Yesterday I watched Will Wilkinson and Ezra Klein on Blogging Heads. Will, as many of you will know, is a pragmatic libertarian (oh, they exist), while Ezra is a liberal. I was struck by (somewhat appalled in fact) by Ezra’s irritation and contempt for the philosophical nerdiness of many libertarians. Ezra’s emphasis on the empirical and the proximate, on a narrow sui generis fixation on a sequence of finite policies was set against a more expansive and theoretically scaffolded conception of the Good Life which Will seemed to be promoting (even a question of the nature of the Good Life). While Ezra held that what is Good and True is self-evidently Good and True, Will seemed to believe that meta-analysis, taking a step back and intellectually decomposing the presuppositions which feed one’s policy positions, is both edifying and may smoke out deeper distinctions and commonalities. As the dialogue continued I was struck by the thought that Ezra Klein was more a man of Burke and Kirk than Locke or Mill!. In other words, Ezra’s aversion to abstract analysis of political positions in a larger context, the deep philosophical structures in which they might be embedded in, to focus singularly on the nitty-gritty of specific issues which loom large contemporaneously, struck me as fundamentally a conservative sensibility.

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Via Retrospectacle.

I’ve received several emails about this website, Understanding Race. Here is a article about the project. I don’t have much to say, the readers of this blog can decompose assertions like this easily enough I assume:

The pattern of DNA across populations shows a nested subset. African populations harbor some alleles (gene variations) that are absent in non-African populations; however, all of the alleles that are common in non-African populations are also common in African populations.

The English here is peculiar. If African populations are more polymorphic, wouldn’t it stand to reason that the common (derived) alleles in non-Africans must be less common in Africans? (since you can’t have more than 100%?) In any case, loci such as MC1R invert this stark narrative. In attempting to replace an outmoded racial typology derived from Victorian imaginations and social contexts anti-racists construct their own ghostly strawmen which are a mirror of the old Platonic constructs.

I have little more to say than to exhort you to hold truth close to your hearts, the follies of the deceivers will then stand naked before you.

Update: Newsflash, Steve Hsu is evil.

In an interesting paper published in the Jan, 2007 issue of Hormones and Behavior, researchers describe a phenomenon they claim is unique to human females; their overt display of fertilty. Specifically, around the time of maximum fertility, women show enhanced “self-grooming” behavior and dress in a more provacative manner in an apparent attempt to solicit copulations. Even more interesting, and in support of a claim I have made previously, is that even females in long term “monogamous” relationships exhibit these behaviors. (difficult to imagine how or why behaviors like this would evolve under the humans are monogamous hypothesis)

I’ll just remind people that while the idea of unconscious regulation of overt behavior that enhances host reproductive opportunities, there are even cooler stories where parasite infection effects sexual behavior similarly.

While this is an intersting study, one might ask the following additional questions:

1. Does the magnitude of solicitation depend on the quality of either the existing mate or extra pair mate? If this is an adaptive behavior, you would predict that solicitation should increase as existing partner quality decreases or as extra-pair mate quality increases.
2. Is there a difference in male perception of this solicitation when looking acoss male quality or relationship status?
3. Does solicitation vary with MHC genes? (Do Women with rarer alleles solicit less?)
4. How might one get a judge-jobs? “hot-woman photograph evaluator”

Any interest in replicating this here at GNXP? Women- submit randomly chosen photos to me or to Razib, one just after your period (low fertility), one about 2 weeks later (peak-fertility). We can assemble an “expert panel” of judges to evaluate …

Paper Abstract (and doi)

Humans differ from many other primates in the apparent absence of obvious advertisements of fertility within the ovulatory cycle. However, recent studies demonstrate increases in women’s sexual motivation near ovulation, raising the question of whether human ovulation could be marked by observable changes in overt behavior. Using a sample of 30 partnered women photographed at high and low fertility cycle phases, we show that readily-observable behaviors – self-grooming and ornamentation through attractive choice of dress – increase during the fertile phase of the ovulatory cycle. At above-chance levels, 42 judges selected photographs of women in their fertile (59.5%) rather than luteal phase (40.5%) as “trying to look more attractive.” Moreover, the closer women were to ovulation when photographed in the fertile window, the more frequently their fertile photograph was chosen. Although an emerging literature indicates a variety of changes in women across the cycle, the ornamentation effect is striking in both its magnitude and its status as an overt behavioral difference that can be easily observed by others. It may help explain the previously documented finding that men’s mate retention efforts increase as their partners approach ovulation.

