Islamic scholar promotes adult breastfeeding:

…Izzat Atiyaa had issued a fatwa, or religious ruling, offering his bold suggestion as a way around the prohibition in Islamic religious law against a woman working in private premises with a man who was not her close relative. Breastfeeding, he argued, would create a familial relationship under Islamic law.
Dr Atiyaa explained to the Egyptian newspaper al-Watani al-Yawm that: “A man and a woman who are alone together are not (necessarily) having sex but this possibility exists and breastfeeding provides a solution to this problem (by) transforming the bestial relationship between two people into a religious relationship based on (religious) duties.“

Note: The authors have a website which summarizes their research (via Language Log).
Speaking in tones? Blame it on your genes:

People who carry particular variants of two genes involved in brain development tend to speak nontonal languages such as English, while those with a different genetic profile are more likely to speak tonal languages such as Chinese.
In tonal languages, which are most common in South East Asia and sub-Saharan Africa, subtle differences in pitch can change the meaning of vowels, consonants and syllables. Nontonal languages, which prevail in Europe, the Middle East and North Africa, use pitch only as a way of conveying emphasis or emotion.
…
He cautioned, however, that the research had so far found only an association that appears to be more than chance, and that more work was needed to confirm a causal effect.

I first started hearing stuff this sort of research (i.e., the correlations between particular alleles and language forms) in 2006, so I’m not too surprised. We’ll see how this pans out, look for it in PNAS.
But, which alleles on which genes? From Scientific American:

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Check out the 2007 writing contest from Seed Magazine. First prize is $2,500.

Note: The authors have a website which summarizes their research (via Language Log).

Speaking in tones? Blame it on your genes:

People who carry particular variants of two genes involved in brain development tend to speak nontonal languages such as English, while those with a different genetic profile are more likely to speak tonal languages such as Chinese.

In tonal languages, which are most common in South East Asia and sub-Saharan Africa, subtle differences in pitch can change the meaning of vowels, consonants and syllables. Nontonal languages, which prevail in Europe, the Middle East and North Africa, use pitch only as a way of conveying emphasis or emotion.
…
He cautioned, however, that the research had so far found only an association that appears to be more than chance, and that more work was needed to confirm a causal effect.

I first started hearing stuff this sort of research (i.e., the correlations between particular alleles and language forms) in 2006, so I’m not too surprised. We’ll see how this pans out, look for it in PNAS.

But, which alleles on which genes? From Scientific American:

The new research, published this week in Proceedings of the National Academy of Sciences USA ties this difference to two genes, ASPM and Microcephalin. The exact functions of both genes are still open to debate, but they are known to affect brain size during embryonic development. “They presumably have something to do with brain structure, because there are deleterious mutations of the genes that lead to microcephaly” (a condition in which a person’s brain is much smaller than the average size for his or her age), says senior study author, Robert Ladd, a professor of linguistics at the University of Edinburgh in Scotland.
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Ladd and Dediu compared 24 linguistic features-such as subject-verb word order, passive tense, and rounded vowels-with 981 versions of the two genes found in the 49 populations studied. Most of the language contrasts could be explained by geographic or historical differences. But tone seemed to be inextricably tied to the variations of ASPM and Microcephalin observed by the authors. The mutations were absent in populations that speak tonal languages, but abundant in nontonal speakers.

First, note that the authors here imply that derived (more recent) forms of the genes in question under strong selection are connected to the spread of non-tonal languages around 6,000 years ago. There’s a lot of question begging here, are tonal languages ancestral? Is this association causal? But look, there’s one thing that jumps out at me from a cursory examination of the various times suggested here: it sees possible that the rise to prominence of non-tonal languages (assuming their derived character) dovetails with the posited expansions of Indo-European and Afro-Asiatic languages around the core of the World-Island (Eurasia + Africa).

Here is the wiki info on the geography of tonality:

In Europe, only Norwegian, Swedish, Scottish Gaelic, the Limburgish language (according to some a dialect of Dutch), Lithuanian, Serbian, Croatian, and some dialects of Slovenian possess tonality, and only Lithuanian regularly marks it in text other than in dictionaries. The tones of Lithuanian are believed to be especially authentic, as they agree for the most part with the tones of Vedic Sanskrit, its ancient cousin. Another Indo-European tonal language, spoken in the Indian subcontinent, is Punjabi.

Most languages of sub-Saharan Africa (notably excepting Swahili in the East, and Wolof and Fulani in the West) are tonal. Hausa is tonal, although it is a distant relative of the Semitic languages, which are not.

