Nice writeup but perhaps no surprise. In a textbook very large neutral population of constant size half the mutants should be singletons, right? Henry Harpending

Sorry to be obscure, I just mean under neutrality. Standard coalescent theory predicts that the number of loci with i copies of a mutant will be proportional to 1/i. So the number of loci with 1, 2, and 3 copies of a mutant should be in the ratio of 1 to 1/2 to 1/3, etc. I don't know where I dug out that 1/2 in my note above: senescence perhaps. Henry

The costs and benefits of helping people, relatives or not, depends on the base population. There is no such thing as 'true' relationship. So we could if we were crazy calculate our relationship with an onion. If I help my brother in a highly inbred population, it doesn't help him as much _with respect to that population_ as it would if in a population of random people. On the other hand _with respect to the species_ it helps him a whole lot more. Two random humans from the same group have an underlying relationship of about 25%, so _with respect to the world_ my brother is worth about 75%, not 50%. Relationship as Hamilton used it is not very well defined anywhere, and thinking about it in terms of pedigree relationship has not helped much. The 25% I use above comes from the world Fst (i.e. kinship) of about 1/8 and doubling 1/8 gives 25%. There are pages and pages of wordspeak in the literature since the 1980s about whether or not group selection and kin selection are the same thing. They certainly are, the only difference is how one writes the models. Henry Harpending

Razib here is a letter I sent to the FDA a week or so ago. Henry Dear FDA: I am writing to comment on the meeting to be held March 8-9 about direct to consumer (DTC) genetic testing (Docket FDA-2011-N-0066). I am especially motivated to write after reading the plea to you by the AMA that any DTC results of possible medical interest be censored to consumers. Their letter reflects an appalling paternalistic arrogance that would violate basic freedoms and impede public scientific understanding. I presume that if they could they would have you ban bathroom scales on the grounds that body weight must only be revealed in consultation with a “qualified medical professional.” The AMA submission has two main themes. The first is that citizens are unable to understand the risks and predicted outcomes that might be reported and that experts are vital to provide guidance. My own experience is that I am perfectly capable of finding empirical risks from current literature, I expect I can do a much better and more thorough job than my personal physician, and even my teenage son can do it with no trouble. My own experience, again, is that only about 1 in 5 medical students know what Bayes’ Theorem is. The second theme is that knowledge of potentially medically relevant genotypes can do some unspecified harm to customers. I have spent a total of six or so years on university IRBs, and this kind of worry is ever present. While there is much public loose talk about psychological harm and the like, within the committee room we all understand that the practice of witholding any data from subjects about themselves is nothing but protection from lawyers. I am perfectly free to refuse to participate in research and in clinical trials but I am not free to refuse to participate in federal censorship of knowledge of my own genotype. I would urge you to keep freedom of information for consumers at the center of the table when you discuss regulation of the DTC genetic testing industry.

I have spent a lot of years with Northern Bush speakers in the Kalahari. They have words for one, two, three, and four (sort of: two-two literally.) On the other hand I have watched my Bushman employees in local stores hand over a five pula note to pay 2.30 for something, count the change, and verify that it was correct. Beats me how they were doing it. Henry

People like this are a real threat to the human sciences. His logic is that attaching importance to the European creative explosion is politically unwholesome. There follows the suggestion that some scratches in ochre from Blombos are really the same as the Euro-bang and that there must have been a bang in New Guinea but no one is reporting on it. Euro-bang also contradicts the assumptions of linguists! None of this kind of talk be acceptable in an undergraduate term paper. 
 
I don't attribute very much significance to the Euro-bang myself but I hope that I could bring up real evidence and theory, not my own politics, in a discussion. It is shameful when prominent journalists exhibit their inability to separate politics and science.

McGraw makes an interesting point, but surely the emigrants to the UK were no random sample of Indian workers. 
 
Henry

When we were working on that paper the big empirical question was whether or not a bottleneck could explain the disease pattern. The bottleneck hypothesis was well established, Monty Slatkin had shown that it was (remotely) plausible using neutral theory, IOW assuming that the effect on homozygotes could be ignored, and so on. All the work went into testing that. Turns out we could have waited a year or so: Olshen et al. and the recent paper from David Goldstein's group show that there is no hint of a bottleneck. We were working from a much poorer set of data but we found the same thing. 
 
