a hormone, which in turn could be influenced by genes, environmental cues, or random effects. If we ask in which way such a phenotype-determining mechanism can be an adaptation, there is the question of the perfection of alternatives being switched between, on the one hand, and the question of when to switch, on the other hand. For the latter, we can regard random variation in liability as adaptive if suitable phenotype frequencies are produced in this way, and any further improvement in the fit of phenotype to selective circumstances achieved by a switching mechanism is then also a possible adaptation. Environmental cues are, of course, candidates to be employed in such better-than-random switching mechanisms, but, as we have seen, heritable genetic variation is also a candidate. Thus, the alternative phenotypes of a multiple-niche polymorphism, together with the switching mechanism, are elements of an adaptation to spatially varying conditions. For genetic switching, spatial variation in phenotype frequencies from recent selection, unless obliterated by extensive gene flow, will be the source of information in the genetic cue. There is some similarity to the idea of local adaptation when gene flow is limited, but the difference is that the alternative phenotypes and the switching mechanism make up one adaptation to a range of environments rather than that each phenotype separately is an adaptation to a single environment. So, in the context of an evolved switching mechanism, like a nonlinear genotype-phenotype mapping, it becomes natural to view genetic determination of the phenotype as potentially an adaptation, falling within the general framework of phenotypic plasticity.

Several decades ago, ecological geneticists were concerned with providing an adaptive interpretation of genetic polymorphism (e.g., Dobzhansky 1951; Cain and Sheppard 1954; Fisher 1958; Ford 1965, 1971), but this interest seems to have declined in recent times. Possibly, the currently dominating idea of the gene as the fundamental unit of selection (Dawkins 1976) has been responsible for the decline because that idea might seem to be in conflict with the notion that genetic variation could play a role in an adaptive device for the organism. In ecological genetics, a traditional but also controversial view was that genetic polymorphism can be adaptive if it renders an organism efficient over a range of environments (Dobzhansky 1951; Cain and Sheppard 1954), corresponding to the modern concept of multiple-niche polymorphism. When examining this idea, Fisher (1958) traced it to the discussion by Darwin (1859) of divergence of character under natural selection and went on to suggest that a "theory of games," with randomized strategies as one feasible evolutionary outcome, could be a way to understand species interactions, such as those between predators and prey. Fisher's treatment is significant as apparently the first explicit suggestion of an evolutionary game theory. It is also clear that Fisher (1958) interpreted balanced polymorphism as an evolved randomized strategy. Ford (1965) had a similar view of genetic polymorphism as a means to regulate phenotype frequencies, and he argued that it would usually be preferable as a switching device, compared to environmental cues, perhaps because he felt that environmental cues would result in excessive fluctuations in phenotype frequencies. It then appears that traditional ecological genetics did not view genetic determination of the phenotype as essentially different from random determination. It was only with the subsequent analysis of bet hedging that this distinction became clear (Seger and Brockmann 1987), although the interpretation of genetic polymorphism as a special case of phenotypic plasticity, which I have argued for here, was not made.

My treatment did not deal directly with environmental phenotype determination, which is possibly the most widespread and important system, because I wanted a simple and focused treatment of genetic and random determination. Nevertheless, environmental determination could be included in the same kind of analysis. By regarding reaction norms as multidimensional "pure strategies," one can investigate whether some component of such a pure strategy would be exposed to disruptive selection, possibly leading to evolutionary branching and genetic polymorphism or, alternatively, whether a randomized reaction norm might evolve. A similar kind of approach has recently been used to study environmental sex determination (Van Dooren and Leimar 2003; Leimar et al. 2004). Factors such as the accuracy of environmental cues and the degree of correlation between environmental cue values observed by different individuals, together with other aspects of the ecological situation, will determine if some component of a reaction norm would be exposed to branching or randomization disruptivity.

Of the examples I used, the effect of competition between relatives on the evolution of alternative phenotypes and on phenotype determination seems not to have been modeled previously. The conclusion that random determination should be favored was, however, reached by Moran (1992), and Day (2001) found that relatedness decreased branching disruptivity in situations where relatives compete. In practice, compared to purely random determination, other mechanisms based on phenotypic cues like relative size or age might often be more efficient in reducing competition between interacting relatives and could thus be expected instead.

On the basis of the simulations for the examples, it is clear that the mutational process can have a marked influence on the system of phenotype determination that evolves. For instance, if there is little additive genetic variation in the degree of random phenotype determination, genetic determination might instead be the evolutionary outcome. A similar point was made by Van Dooren and Leimar (2003) and Leimar et al. (2004) in the context of sex determination. The explanation is that genetic and random cues can sometimes serve equally or nearly equally well for phenotype determination. As a consequence, in situations where branching and randomization disruptivities are equal, it seems appropriate to regard a genetic determination of the phenotype as a randomization device. Nevertheless, considering general fitness functions, the theory developed here shows that those situations are marginal. Using heritable genetic variation for phenotype determination will generally either be selectively favored and thus be a case of adaptive genetic determination of the phenotype or instead have a selective cost as compared to random determination.

Posted by razib at 10:11 PM | | TrackBack


Sunday Times

A couple of items of interest from today's London Sunday Times.

First is this front page story on the level of illegal immigrants in the UK, allegedly estimated by Home Office officials at around 500,000.

