The 10,000 Year Explosion: How Civilization Accelerated Human Evolution
Just wanted to give everyone a heads up, Gregory Cochran’s new book, The 10,000 Year Explosion: How Civilization Accelerated Human Evolution, is available for pre-order on Amazon. Of course, I wouldn’t trust Amazon’s publication date too much….
Labels: Human Evolution
When is Steve Sailer’s new book going to be available AT AMAZON ?
i’m sure it’ll show up at some point, but until then,
http://www.lulu.com/content/4576443
Is it anything more than Muller’s rachet?
However, I will buy the book … rest assured.
Going by the recent movie “10,000 B.C.,” humans were already quite civilized 12,000 years ago: they had developed agriculture, domesticated the horse, used metal weaponry, and the Egyptians were well on their way toward completing the Pyramids. And, according to one blooper site, even though it was 10,000 years, well, B.C., one character exclaimed “Jesus!” when startled.
Whatever happened to Cochran’s theory of where to find real, live Neanderthals? Since that was two and a half years ago, I guess it didn’t work out, but I’m still interested in what the theory was.
A great moment in intellectual history.
As for the hidden Neanderthals: the possibility still exists. Look, once upon a time I argued that there ought to be mitoviruses, viruses that hijack the _mitochondrial_ replication apparatus instead of the nuclear machinery. I had to wait ten years for someone to find one.
Be patient.
Beat you to it!
So what is his general thesis for folks who enjoy this topic but aren’t as up on the intricacies of the literature as specialists are? I’ve really liked all the books on this I’ve read from different views (and disciplines – although I’m partial to the cognitive science approach).
Amazing! It’s just been a couple days since I e-mailed Razib inquiring after the health of the Neandethals or at least of G. Cochran’s overdue announcement of where we can meet up with some of ‘em (other than the pair to whom we’ve been introduced in the Geico commercials).
Congrats on your new book Greg! Since you are floating around I thought you might find it interesting that the Fraternal Birth Order Effect just hit a speed bump.
A new study with a 10,000+ sample by Andrew Francis of Emory University couldn’t detect it.
Family And Sexual Orientation: The Family-Demographic Correlates Of Homosexuality In Men And Women
Please tell me the Cochran book is a popular introduction to recent developments in haplotype structure analysis/extended haplotype homozygosity and selection – because I NEED one really, really bad. (Unless anyone can recommend one? Maybe one that’s already available?)
Sister Y:
Try here for a 2006 review, and follow the citations:
http://www.scienceonline.org/cgi/content/abstract/312/5780/1614
I would say that we managed to come up with plausible explanations of several of the major unsolved questions of history and prehistory, including some contemporary questions. The approach is different, in that we take biology seriously – in particular, mathematical genetics.
Key topics: ed, how Neanderthals may have played a key role in the birth of behavioral modernity, how human evolution has accelerated, adaptation to agriculture and complex societies (which includes human domestication), how trade and conquest stirred the genetic pot in Eurasia, the expansion of the Indo-Europeans, the European conquest and settlement of the Americas and Australasia, historical progress, and how the Ashkenazi Jews got their smarts.
And you should have seen the stuff they wouldn’t let us put in the book… though in fact, you probably will.
“Be patient.”
We haven’t got all millenia, you know.
Obviously, relict archaics would probably be smart enough to hide from sapiens, intentionally and systematically. That seems like the biggest a priori point in favor of their possible persistence. But there are lots of different infectious psychoses, and so it’s hard to imagine that one of the archaics wouldn’t have blundered into sapiens territory due to madness. Or, one might come our way intentionally due to some extreme duress.
relict archaics would probably be smart enough to hide from sapiens
Sasquatches?
LOL
I am pretty sure that this is not what is meant by “Neanderthals among us”.
Whoops, the neander comments didn’t seem like a metaphor (for introgression) to me, but I could be mistaken. The “not panning out yet” part made me think something else was being discussed – has the introgression hypothesis of microcephalin etc been refuted?
I recall there was some talk about Homo floresiensis, since they persisted so late, assuming they are a bona fide taxon. I didn’t see any scientists wanting to go on record about living floresiensis being anything more than an “utterly vanishing possibility” or something like that, but I think the possibility was acknowledged once or twice in interviews, brought up by the interviewer.
