gaps in books? gaps in personal knowledge?
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Aquest tema està marcat com "inactiu": L'últim missatge és de fa més de 90 dies. Podeu revifar-lo enviant una resposta.
Or, if like me, you don't even know what you don't know, what sorts of areas area gaps in your knowledge/interest that you're looking to fill?
In archæology you're dealing with material culture, and a huge body of ethnographic evidence shows quite clearly that variation in material culture maps onto human social groups/populations in extremely complex ways: so you can't just "read off" group relationships or population history from archæological data. Plus, the European landscape has been pretty intensively exploited for millenia, so a vast amount of archæological remains are simply gone.
However long the Basques as such have been around, there's been intermarriage with surrounding populations, so genetic data are imperfect.
A similar sort of question arises in the Americas: there are lots of existing Native American tribes, so why can't we trace them back into the pre-Columbian period? Aside from the above, the introduction of Old World diseases into the Americas so decimated the indigenous population that it appears (from early explorers' records as well as archæology) many formerly independent groups had to band together simply in order to survive.
This is not, of course, to say that we can't know more than we do: archæologists can be among the most intellectually conservative of scholars, and the history of the discipline around the world shows a poor record of paying attention to what local people might have to say. On the other hand, the Basques have been there throughout all of recorded history, which is a pretty substantial chunk o' time with many social and cultural upheavals, so it is unlikely that extant legends and traditions will go very far in illuminating Basque origins.
I don't know how well this answers your question. I'm not a European prehistorian, so I can only speak in general terms; but if a Euro. prehistorian doesn't show up, I'd be happy to try to answer any others you may have.
#3, sure "genetic data are imperfect," but that's part of the frustrating thing for me, the Basques are so clearly different physically--"the highest concentration of type O blood in the world" (!) according to one of the few books on the Basques, The Basque History of the World by Mark Kurlansky, with the O percentage in the hard-core Basque areas (the Basques are very committed to their homeland) even higher. I'm just wondering if the lack of information is due to lack of research that in turn's due to lack of interest or what?
Are you familiar with basic microevolution: the importance of population size, 'founder effects,' genetic drift, that sort of thing?
In microevolution, the basic units are genes and alleles. Alleles are different versions of a gene, in the way that full, gored, A-line, and straight are all kinds of skirts. So, for the blood-group gene, there might be alleles for A, B, and O blood groups. (I'm just giving examples here, so even if my particular facts are wrong, it shouldn't misrepresent the principles I'm trying to illustrate.) So, strictly speaking, nobody has "the gene" for anything: one can have "the allele" for type-O blood, or "the allele" for type-A; what everyone has is a gene (or, rather, an allele) for "blood type." I've heard that the ability to curl the sides of one's tongue up so that the tongue looks like a taco shell is genetic; my parents and sisters can all do that, but I can't. So, assuming it is genetic and that it is straightforward, it's not that my family has the taco-tongue gene and I don't, it's that they have the "taco-tongue-capable" allele and I have the "taco-tongue-incapable" allele. So, in a sense, a "gene" is a sort of abstraction, a group of alleles.
In microevolution, one of the basic measures is the relative frequency of different alleles in a population. It's important to keep in mind that we're talking about populations and not individuals, or, necessarily, social groups. And there's no standard "population size," because we're talking about relative frequencies.
So: alleles and populations.
For starters, assume an infinite population with completely random mating throughout. In that case, "gene frequencies" (the term usually used, although "allele frequencies" is what is meant) won't change within the population. This is the "null hypothesis" state, doesn't really exist, never has, just a basic steady-state situation to use as a comparison for getting concepts across.
Now, suppose you take a small, random sample of individuals from that infinite population and stick them somewhere out of contact with the infinite population. For most genes, the allele frequencies in the little group will be representative of the allele frequencies in the infinite population. But for some and which ones will be completely random the allele frequencies in the little group will be different. The randomness is simply a matter of sampling error: if you take a small random samples a large enough number of times, eventually you will get an unrepresentative sample. Only, rather than taking lots of little samples of one gene, we're taking one little sample of lots of genes (since individuals are, genetically speaking, collections of genes).