There are numerous tonal languages in East Asia, including all the Chinese “dialects”, Thai, Vietnamese and Burmese (but not Mongolian, Cambodian, Malay, standard Japanese or standard Korean). In Tibet, which is riven by harsh geography, the Central and Eastern dialects of Tibetan (including that of the capital Lhasa), are tonal, while the dialects of the West are not. Much speculation has been generated over the reasons for this partial tonogenesis.

Some of the native languages of North and South America possess tonality, especially the Na-Dene languages of Alaska and the American Southwest (including Navajo), and the Oto-Manguean languages of Mexico. Among the Mayan languages, which are mostly atonal, Yucatec, with the largest number of speakers, has developed tones.

Finally, from the authors’ website:

The next step is to do experiments in which we look for evidence of the nature of the predisposition or bias. The work of Patrick Wong and his colleagues provides one possible lead here: they have shown that some monolingual adults find it much harder than others to learn an artificial language vocabulary that makes use of tone or pitch distinctions, and that the differences between these groups show up in subtle differences of brain structure as well. If we could show that these differences also reflect differences in genetic make-up, it would go some way to showing that the correlation we have found is based on a real causal link.

Related: This is Bruce Lahn’s brain on ASPM and MCPH1. ASPM, Microcephalin, and intelligence. Developmental cell biology of ASPM. Brain size & genes.

Kambiz @ Anthropology.net has an excellent review of the case of the Chinese warlord with “European” ancestry.

Chris has a long response to Paul Bloom’s recent argument about intuition & science & education. You can also see Jake Young’s critical take here, as Chris responds in part to some of his issues with the piece.

Recently Razib walked readers through a scenario where a population passing through a bottleneck would, by sampling error, experience a change in allele frequencies and thereby convert some of the variance due to dominance into additive genetic variance — the kind that matters most for a population to respond to selection. If we recall the Breeder’s Equation — R = S*h^2 — the increase in the population mean for a trait (R) equals the mean of the sub-population selected for breeding (S), multiplied by a fraction between 0 and 1 that shows how fully the potential for change is exploited by selective breeding (h^2). This fraction is called the heritability and equals the fraction of the entire phenotypic variance that is accounted for by just additive genetic effects. Clearly, this fraction increases as additive variance increases.

To review a key difference between additive vs multiplicative scenarios, the components in an additive case don’t interact, or the context in which they appear doesn’t matter. Since such effects are blind to all other contingencies, they matter most in trying to breed a trait in a desired direction. Non-additive effects throw sand in the gears: for instance, if the alleles within a particular locus interact, we have dominance. The other type is due to epistasis, or the interactive effects between loci. Since these effects blunt the power of directional selection, we ask what if we could magically convert the retarding type into the promoting type? Razib’s post linked above has already showed how, in detail, this could happen when a bottleneck converts dominance variance into additive variance. Now, to see how a bottleneck could convert epistatic variance into additive variance, consider the following table*:

—- AA — Aa — aa
BB.. 8……. 6…… 4
Bb.. 2……. 4…… 4
bb.. 1…….. 1….. 3

Let’s call the locus with the A and a alleles locus 1, and that with the B and b alleles locus 2. We’ll say the entries correspond to a phenotype that depends on the genotypes at both loci, and that fitness is positively correlated with this phenotype. Consider locus 1: the A allele is associated with greater fitness if you look just at the first row, where it interacts with just the BB genotype. In fact, A’s effect is perfectly additive: each copy of A adds 2 units to the baseline, and the heterozygote’s value is the average of those of each homozygote. If the b allele were lost somehow, then the only possible genotype at locus 2 would be BB (only the top row would show up), and the greater fitness of A combined with its non-trivial heritability (i.e., greater additive variance) would then drive A to fixation. The trouble is that when A teams up with the Bb and bb genotypes, its effect is non-additive and it’s associated with lower fitness. We therefore have epistatic variance in this trait: the fitness of the alleles at locus 1 depend on the larger genetic context in which they appear.

For readers not used to this jargon, consider a real-world case of the market success of musical styles. Let’s say that locus 1 represents the musical styles, such that AA is a pure classical, Aa is classical-jazz fusion, while aa is pure jazz. Now, locus 2 represents the critics, such that BB prefers classical and increasingly winces as he hears more jazz intrude into a style; Bb prefers music that has even a hint of jazz; while bb is a jazz purist. Here, the success of a particular style depends on who’s judging it, and since the judges have dissimilar opinions, a diversity in musical styles will be maintained.

But suppose that, due to the whims of fashion in criticism, the pool of critics was suddenly depleted of those who valued jazz at all, leaving only the classically minded critics (BB). Then we would quickly see jazz musicians removed from the concert halls and record stores, replaced by pure classical musicians. This loss of diversity in the pool of critics wouldn’t have to result from caprice — maybe somebody important in the world of criticism fired all of the critics even somewhat sympathetic to jazz.

To bring this back to genetics, the loss of the b allele at locus 2 could result from a population bottleneck, which increases sampling error, or it could result for more selective forces. We already see that b is associated with lower fitness (values descend as you move down any of the three columns), so it could also be lost due to selection against it. In the past 10,000 years, it has been possible for a few people to affect large numbers of others — maybe a satrap decides that he doesn’t like people with blue eyes and tries to kill them off. Or perhaps an imperial ruler or ruling elite make good on a promise to execute anyone who steals. By purging a locus or loci of their diversity in any of these ways, any other loci that had been interacting with the suddenly homogenous loci are now more free to undergo directional selection. Crucially for humans, the new socio-cultural and institutional structures that came into being only after agriculture probably rubbed out some diversity at loci that were only of marginal importance in a hunter-gatherer society, but whose diversity could not be tolerated in an agricultural one. This applies equally to loci affecting traits above the neck as well as below.

* Shamelessly using the same numbers as Table 2.3 on p.21 of Mazer & Damuth (2001). Evolutionary significance of variation, in Fox, Roff, & Fairbairn (eds.). Evolutionary ecology: Concepts and case studies. New York: OUP.

Kambiz @ Anthropology.net has an excellent review of the case of the Chinese warlord with “European” ancestry.

‘Smart’ mice teach scientists about learning process, brain disorders

Mice genetically engineered to lack a single enzyme in their brains are more adept at learning than their normal cousins, and are quicker to figure out that their environment has changed, a team led by researchers at UT Southwestern Medical Center has found.
…
The group is also beginning a search for drugs that might create the same effects without genetic manipulation and monitoring the animals’ health and behavior over time.
…
The key in this study was being able to “knock out” the gene for Cdk5 only in the brain, and only when the mice were adults. This technique, only recently developed and called conditional knockout, allows much more sophisticated experiments than traditional knockout, which entirely eliminates the gene.
…
Normally, Cdk5 works with another enzyme to break up a molecule called NR2B, which is found in nerve-cell membranes and stimulates the cell to fire when a nerve cell signaling molecule, or neurotransmitter, binds to it. NR2B previously has been implicated in the early stages of learning.

The new research showed that when Cdk5 is removed from the brain, the levels of NR2B significantly increase, and the mice are primed to learn, Dr. Bibb said.

Evolved biological systems aren’t optimal…just good enough. Knowing how the system works should lead to interventions that improve function. In the coming decades there should be nutritional, drug, training, genetic, and cybernetic enhancement of brain function.

Redefinition / turnin’ your play into a tragedy / exhibit level degree on the mic / passionately – Kweli

Nature has an Insight section up ostensibly about epigenetics starting with an article by Adrian Bird suggesting a re-definition. It’s free. I think the term is useful to the extent that you can predict something about a phenomenon or mechanism by knowing that it is ‘epigenetic’. Bird’s suggestion is to make the term less useful and more inclusive. The last section is labeled ‘Refining a definition’ when in fact he is doing just the opposite:

…there might be a place for a view of epigenetics that keeps the sense of the prevailing usages but avoids the constraints imposed by stringently requiring heritability. The following could be a unifying definition of epigenetic events: the structural adaptation of chromosomal regions so as to register, signal or perpetuate altered activity states. This definition is inclusive of chromosomal marks, because transient modifications associated with both DNA repair or cell-cycle phases and stable changes maintained across multiple cell generations qualify.

He wants to allow transience and yet use epigenetics to explain stable phenomena:

A growing idea is that functional states of neurons, which can be stable for many years, involve epigenetic phenomena, but these states will not be transmitted to daughter cells because almost all neurons never divide.

Without such epigenetic mechanisms, hard-won changes in genetic programming could be dissipated and lost;

With this refinement, epigenetics is everything and nothing. The only thing you can infer about an epigenetic event is that it doesn’t change the DNA sequence. Bird wants to claim that a unifying trait is that epigenetics is ‘responsive’ rather than ‘proactive’. I don’t understand. If you’re going to introduce new terms, why not choose to bring into to broader use the distinction between meiotically and mitotically heritable or force people to be specific about which chromatin modification they are referring to instead of saying ‘epigenetic modifications’? Responsive and proactive are more loosely defined concepts destined to muddy waters and lead away from insight.