Since it’s been two years, I suppose I should give out a clue.
Here it is:
“What for you bury me in the cold, cold ground?”
Australian aborigines?
Tasmanians? They were contemporaries, if that’s what you mean. Different races of of the same species?
By that logic, Andaman Islanders should be Neanderthals too.
I’m not sure what that means, but at least it confirms that I have no idea what we are even talking about.
Let’s see: the Jews didn’t have a reputation for being particularly clever in the classical world.
Modern European Jews, though, are real cleverclogs.
Meantime, everyone asks “where did those old-time Europeans, the Neanderthals, go?”
I feel a conjecture coming on.
I’ll go with Jews. It’s Dec. and Jews must be buried within 24 hours of death…
Sheesh, no one is even taking proper advantage of a giveaway. Another hint: It’s a quote, and any properly educated person would recognize it.
right, we have google and it’s the tasmanian devil…
If it is the Tasmanians, they have plenty of living descendants (mixed, of course) so it should be possible to find genetic traces of Neanderthal ancestry.
gcochran:
I’m going to take a shot in the dark here and go back to the earliest reference that I can recall to being buried in “…the cold cold ground.” namely a song either written or written down by Stephen Foster in 1852 (of whom someone at Warner was deeply interested in if you count how much of his oeuvre is used in the old cartoons, hence the Taz riff).
Of course if that’s the clue, then it leaves more damn questions than answers, particularly with all the variant verses to the song I’m thinking of.
I could be totally off, though.
Greg, David Boxenhorn got it a few comments up.
“All species are destined to become extinct, but, except as they are parts of a species, subspecies need not follow this rule. By definition, species do not ordinarily interbreed, but subspecies do. The Tasmanians were absorbed by the Caucasoids who replaced them on their island. . . . When subspecies disappear, they usually, if not always, do so by absorption. Their genes linger on polymorphously with those of their conquerors . . . The principle is that when a population has been invaded by members of another race the genes that give it its special adaptation to its local environment retain their selective advantage and eventually come to characterize the mixed population through the process of natural selection.”
– C.S. Coon, The Origin of Races (p. 34)
Slightly OT, but there’s also an interesting section on dwarfing (among other interesting things). Did anyone else know that “Dutch anthropologists found six or more fossil skeletons of small people in a cave on the island of Flores, Indonesia in 1955“? I’d never come across this bit of info in anything I read about the Hobbits.
The clue points to the Tasmanian Devil, damn it. Think !
So is Greg saying it is something to do with the Tasmanian Devil but not the aboriginal Tasmanians themselves? Too hard for me!
The clue points to the Tasmanian Devil, damn it. Think !
Um, Tasmanians? Or rather, their descendents? Like David guessed several comments ago? That’s the logical guess.
If so, looks like we have a picture of what a Neanderthal might have looked like. If not, then I think we’re going to need another clue.
Taz devils have been in the news for their transmissible tumors. Are you suggesting that living sapiens could bear transmissible tumor lineages acquired from neanders? I hear that tazzies are apparently almost uniform at MHC loci, but “Canine Transmissible Venereal Tumor” appears to pass between MHC-diverse dog hosts, and has even been claimed to be closer to wolves than to dogs:
http://www.iayork.com/MysteryRays/2007/10/11/creepy-cancer-post-of-the-month/
I think the latter would suggest that it actually crossed from wolves into dogs. If you suppose that it had instead gone all the way down the wolf-to-dog path in tandem with the original wild ancestors of dogs, then you must conclude that it has a lower mutation rate than the wolf-dog lineage. But being a cancer, it should – I think – have a higher mutation rate than the wolf-dog lineage.
Oops, I messed up: I’ll stick with my first paragraph, but nevermind my second paragraph. A transmissible tumor lineage that originated in wolves wouldn’t be having “sex” with the wolf-to-dog lineage germline (or the germline of any other lineage). So it should go off through sequence space in its own independent direction, and the lineage infecting dogs should remain closer to wolf than to dog, even if it passages through canids all the way from its wolf origin down the entire wolf-to-dog lineage. So a jump from wolves to dogs is not supported and not parsimonious.