Now folks are picking at us for not testing the disease part of the hypothesis but I see an easy out. Who has access to the Jewish disease community, who has the name in this field? Risch, of course. I am sure he will step right in and help us out with the study everyone wants us to do. 
 
Henry

pconroy said "How do you know this?" in response to Peter's assertion that Neanderthals were covered with fur. 
 
A clue is that the finger bones of an infant chimp are quite rugose because the baby uses his hand to cling to mom's fur. Human infant finger bones are not rugose at all because they have not been exposed to a lot of muscle pull. 
 
Neanderthals are like chimps in this respect, suggesting fur to many of us. 
 
Henry

I think Clark is still partially blinded because he is an economist who wants to talk about "production." Evolutionary biologists want to talk about "fitness" and would claim that optimizing in the economists' sense is a small subset of fitness maximizing. 
 
He describes Highland PNG in his rebuttal but doesn't seem to "get" the difference between PNG and, say, Japan. Following Fisher and Dawkins, reproduction is mating and parenting. Among tropical gardening groups all over the earth land is essentially free, women can produce enough to feed their children and the men, production does nothing for men, so they spend their time competing with other males, i.e. in mating effort rather than parenting effort. 
 
It is only when there is a fitness payoff to male work that we see what Clark takes to be the normal agricultural pattern. This happens, it seems, when polities arise, suppress local raiding and warfare with constabularies, and population growth and agricultural intensification follow. Highland PNG is such awful broken terrain that polities could never persist there.

I learned in graduate school in 1967 that IQ was the best predictor of lifespan that there was. I have no idea what the references were, but it was common knowledge among the social science crew at Harvard. 
 
Then after Jensen's monograph the curtain came down on studies of cognitive variation and something like the dark ages followed.

Razib the history is that in the 1970s the idea was widespread that foragers have lower fertility than farmers, most of it based on low completed family sizes in !Kung Bushmen developed in Nancy Howell's monograph. Central African Pygmies had comparably low completed fertilities. 
 
Then we realized that both these groups were in the so called "sterile crescent" of venereal infertility in Africa and that the low fertility was a result of VD not backload and all that. Then Jim Wood and later Gillian Bentley did literature surveys showing that completed family sizes in foragers and gardeners did not differ at all--they were all five or six. 
 
I can't see any support for any pervasive reproductive career differences between foragers and farmers myself. 
 
A handy source is  
@article{pennington1996ceh, 
title={{Causes of Early Human Population Growth}}, 
author={PENNINGTON, R.L.}, 
journal={AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY}, 
volume={99259}, 
pages={274}, 
year={1996} 
} 
 
I know, I know, if I knew how to put in a link to a URL I would. 
 
Henry

Here is a piece of data relevant to GC's fears of censorship of data in our future: 
 
Dear Dr. Harpending: 
 
The National Human Genome Research Institute (NHGRI) is planning a 
workshop to explore the ethical, legal, and social issues (ELSI) raised 
by research on natural selection in humans. The impetus for this 
meeting is the sense of a growing need for more thoughtful deliberation 
by genomic researchers, ELSI researchers, science writers and science 
editors regarding the societal issues raised by natural selection 
research. The goals of the meeting will be to: 1) discuss the 
scientific design and interpretation issues pertinent to this research 
to determine whether a set of "best practices" can be identified for 
investigators and peer reviewers in this area; 2) discuss the relevant 
ethical issues and issues surrounding public understanding and reporting 
of the findings of this research to assess what issues science editors 
should consider when dealing with papers in this area; and 3) discuss 
future directions for genomic and ELSI research related to natural 
selection. 
 
We would like to invite you to attend this workshop, which will be held 
in Rockville, MD on October 28, 2008. NHGRI will cover your travel 
expenses. An agenda for the workshop is attached.

Very nice plot of the frequency spectra: I missed your older post. But if these were ascertained in a single pair of chromosomes then it matters where those chromosomes came from. Do we know? Were there really only two? If so then inferences about more or less drift in Europeans and Asians are tenuous. 
 
Henry

G: 
 
Very nice--a real hypothesis test. Can you give us some good sources? 
 