Jonah over at The Frontal Cortex has some commentary up on the gay sheep story. A reader pointed out that this controversy started off with some wild claims made by PETA. Nevertheless (more at Andrew Sullivan’s), no matter the details of the claim, there are a few points I’d like to pick up on….
Jonah says:

So here’s my hypothesis: if you select against homosexuality in a biological community, you will also be selecting against our instinct for solidarity. The same genes that give rise to gayness might also give rise to cooperation. When scientists create a population of all heterosexual sheep – this would be a boon to ranchers, since a high percentage of male sheep are gay – they will find that their sheep are now more violent as well.

Assume that Jonah is correct and that some of the loci with a range of alleles which allow for human predisposition to sociality also result in small number of obligate homosexuals. It seems that the evolutionary logic demands that modifier genes emerge which mask this fitness killing trait. What Roughgarden (and Jonah) would have us believe is that there are structural-biophysical reasons why this can not happen, because if it could, it should. I can believe and accept some level of homosexual behavior emerging facultatively (e.g., bonobo females) as part of conditional behavioral strategies (some human populations have also engaged in facultative ritual homosexuality). But that does not entail obligate homosexuality as a necessity. The evolution of selfish genetic elements shows us that genomic dynamics can result in deleterious consequences for individuals, and these consequences can persist in a metastable form because of the long term ubiquity of various parasitic elements. Not only does this apply intragenomically, but there are also parasites which modify human behavior. The paradox of worker sterility in eusocial insects forced us to come to grips with inclusive fitness and Hamilton’s Rule, but the mathematics doesn’t pan out for obligate homosexuality in such a fashion. We have a range of somewhat baroque and peculiar choices before us to explain the biological root of this behavior, and I don’t place Roughgarden’s hypothesis very high on the chain of parsimony. So when Jonah says:

Selecting against homosexuality isn’t just immoral and unethical: it’s also just a terrible idea, driven by bad biology.

I say hold up brother! Let’s not put the cart before the horse here. Roughgarden’s thesis is speculative, to be charitable, so the inference that more obligate homosexuality leads toward more sociality is itself stretching the foundations of established biology. Fundamentally the evolutionary logic is pretty uncharted here. I suspect that the evolutionary rationale won’t be adaptive at all, but some sort of selfish element, whether it be intragenomic, or extra-genomic (e.g., a parasite). I also wouldn’t be surprised if medicine does get advanced enough that the proximate biological processes which underpin obligate homosexuality are nailed down (and many other psychological predispositions). As for morality, I think it is all about choice, and let’s get real, in a world where white parents make sure that their kids don’t go to school with blacks (no matter the test scores of the school!) you’ll not be hearing many of the silent screams of any fetuses diagnosed with a high likelihood of obligate homosexuality.

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Razib has several times mentioned an important theorem of population genetics, credited to J. B. S. Haldane, that the probability of a single favourable mutation surviving and spreading throughout a population is approximately 2s, where s is its selective advantage relative to other alleles. So for example if a mutation has a selective advantage of 1 per cent, it will have approximately a 2 per cent chance of ultimately sweeping through the population. This may seem a low probability, but if the same mutation recurs more than a few dozen times in the species, it is virtually certain to be successful. A recent paper by John Hawks and Greg Cochran makes a central use of Haldane’s theorem.

As a matter of historical curiosity I wanted to see Haldane’s original statement of this principle, and how he derived it.

Hawks and Cochran give the citation ‘Haldane, J. B. S. (1927): A mathematical theory of natural and artificial selection, part v: Selection and mutation. Proceedings of the Cambridge Philosophical Society, 28, 838-44.’ I find that the correct volume number is 23, not 28. The same incorrect citation is given by Crow and Kimura’s An Introduction to Population Genetics Theory (1970).

The paper is also reprinted in Selected Genetics Papers of J. B. S. Haldane, edited with an introduction by Krishna R. Dronamraju, Garland Publishing, NY, 1990, at pp. 90-96. I have transcribed the key passage from the paper below. Incidentally, Haldane uses k, rather than s, for the selective advantage, but this is a trivial matter of notation. More important, Haldane’s theorem only applies where the population is sufficiently large. If the breeding population n is very small (less than about 50) there is a significant chance that a single mutation will be fixed by genetic drift before selection has had much effect. For a single neutral or favourable mutation there is always a probability of at least 1/2n that it will ultimately be fixed, since in the absence of recurrent mutation one of the 2n genes in the population will ultimately be the ancestor of all surviving genes.