The general idea is that host cell line infections can occur (TVT, Tasmanian devil facial tumor, and a contagious leukemia in Syrian hamsters), can mutate into something that is nonlethal and/or chronic if selection favors that (TVT usually goes away with time), can infect related species (TVT can be experimentally transmitted to wolves, jackals, coyotes and red foxes), and might exist in humans today. There are human diseases that appear infectious for which the transmissible agent has not been identified – sarcoidosis, for example.
So modern humans might suffer from infectious organisms directly derived from Neanderthals or other archaic humans. As far as I know, no one has yet thought of looking for Neanderthal-derived cells inside people.
Since such cells would have the required genetic code for making human signal molecules, they might be particularly likely to employ baroque forms of host manipulation. I’ll leave that topic as an exercise for my readers.
I hate to wind up your overclocked ego, but that is by far the most fucked up idea I have ever heard. In a good way of course; it is after all a far-from-impossible idea for pathogenesis, for all I can tell. I would never have thought of that in a million years without the clues. What kind of crack are you on and where can I pick some up?
A goddamn NEANDERTHAL infection? Dude, that is soooooooooo gross!
Since dispersal is the main cause of stable virulence for an infective agent, I guess that’s the key angle for evaluating whether a very-low-virulent transmissible tumor could exist, ja?
So any word on when the book will be published? I have a certain lefty friend I would love to give it to as a Christmas gift for the section on Ashkenazi intelligence alone.
Greg, the idea is plausible enough but aren’t these things just as likely to be from non-archaics? Or do you think that they’d have to be old in order to have evolved to hide themselves well?
The book is supposed to come out January 25th, but you can preorder a copy from Amazon for your friend.
Matt: of course, a cell line infection could have originated from modern humans, even from your cousin Frank last year. And that must be far more likely: in fact, with the big world population and relaxed sexual mores, the probability of generating such an infection must be higher than ever before. However, there _could_ be Neanderthal-derived cell line infections, and this is really the only scenario I’ve been able to come up with that gives us live Neanderthals – hiding in your sinuses, or maybe your prostate. The only one so far.
There are other known infectious diseases in which some metazoan has completely chucked complexity and gone back to being a germ: whirling disease in fish, for example.
I’m starting to think this book from Cochran and Harpending might turn out to be kind of interesting. Maybe I’ll take a look at it some night if there’s nothing good on TV.
How to seek for amoebic neanderthals? Wouldn’t there be a ton of mutations in a tumor that old? Hence you don’t really know what PCR primers to try, because a given sequence from neanders might no longer be intact in the tumor. So how about just using many different primers all at once; it doesn’t matter how many, as long as they all fail to amplify sapiens DNA.
Also, it would be good to look in a lot of different species, not just humans, since any low-virulence transmissible tumor would be a very important discovery, not just a neanderthal one. If they exist, and humans have them, they would be a possible etiology for any autoimmune disease or basically any complex disease, especially if the disease has a high fitness load.
If you wanted to look for a tumors whose progenitor is the same species as the host species, you could MHC-type a bunch of individuals, then use PCR to check each individual for MHC sequences foreign to that individual.
These Neanderthal infections, they’d probably still have Neanderthal mitochondria, right?
Cochran,
What’re the odds some recently extinct species, moa birds maybe, or passenger pigeons, are actually still around as infections and could be resurrected?
We have some reconstructed Neanderthal mtDNA, and Neanderthal tumors should still have Neanderthal mitochondria. we can do PCR for the mtDNA to screen lots of tissue samples.
If living cells can be distinguished by mtDNA or mitochondrial features, maybe whole, live Neanderthal cells can be isolated.
Host manipulation eh?! The possibilities are interesting.
When it comes to resurrecting moas and stuff, the problem would be a lack of purifying selection on all the morphogen genes, not to mention all the neuron-specific genes, etc. The tumor doesn’t need any of that stuff. How fast they would all turn to garbage, I don’t know. Probably pretty fast.
It’s pretty hard to guess from theory how likely it is that hypo-virulent transmissible tumors exist. There don’t seemt to be a lot of high-virulent TTs, though there could certainly be more out there that we don’t know about. You can read a lot about virulence theory on Bruce Levin’s website, where he has a lot of his papers. Until about a generation ago most people thought virulence belonged to poorly adapted parasites, and that all parasites should evolve monotonically to avirulent commensalism – why harm the host, the parasite’s resource and home? To some extent this is true. But this is naive, because you may have to break a few eggs to make an omlette – spread to new hosts, that is (or other favorable enviroments, since not all parasites are obligate). There is often a stable trade-off between hurting the host and spreading. Not every parasite is on an evolutionary trajectory where virulence should progressively approach zero.