A difference in the little group's allele frequency can lead to what is called a "founder's effect." Suppose the infinite population has one gene with five alleles, all with a frequency of 20%. And suppose that our little group's frequencies are a bit different because of sampling error: 35%, 20%, 20%, 20%, and 15%. Over time, that unusually well-represented allele can come to dominate the small population's allele frequency in time (say, on the order of 70%, or even higher), simply because it starts out with that numerical advantage, and even though it offers no advantage over the other alleles.
A "bottleneck" is sort of a founder's effect in reverse: instead of plucking out a small, random sample from the source population, you kill off individuals in the source population until you are left with a small, random sample. Something like this is believed to have occurred with cheetahs: the genetic variation in cheetahs is so small that they think something happened in the past so that there was at one point only a minimally viable population of cheetahs, and today one of the chief goals of the cheetah breeding program among zoos is to maximize cheetah genetic variation.
As you can see, population size is an important factor: the smaller the population, the more pronounced these effects. This is true also for genetic drift, which is simply random fluctuations in allele frequency between generations. In the real world where there has never been an infinite population, allele frequencies can fluctuate through time, but in a large enough population, the average frequency will remain stable (think of normal temperatures and precipitation for a given day of the year, compared to what actually happens that day in specific years). As population size decreases, genetic drift becomes increasingly likely to result in permanent changes in allele frequency in the population (this is how, in my founder's effect example, the allele with a 35% frequency can, over time, acquire 70% frequency: in a small enough population, a small but significant difference can be magnified into a large difference simply by random processes).
The important thing in all of this is that, so far, everything I have said does not involve any question of genetic fitness: these are random processes, and which alleles benefit has nothing to do with how beneficial or harmful they may be. Throw in genetic fitness, and these processes can be accelerated, minimized, or who knows what else. The classic examples are hemoglobin variants, in which normal hemoglobin is best for oxygen transport but variant hemoglobin is best for resistance to malaria: if you have two normal alleles, you die of malaria; two variant alleles, you die of sickle-cell disease; one of each, you survive both. Both have advantages and disadvantages, and they are such that the ideal allele frequency is 50% for each as long as you're in a malaria-ridden area. In areas not subject to malaria, variant hemoglobin loses its advantage and normal its disadvantage, and so you get selection in favor of normal hemoglobin.
A couple of other points: humans have many thousands of genetic variations. Even among the ones with selective advantages, most have nothing whatsoever to do with how people group themselves socially: you do not find people included or excluded from communities because they have type-B blood or carry an allele for variant hemoglobin. In fact, of all genetic variants in the world, any given population has about 70% of them. Not all populations will have the same 70%, and some have less while others have more. Overall, then, virtually all human genetic differences are shared between two or more populations. This means that, effectively, there are no individual genetic markers that will tell you to which population an individual person belongs.
The best that can be done is to look at groups of genetic variants, and make statistical estimates of closeness of association between populations and individuals or other populations. In fact, it's really unsafe to make inferences about single individuals in comparison to a known population, because on average there will be about 25% variation within a population, so without knowing the variation of the individual's source population, you can't know anything about whether they're representative or not. Women's pelvises tend to be wider than men's, but there is overlap.
This becomes more difficult as time differences between the populations grow, because of random and/or selective genetic change. Forensic anthropologists (think TV's Bones) use data about the distribution of various skeletal attributes within races, sexes, and ages. However, these data were obtained from 20th century American populations. Use them on modern populations from other places, or older populations from America, and their utility is less. This is what happened with "Kennewick Man," a 12,000 y.o. skeleton from Washington State that was initially identified as Caucasian, which conflicts with all archæological knowledge. Yes, if you use 20th century data. But he's not a 20th century person, and if you look at the sample of 12,000 y.o. skeletons from America, they all kind of look alike, they don't really look like any modern populations particularly, and the ones they're least different from, as a group, are some SE Asian/Pacific populations.
OK, I'll stop here because this is changing from a post to a book. As I say, this all very brief. The main points I hope you take away are that population size matters, that the genetics of a population can change through time for no apparent reason, and that there is almost no genetic variation that is specific to any social group.
With regard to several Native American tribes, 1491 offers a synthesis of some new information. This book has been talked about a lot on other threads and in other groups as well.
I am still looking for some information regarding the Native American tribes along the Delmarva Peninsula, but have not yet acquired any books specific to them yet. (Let me know if you hear of anything!)
What other people is there a general lack of knowledge (academic, popular, personal, etc.) or gaps in the history that you would be interested in hearing about?