Henry

There is lots of worry out there that the Mungo mtDNA sequence is an artifact. 
 
Henry

"re:bottlenecks. any model for recent human history that doesn't include some form of strong genetic drift (via bottlenecks or small Ne or something) in non-African populations simply will not fit the data well. a very nice paper that serves as an example:" 
 
Or genetic draft. 
 
Henry

I don't think there is any argument with some form of the general Out-of-Africa model. What Hawks is addressing, I think, is the widespread fear-of-selection and consequent invocation of bottlenecks to explain everything. There is no support for these supposed bottlenecks outside the particular data sets that are being explained away. 
 
This bottlenecks-everywhere mentality is part of a larger funny kind of  bias in human genetics. The paradigm recently in genomic surveys has been to do careful elegant analysis, beautiful computations on huge datasets, then wave the arms back and forth about bottlenecks with no thought of testing any hypotheses. All the attention is to the technology, none to the scientific issues supposedly being addressed.  
 
Another wonderful example is the Olshen et al. paper discussed here a while ago. Beautiful data showing with absolutely no ambiguity that there never was any Ashkenazi bottleneck. But the authors paid no attention, prattled on about the Ashkenazi bottlenecks (3 of them!) anyway without even looking at their data. 
 
We have had the same same tradition a long time with the mtDNA and Y chromosome tree-makers. Careful genetcs, careful computation, then stare at the output and make something up to explain it. No testing of prior hypotheses ever-the concept is foreign. 
 
Henry

I just realized that I have no idea what Luca's maps actually portray: I dropped out of this business for a few decades and never paid much attention to this stuff. 
 
If we have some kind of data matrix we can compute eigenvectors of covariances among genes and another set among populations. The first gives synthetic alleles, the second synthetic populations. We could then smooth and interpolate either one. Which one is Luca plotting in his book? I do know that one is called principal components, the other principal coordinates, but I don't know which is which. 
 
And what happens when one makes a map of the other one, the one Luca didn't use? We used to do both because the axes are the same. 
 
Thanks, Henry

We hadn't seen previous PCA references and had read he was the first to apply PCA to gene frequency data, so we may simply have not dug deep enough on this. However, in the History and Geography of Human Genes he describes developing the "synthetic maps" approach, and I think our statement that "he pioneered the use of PCA in population genetics" is still fair. 
 
Here is an old paper that uses PCs: mine because the reference is handy. There was a cottage industry of this stuff in the 1970s. Luca did come up with th idea of plotting one pc at a time as a synthetic map. 
 
Henry 
 
item 
Harpending, H.C. and T. Jenkins. 1973.  
Genetic distance among southern African  
populations, in {em Method and Theory in Anthropological Genetics}, edited by M.  
Crawford and P. Workman, Albuquerque: University of New Mexico Press.

i think this is most easily interpreted as orthogonal; it's talking about a totally different question. consider the specific case of a SE -> NW PCA map in europe. cavalli-sforza et al. famously interpeted this as a signal of a neolithic demic diffusion which manifested as a range expansion/wave of advance. 
 
If I remember correctly the second European PC is NE->SW, and an edited volume from the UK was focused on interpreting it. The editors did not appreciate that it was simply at right angles to the first one and likely meant nothing. 
 
Henry

so the shape of the habitat (in these ideal cases) determines the class of matrix, which in turn determines the structure of the eigenvectors. if I understand correctly, this should hold true regardless of the size of the matrix. 
 
Yes, of course, I have been thinking about the eigenvalue spectrum. I ought to wait until later in the day, when I'm awake, to comment. 
 
HCH

right, yes, that's cited in the abstract. but I don't think these patterns are "edge effects". this paper tells you mathematically why these artefacts arise when migration patterns are constant. 
 
If not, what happens when your space is a circle or a torus? When the space gets larger and larger? 
 
Henry

Bob Sokal wrote a paper pointing out that lots of Luca's PCs were likely edge effects and showing that completely random data, white noise, on continent maps generated the same patterns. This was in the late 80s. 
 
And contra the abstract of the article folks in human genetics have been using PCs since the 1960s-Luca came up with looking at one at a time, which I am not sure is an advance. 
 
Henry