It is interesting that Haldane himself does not claim great novelty for his 1927 theorem, but presents it as an application of the methods set out by R. A. Fisher in his 1922 paper ‘On the dominance ratio’. Fisher himself later gave a more elaborate treatment of the same problem in a 1930 paper, ‘The Distribution of Gene Ratios for Rare Mutations’, Proceedings of the Royal Society of Edinburgh, 1930, 50, 205-20. (Like most of Fisher’s papers, this is available online from the Fisher archives at Adelaide.) This includes the conclusion that:

The probability of a mutant, enjoying a small selective advantage a, spreading until it establishes itself throughout the entire population is thus found to be 2a/(1 – e^-4an); it is easy to see that with an indefinitely large population, or in any case if 4an [population size x selective advantage] is large, this expression reduces to 2a. Thus a mutation conferring a selective advantage of 1 per cent will have practically a 2 per cent chance of establishing itself.

In 1930 Fisher, rather characteristically, did not cite Haldane’s 1927 treatment of the selection problem. Sewall Wright, in his 1931 paper on ‘Evolution in Mendelian populations’, states a similar proposition and credits Fisher, but not Haldane, with prior publication. This might raise a question whether Haldane or Fisher should be given the main credit for the theorem. As far as I can judge, Haldane does make a heavy use of Fisher’s 1922 methods, but Fisher himself did not (in 1922) explicitly calculate the probability that an advantageous mutation would survive, and Haldane’s application of Fisher’s methods in 1927 was by no means as easy as falling off a log. I think therefore that Haldane does deserve the credit for the theorem itself.

In any case, as often turns out in issues of priority, there are neglected earlier candidates. As early as 1873, the Rev H. W. Watson, in response to a request from his friend Francis Galton, had published a method for calculating the ‘extinction of surnames’ which contains much of the technique later used by Fisher for calculating the random extinction of genes. And even earlier, in 1845, a French mathematician called Bienayme had published a brief paper with results suggesting that he may have discovered some of the same methods, though he did not give details. (See Michael Bulmer, Francis Galton: Pioneer of Heredity and Biometry (2003), pp.156-60.) There is nothing to suggest that Fisher or Haldane knew of these earlier efforts.

The following extract from Haldane’s 1927 paper contains his proof of the theorem. I cannot reproduce all of the mathematical notation, so I will use S to indicate summation, x^n to indicate the n’th power of x, and x_a (etc) to indicate subscripts. I have added some comments (in square brackets) and notes in an attempt to explain the derivation, as far as I can follow it myself. No doubt much of this will be self-evident to expert mathematicians, but expert mathematicians have a tendency to underestimate the difficulty of following mathematical proofs for the rest of us.

EXTRACT

…the treatment of Fisher [1922] is followed.

In a large population let p_r be the chance that a factor [allele] present in a zygote at a given stage in the life-cycle will appear in r of its children in the next generation. If the individual considered is homozygous, this is the chance of leaving r children, if mutation is neglected. Let S p_r(x^r) = f(x) [note 1]. Therefore f(1) = 1, f(0) = p_0 [note 2], the probability of the factor disappearing, while f ‘ (1) = S rp_r, [note 3] i.e. the probable number of individuals possessing the factor in the next generation. The probability of m individuals bearing one each of the factors considered leaving r descendants is clearly the coefficient of x^r in [f(x)]^m, if we neglect the possibility of a mating between two such individuals, which we may legitimately do if m is small compared with the total number of the population. If then the probability of the factor being present in r zygotes of the nth generation be the coefficient of x^r in F(x), the corresponding probability in the (n + 1)th generation is the same coefficient in F[f(x)]. Hence if a single factor appears in one zygote, the probability of its presence in r zygotes after n generations is the coefficient of x in S(x) [S has subscript f and superscript n], i.e. f(f(f…f(x)…)), the operation being repeated n times [note 4]. The probability of its disappearance is therefore LtS(0) [note 5]. By Koenigs’ theorem this is the root of x = f(x) in the neighbourhood of zero [note 6].

Now in the case of a dominant factor appearing in a population in equilibrium, and conferring an advantage measured by k, as in Part I(5) [of Haldane’s series of papers] f ‘ (1) = 1 + k. Since f ‘ (x) and f ” (x) are positive, x = f(x) has two and only two real positive roots, one equal to unity, the other lying between 0 and 1, but near the latter value if k be small [note 7]. Hence any advantageous dominant factor which has once appeared has a finite chance of survival, however large the total population may be.

If a large number of offspring is possible, as in most organisms, the series p_n approximates to a Poisson series, provided that adult organisms be counted, and since
f'(1) = 1 + k, f(x) = e^(1 + k)(x – 1). Hence the probability of extinction 1 – y is given by 1 – y = e^-(1 + k)y [note 8].

Hence (1 + k)y = -log(1 – y) [note 9]

and k = y/2 + (y^2)/3 + (y^3)/4 + … [note 10]

and if k be small, y = 2k approximately [since the terms after y/2
are orders of magnitude smaller]. Hence an advantageous dominant gene has a probability 2k of survival after only a single appearance in an adult zygote, and if in the whole history of the species it appears more than log_e2/2k times [the natural logarithm of 2, divided by 2k] it will probably spread through the species. But, however large k may be, the factor may be extinguished after a single appearance. Thus, if k = 1, so that the new type probably leaves twice as many offspring as the normal, the probability of its extinction is still .203. If in any generation there are m dominant individuals the probability of extinction is reduced to y^m, where y is the smaller positive root of x = f(x). When k is small this reduces to (1 – 2k)^m. Hence if in any generation more than log_e2/2k adult dominants exist, the factor will probably spread through the whole population.

NOTES

[Note 1] Summation is over values of the subscript r from zero to infinity. Since r is the number of an individual’s offspring, it can only take integer values.

[Note 2] The sum is p_0(x^0) + p_1(x^1) + p_2(x^2) + p_3(x^3)… For the value x = 1 this equals p_0 + p_1 + p_2 + p_3… , which sums to 1, since the probabilities are mutually exclusive and cover all possible outcomes. For the value x = 0 the terms from p_1(x^1) onward are all equal to zero, so the series reduces to p_0(0^0), which = p_0 if we accept that 0^0 = 1. I am not sure that there is any agreed convention on this point, as the usual proofs that x^0 = 1 (e.g. 1 = (x^a)/(x^a) = x^(a – a) = x^0) break down for the case x = 0. Fisher, in his formulation of the series, presents it as p_0 + p_1(x^1) + p_2(x^2) + p_3(x^3), which avoids any doubt on this point.

[Note 3] Summation is over values of r from zero to infinity. The expression f ‘ (1) evidently means the first derivative of the function f(x) with respect to x, for the value x = 1. Each term in the sum f(x) has the form p_r(x^r), so by elementary calculus its first derivative is rp_r(x^(r – 1)), and the first derivative of the sum f(x) as a whole is the sum of the first derivatives of its component terms. But for the value x = 1 these each reduce to rp_r, so the first derivative of f(x) is equal to S rp_r, as in Haldane’s formula.

[Note 4] Haldane’s treatment here is closely based on Fisher, but uses different notation.

[Note 5] Lt is the limit as n goes to infinity, in other words as the function is iterated indefinitely with its own previous value as argument.

[Note 6] This part of the derivation evidently requires advanced knowledge of the theory of functions, and I can only take it on trust. Haldane gives the cryptic reference ‘Koenigs. Darb. Bull. (2) 7, p.340, 1883.’ I wondered if ‘Koenigs’ might be an error for ‘Koenig’, possibly Julius Koenig, but on consulting the Dictionary of Scientific Biography I found an entry for a French mathematician, Gabriel Koenigs (1858-1931). Among his many accomplishments, according to the DSB, Koenigs was ‘one of the first to take an interest in iteration theory’. Koenigs was also a pupil of Gaston Darboux, founder and editor of the Bulletin des Sciences Mathematiques et Astronomiques, sometimes known as ‘Darboux’s Bulletin’. So Haldane’s cryptic reference to ‘Darb. Bull.’ is probably to an article by Gabriel Koenigs in the Bulletin des Sciences Mathematiques et Astronomiques, 2nd series, volume 7, 1883, at p.340. I find that there is indeed an article by Koenigs, ‘Recherches sur les substitutions uniformes’, at the cited place, but its mathematics is far beyond me.