I suspect that another aspect of virulence may be competition. This occurs most when immunity is strongest. For some infections there is sterilizing immunity, and an infected host eventually becomes totally immune. If you and I are two strains of some parasite, then it is not much good cosseting the host – I don’t have an indefinite amount of time to get into the clean hosts, because if you get there first, I am excluded. This can probably produce a pressure towards higher virulence. For many taxa of parasites, the immune response is not terribly effective, and superinfection by multiple strains can occur without too much disadvantage to any of the strains.
There are at least a couple other causes of virulence, but I don’t think they apply much to this question. So if low-virulent tumors can spread and survive, they will exist. To do this, they will first of all have to be potent. Syphilis, perhaps largely because of its low immunological visibility (see J Radolf), is extremely potent – injecting about 5 organisms into your skin makes you about as likely to come down with syphilis as not. For many parasites the median infective dose is more like a zillion. If it can be potent, it doesn’t need to grow to very large numbers in the host, which is good because that usually makes a mess of the host. If it can make an efficient egress from the host, by provoking coughing, moving into bodily fluids, replicating to gonzo levels in some disposable vector-host like a mosquito – that also helps.
TTs certainly have a ton of DNA to work with, as GC pointed out, and the corresponding proteins already fit the host ones like a glove. That point probably favors the possibility of their being able to do well with low virulence. Also, since many, probably most genes are suddenly released from purifying selection, that means they are free to do whatever needs doing.
The biggest black box here, is that normal tumors don’t passage between hosts. That’s why they are so extremely ugly and indisciplined in their acts – a herpesvirus would blush, I think. Normal tumors aren’t an organism; TTs are. So the virulent TTs are our only window on what level of stealth and sophistication tumors are perhaps capable of. A small window. The crassness of normal tumors doesn’t really tell us anything.
Amoebic neanderthals swarming around in my blood, good grief, I still can’t get over it. Science is way too cool, I’m not sure how people used to get by without it.
Hey, there may be a problem here for this whole idea: a lot of MHC typing is already done, so if very-low-virulent transmissible tumors exist, why haven’t they been detected yet? If a mammal is infected with a conspecific transmissible tumor, the latter will rarely have the same MHC alleles as its host, since there are, eg, 300+ MHC-I alleles in man; they are the most diverse loci, by miles and miles, in essentially all vertebrates. Thus, the tumor-infected mammal will look like it has an excessive number of MHC alleles. (As a human you ought to have three MHC-I and three MHC-II loci.)
R_White_Paper_Jill_Henault.php
Formerly, all MHC typing was serological or immunological – which both mean the same thing, recognition of a protein using specific antibody (which is typically conjugated to eg some enzyme that makes some indicator substance become colored, that’s how you see it, you get a nice spot). Any TT that infects a mammal should be a real minority of the mass of the mammal, so the tumor’s alleles proabbly won’t show up in any antibody based method. 1/1000 of a spot just looks like background noise – some antibody got stuck to the surface; they do that.
But there is such a thing as PCR based MHC typing – using full sequences or microsatellites – and there, of course, the result is not a linear function of the amount of DNA present in the sample. For example, here is a pretty sweet graph where PCRs were run on different amounts of template man’s second best friend, Bartonella henselae – from 4 pg to 4000 pg:
http://clongen.com/Real_Time_PC
As you can see, the amount of DNA used makes a difference – otherwise there’d be no such thing as quantitative PCR. But by 50 cycles out, the amount of amplicon is basically the same for 40, 400, and 4000 pg initial template.
50 cycles seems really long to me, but I’m truly a PCR neophyte (not to mention I also suck at it). The differences are greater earlier in the reaction.
For the real answer to whether extraneous MHC alleles in various vertebrates should have been noticed already by accident using PCR, the devil is in the details. How many of the TT cells are in the blood, assuming blood is what’s used? How many cycles are done, since more cycles is more favorable for seeing really small amounts of DNA. Etc. