Neolithic Y DNA from Southwestern France

A post by Dienekes brings to my attention a paper in PNAS, "Ancient DNA reveals male diffusion through the Neolithic Mediterranean route":
The Neolithic is a key period in the history of the European settlement. Although archaeological and present-day genetic data suggest several hypotheses regarding the human migration patterns at this period, validation of these hypotheses with the use of ancient genetic data has been limited. In this context, we studied DNA extracted from 53 individuals buried in a necropolis used by a French local community 5,000 y ago. The relatively good DNA preservation of the samples allowed us to obtain autosomal, Y-chromosomal, and/or mtDNA data for 29 of the 53 samples studied. From these datasets, we established close parental relationships within the necropolis and determined maternal and paternal lineages as well as the absence of an allele associated with lactase persistence, probably carried by Neolithic cultures of central Europe. Our study provides an integrative view of the genetic past in southern France at the end of the Neolithic period. Furthermore, the Y-haplotype lineages characterized and the study of their current repartition in European populations confirm a greater influence of the Mediterranean than the Central European route in the peopling of southern Europe during the Neolithic transition.
Note: contra the authors' assertion, lactase persistence was probably not carried by Neolithic central Europeans; the most common European LP-associated allele has been absent in all central European Neolithic samples tested to date.

Dienekes writes:
R-M269 which, because of its apparent young Y-STR age has been tied by some to either the Mediterranean or Central European Neolithic is conspicuous absently from both at the moment. It may yet surface in a Neolithic context, but its absence this late from a region where, today, it is abundant only adds to its mystery.
In fact, the amateur estimates using actual mutation rates put the spread of R1b into Western Europe clearly post-Neolithic.

R1b and LP in Western Europe are in all likelihood associated with the dispersal of Indo-European languages.

These findings add to ancient DNA evidence indicating large-scale post-Neolithic population replacement in Europe. Coon and other traditional physical anthropologists, it turns out, probably had a better handle on European prehistory 70 years ago than population geneticists did five years ago.

DNA tests show Ingmar Bergman not his mother's biological child

Who was the mother of Ingmar Bergman?
The mystery is even greater given that Karin Bergman, who kept extensive diaries, recording both events and thoughts, was by all accounts unaware that Ingmar was not the child to whom she gave birth July 14,1918 but a surrogate child. [. . .]

The analysis, which reached her April 12, 2011, established with certainty that Ingmar Bergman was not the son of Karin Bergman, supporting Tillberg’s hypothesis about her own family. It is not yet certain who Bergman’s mother was, but a great deal of circumstantial evidence suggests that it was Tillberg’s grandmother, Hedvig Sj√∂berg (later Tillberg), who in July 1918 gave birth to a son in Stockholm who was immediately given up for adoption.

Racial differences in genetic load?

Another point of confusion in Kanazawa's deleted post:
There are many biological and genetic differences between the races. However, such race differences usually exist in equal measure for both men and women. For example, because they have existed much longer in human evolutionary history, Africans have more mutations in their genomes than other races. And the mutation loads significantly decrease physical attractiveness (because physical attractiveness is a measure of genetic and developmental health). But since both black women and black men have higher mutation loads, it cannot explain why only black women are less physically attractive, while black men are, if anything, more attractive.
Actually, the ancestors of present-day non-Africans existed for the same amount of time as the ancestors of present-day Africans. Any racial differences in the number of deleterious variants per genome would need to be explained in terms of population differences in mutation rate, or strength of purifying selection, or some other relevant population genetics parameter.

A few years ago, an academic geneticist affirmative-action beneficiary made the opposite claim: that due to a population bottleneck, Europeans harbor more deleterious variation than Africans. John Hawks pointed out the impossibility of that study's conclusion around the time it was published:
What is amazing to me is that these same geneticists embrace hypotheses of population history that cannot possibly have happened. The other geneticists quoted in the article, Carlos Bustamante and his graduate student Kirk Lohmueller, wrote a paper earlier this spring arguing that deleterious mutations have reached high frequency in Europeans (moreso than Africans) because of a bottleneck during European history. The press reported this work as "Whites genetically weaker than blacks, study finds." The hypothesis in the paper is that protein-coding sites otherwise conserved in most mammals may differ among humans because of relaxed selection in a bottleneck.

Here's why they're wrong: their bottleneck is impossible. They propose that the European population was a small, isolated population of 5,700 effective individuals from 214,000 years ago up to the Last Glacial Maximum. I suppose I should take some encouragement that they believe Neandertals were European ancestors (because otherwise, where exactly would this small, isolated population of Europeans have lived). But it's still quite impossible -- it implies no gene flow between Africans and Europeans across that entire span. You see, that is the only way that genetic drift can lead to this kind of result -- large differences in frequencies between continents for hundreds of deleterious alleles. It takes a bottleneck of exceptional length, along with complete isolation.

In what has become a troubling trend, these details were hidden away in the online supplementary information of the paper.
Empirically, there seem to be no major racial differences in genetic load. Compared to whites, blacks have much higher rates of spontaneous abortion and infant mortality -- superficially consistent with higher genetic load among blacks -- and an early attempt in Brazil to assess racial differences in genetic load by examining the effects of inbreeding did conclude that blacks have more lethal equivalents. However, a subsequent Brazilian study, with better controls, found no racial differences in inbreeding load:
A new investigation using sib and cousin controls, made in the same Brazilian area where whites and nonwhites (mulattoes and Negroes) had before shown inbreeding loads of different magnitudes, failed to support these findings. Our present data show that the number of lethons is the same in both ethnic groups. A review of all investigations on Brazilian whites and nonwhites suggests that the number of lethons may be accepted as roughly 2 in both ethnic groups.
Similarly, "An analysis of consanguineous marriages in Nigeria" finds:
The total number of heterozygous deleterious genes carried per person in this population was estimated to be 8.71 +/- 3.92 (SD), which is not too different from estimates for several other racial groups.

Black women rated less physically attractive than other women; white men rated better looking than black men

Via the isteve comments section, I learn of a now-deleted Psychology Today blog entry by Satoshi Kanazawa, headlined "Why Are Black Women Rated Less Physically Attractive Than Other Women, But Black Men Are Rated Better Looking Than Other Men?" Prissy, terrier-faced "science" blogger / wannabe PC enforcer PZ Myers helpfully includes a link to a pdf copy of the post. (PC's own reaction includes this amazing bit: "Good grief…shades of Francis Galton! For those of you who don't know, creepy old man Galton ogled women and judged them for looks[!].")

Kanazawa explains:
The physical attractiveness of each Add Health respondent is [rated] three times by three different interviewers over seven years.

From these three scores, I can compute the latent "physical attractiveness factor" by a statistical procedure called factor analysis. Factor analysis has the added advantage of eliminating all random measurement errors that are inherent in any scientific measurement. The latent physical attractiveness factor has a mean of 0 and a standard deviation of 1.
Kanazawa finds that black women are "far less attractive than white, Asian, and Native American women", while "races do not differ in physical attractiveness among men, as the following graph shows". In fact, the second graph clearly shows that white men have higher "mean latent physical attractiveness" scores than black men, and that the difference is statistically significant. Kanazawa goes on to write:
Black women are still less physically attractive than nonblack women net of BMI and intelligence. Net of intelligence, black men are significantly more physically attractive than nonblack men.
Inconveniently for black men and Kanazawa, the real world does not control for intelligence. Further, if the association between intelligence and physical attractiveness rests on some underlying "good genes" factor, it makes little sense to try to "control" for intelligence when comparing races. The intelligence and attractiveness of someone with average genes for his race are what they are.