[Note 7] Haldane does not consider the trivial cases p_0 = 1, where the gene is always extinguished immediately, or p_1 = 1, where it always produces one and only one offspring per generation. In the first case f(x) would have the value 1 for all values of x, while in the second case it would have the value x for all values of x. For non-trivial cases the value of the function f(x) increases continually and at an increasing rate with increasing x, so the first and second derivatives of f(x) are positive. Haldane also states that the equation x = f(x) has two and only two real positive roots, one of which is 1, and the other between 0 and 1. I am not sure I could give a rigorous proof of this, but I suggest the following approach. If we plot a graph of the function y = f(x), for real positive values of x, then f(x) = y = x wherever the curve representing the function touches or intersects a line through the origin at 45 degrees to the axes. As f ‘ and f ” (the first and second derivatives) are both positive, the curve is concave upwards, i.e. it has just one ‘bend’, with the inner part of the bend on its upper side. The curve must start from the y axis at the value p_0, since we know that f(0) = p_0, which is somewhere between 0 and 1. We also know that f(1) = 1, so the curve must touch or intersect the 45 degree line at x = y = 1, which is accordingly a real positive root of x = f(x). The curve must therefore pass in some way from the point (x = 0, y = p_0), which is above the 45-degree line, to the point (x = 1, y = 1), which is on that line. As the curve is concave upward, it cannot touch or intersect a straight line in more than two points. Since it touches or intersects the 45-degree line at the point (x = 1, y = 1), there are three possible ways of doing so: (a) it is a tangent to the line at that point; (b) it intersects the line at that point from above the line (in its approach from its starting point on the y axis); or (c) it intersects the line from below the line. But it cannot be a tangent to the line at that point, because the first derivative of the function would then be equal to the slope of the line, which is 1, whereas by assumption the first derivative at that point is 1 + k, with non-zero k. Possibility (a) is therefore excluded. Possibility (b) can be excluded for a similar reason. If the curve intersects the 45-degree line from above, a tangent to the curve at that point must make an angle of less than 45 degrees with the x axis. But this means that the first derivative of the function at the point of intersection must be less than 1, whereas by assumption it is greater than 1. This leaves only possibility (c), that the curve intersects the line from below, which is consistent with the fact that the first derivative is greater than 1, so that a tangent to the curve would have an angle greater than 45 degrees. But this implies that in passing from (x = 0, y = p_0), which is above the line, to (x = 1, y = 1), it has first intersected the line at some other value of x between 0 and 1, which is another real positive root of x = f(x), as required by Haldane’s proof.

[Note 8] Here Haldane follows Fisher closely, but with a significant modification. Fisher (1922) had given the formula f(x) = e^m(x – 1), where m:1 is the ratio of the total population in generation (n + 1) to the population in generation n; in other words he allows for the growth of a neutral allele in line with any expansion of the population as a whole. Haldane’s significant innovation is to allow for genes which increase in numbers because of a selective advantage, k, relative to other genes in a static population. Fisher’s f(x) = e^m(x – 1) then becomes Haldane’s f(x) = e^(1 + k)(x – 1), and Haldane is able to find an explicit expression for the chance of survival in terms of the selective advantage k (see Note 9).

[Note 9] Haldane denotes the probability of the gene surviving as y, so the probability of extinction is 1 – y. But the probability of extinction is the appropriate root of the equation x = f(x) = e^(1 + k)(x – 1). So substituting 1 – y for x we get 1 – y = e^-(1 + k)y. In the right hand side of this equation the expression -(1 + k)y is the (natural) logarithm of the left hand side, which is 1 – y, so, taking the negative of both sides, (1 + k)y = -log(1 – y).

[Note 10] Here Haldane assumes knowledge of a theorem equivalent to -log(1 – y) = y + (y^2)/2 + (
y^3)/3 + (y^4)/4: see this Wiki article on logarithms. Given this theorem, we have

(1 + k)y = -log(1 – y) = y + (y^2)/2 + (y^3)/3 + (y^4)/4 …

therefore, dividing both sides by y and then subtracting 1 from both sides, we get

k = (y^2)/2y + (y^3)/3y + (y^4)/4y … = y/2 + (y^2)/3 + (y^3)/4 + …

as stated by Haldane.

If any readers are associated with Montgomery Slatkin’s lab, could you email me? (contactgnxp -at- gmail.com). Thanks.