Second, an interesting feature article (book extract) by Tarquin Hall on the immigrant 'community' in East London. (Read it and you'll see why I put quotes round 'community'.) The article reads not unlike a spoof by Sacha Baron-Cohen, but it is, apparently, genuine.

(Added) ...and here's another extract from Tarquin Hall's book, that I thought was part of the same article, but has a separate URL.

Posted by David B at 10:29 AM | | TrackBack


The second american civil war

Why are Americans so conservative, so religious, and so resistant to modern western ‘Liberalism’? These subjects, with some variation, are a staple of European discussion regarding the United States. While explanations tend to focus on the metaphysical (“That redneck God of theirs!”), I believe another very significant factor is to be found in empirics – to be specific, in a single graph.

murder rate.JPG

This is the US annual murder rate per 100 000 inhabitants. The US murder rate hovered around 4,5 per 100 000 during the fifties. Then, in a few short years in the mid-to-late sixties, the rate doubled. What happened? In short: Liberalism happened, and Americans haven’t forgotten yet.

The murder rate has been debated quite a bit recently, because of the Levitt-Sailer dispute regarding the impact of abortion. Sailer also recently used the murder rate explosion, and all those factors that it is a proxy for, as an explanation for the resilience of the US white working class – People were simply scared off from getting too carried away by all their newly-won social freedoms by witnessing the drastic deterioration of social conditions in Black America.

Still, in the general debate on why the US political scene looks the way it does, the “murder rate factor” has never gotten enough attention. When it did, the material presented was often of dubious informational value. (Read: “Bowling for Columbine”)

Still, in order to be able to quantify the political impact of the social upheaval that led to the murder rate explosion, some raw numbers can be helpful. The graph below shows the absolute number of murders per year, and the number of murders as it would have been, had the average 1950-63 murder rate remained constant.

murders.JPG

In this way, we can determine that all in all, the US had roughly 300 000 more murders between 1964 and 2002 than had been the case if the sixties ‘explosion’ had not happened. The ‘excess murder rate’ causalities during the Vietnam War years of 1965-75 alone number roughly 74 000 people – well above the number of US soldiers killed in Vietnam.

Vast amounts of ink have been spent detailing the impact of Vietnam on the American psyche. Some of that ink would probably have been better used in determining just how the great killing spree that lasted from the mid-sixties to the mid-nineties changed how Americans view the world.

UPDATE:
As pointed out in the comments, having some data on how large the murder-prone part of the population is can be handy when discussing these kinds of issues. Added this graph, showing the indexed murder rate and the (indexed) share of the population that is between 14 and 34 years old:

youngmurder.JPG


UPDATE 2:

Steve Sailer fleshes it out in comments:

"The FBI's "homicide offending" statistics broken down by age, race, and gender only go back to 1976. Before that, they just are by total population.

What I don't know for sure is whether the black crime rate went up sharply in the 1960s or whether simply the number of blacks in big cities went up due to the Great Migration out of the South following the mechanization of cotton farming in the mid-1940s.

I suspect that what happened was that the black crime rate in Northern cities was fairly low from 1945 into the early 1960s because blacks newly arrived from the South were still feeling intimidated. Then, the Civil Rights movement and the Warren Court taught Northern urban blacks not to fear The Man, and indeed to actively resent whites.

Meanwhile, in the 1960s, Northern liberal states began raising welfare payments and stopped hassling unmarried mothers. This led quickly to a breakdown of marriage among young urban blacks, which freed young men from the supervision of wives, allowing them to live a disorderly life while still allowing them the comforts of a woman's bed.

Meanwhile, restrictions on where blacks could live in Northern cities were breaking down -- for example, blacks were restricted to a sharply defined ghetto on the South Side of Chicago throughout the 1960s -- both due to legal changes and to sheer numbers arriving from the South and the high birthrate. So, blacks began pouring into formerly all white working class neighborhoods.

After integration in their neighborhood began around 1967, my late inlaws, being nice liberals (he was a classical musician and union leader, she a special-ed teacher), joined a pro-integration activist organization in their West Side of Chicago neighborhood to keep the neighborhood from going from part black to all black. All the members pledged not to sell.

But within 18 months, the first wave of middle class black home buyers in their neighborhood had been driven out by underclass blacks pouring in and driving the crime rate through the roof.

After their kids were mugged three times and the vast Martin Luther King riot occurred in their neighborhood in 1968, my inlaws finally sold out at a very low price, being just about the last whites to leave the neighborhood, losing much of their life savings because they had tried to make integration work.

They moved to what are now the distant exurbs and voted Republican after that.

So, I think four things happened in the 1960s: the number of blacks in the North went up, the black crime rate went up, contact between black and white went up, and black animus toward whites became active. Put them all together and the number of whites violently victimized by blacks shot through the roof in the 1960s, leaving a permanent impact on American politics.

The fifth thing that happened in the 1960s was that liberals permanently became associated in the popular mind with murder:
Lyndon Johnson won 61% of the vote in 1964 running as a staunch liberal, but his Veep, Hubert Humphrey, won less than 43% in 1968. In 1972, McGovern won about 38%. Watergate helped Carter squeak in with 50% in 1976, but he was the last Democrat to get that high a number."

SOURCES:

US Dept. of Justice (Murder rate)


US Census (population statistics)


Posted by dobeln at 05:59 AM | | TrackBack