Jason Rosenhouse and John Hawks have both commented on the introgression of cattle alleles into wild bison. J & J have hit many of the salient points, but let me suggest one issue: not all genetic loci are created equal. That is, “neutral” markers should be weighted less than “functional” markers. Of course, neutral markers probably aren’t all neutral, and many functional markers are functionally relevant only in specified environmental contexts. The problem with these sort of questions is that I believe our “species concepts” are derived from gestalt psychology and our intuitive tendency to categorize “kinds” based on a few visible traits, and these few traits often derive their characteristics from a subset of genetic loci. The mapping of the words to the genetical reality of a flux of allele frequencies across populations is imperfect, and it is through the filter of these words that we elucidate our values about what is important. When we say “we need to maintain genetic diversity” what we really mean is that we wish to maintain correlation structure. But what does correlation structure of the vast sea of ancestrally informative neutral alleles really tell us? Is there some ancestral “bison essence” that is passed along neutral non-coding lineages? I say no! Cognitive psychologists, for example Paul Bloom, have been developing models which suggest that “innate dualism” and “essentialism” are prefab structures through which we comprehend our world, and so we have based our conservation policy from the bedrock of these intuitions. But if science is the ultimate arbiter then we need to reconsider the context of our values, because the full set of loci likely do not contribute to the “essence” which we seek to perpetuate. Alleles are more than the sum of their parts, consider the Africanized honey bee, they might be hybrids, but these “killer” bees have nasty traits which evoke less than a middling level of concern. Rather, particular behavorial tendencies inherited from their tropical forebears loom large, their docile European ancestry be damned! The blood does not tell I say, damn by phenotype and praise by phenotype!

Squirrels lose half of their synapses when they go into hibernation. The synapses fall apart in relation to temperature changes. The proteins aren’t destroyed. They are just detached, possibly as protein complexes floating in the cytoplasm. They get more synapses when they wake back up, but it’s not clear that they are the same ones. In fact, they are impaired in recognizing squirrels they’ve met before after hibernation. Can you imagine? Half of synapses in thalamus, hippocampus, and cortex? If Synaptic Self is at all appropriate book title, do squirrels lose their squirreldentity every winter? Maybe some place holder protein is left behind so the synapses can grow back how they’re supposed to. It’s not easy to tell that you got the same synapses before and after hibernation. Guess you could induce in vivo LTP and see if it can be maintained over that span. Or use one of Svoboda’s fancy window-on-the-brain techniques.

I am currently reading The English Civil War. When I read God’s War, a history of the Crusades between 1100 and 1400, it was a rather detached affair. My conscious partisanship toward the West expressed itself in a mild sentimental bias toward its medieval Christian percursor.1 Nevertheless the medieval period is a distant land and it was a survey of a shadow alien landscape from which I wished to glean facts in the service of a general understanding of human affairs and action. Yet my reading of The English Civil War is different, I seem to always “root” for the Roundheads against the Cavaliers. Perhaps this is because I am an American, and will always smile upon the tribunes of the plebs who have the gall to rise against the armies of the king, but sometimes I wonder if the sentiment does not have deeper origins. In Albion’s Seed David Hackett Fisher identified “Four Folkways” in the United States which derive from the pre-1776 British Settlers:

Families of zealous, literate Puritan yeomen and artisans from urbanized East Anglia established a religious community in Massachusetts (1629-40); royalist cavaliers headed by Sir William Berkeley and young, male indentured servants from the south and west of England built a highly stratified agrarian way of life in Virginia (1640-70); egalitarian Quakers of modest social standing from the North Midlands resettled in the Delaware Valley and promoted a social pluralism (1675-1715); and, in by far the largest migration (1717-75), poor borderland families of English, Scots, and Irish fled a violent environment to seek a better life in a similarly uncertain American backcountry.

My own personal background is at the nexus between the Puritan and Midland folkways. I once told a friend that when going through the Civil War period I always knew who the good guys were. (the Blues of course!) Only later on with the awareness of adulthood did I comprehend the nature of “the Lost Cause,” or the reality that the Roundheads were arguably more tyrannical than the Cavaliers. Other biases lurk in my mind, when I read The Reformation I leaned toward the Protestants, even though I knew the rough sketch of the outcomes. This, though I am aware of, and attempt to ward myself from, the sin of anti-Catholic prejudice which suffuses the Anglo-American intellectual tradition.

I am immigrant, strictly speaking, to this nation. Though schooled nowhere else I am visibly different from the majority of the citizens, and was a conscious alien as a child. Nevertheless, it is clear that I have internalized the subtle biases and outlooks of the “the Yankee,” whatever that is. Part of the explanation perhaps lay with the thesis of The Nurture Assumption, my peers have generally been northern Yankees, and so I became. Additionally, my teachers always knew who the “good guys” were, even if they wouldn’t say it in so many words. I am curious, what biases do readers feel themselves stumbling upon? In our society we are taught to reflect & explore “latent” bias on the dimensions of sex and race, but what about the unconscious “folkways” which we imbibe through the banal processes of socialization?

1 – Though I have admitted a faint and reflexive attraction to the harmonies of the call to prayer because of childhood memories, in general I find Islamic civilization a cold and dour affair and am not particularly disposed toward it.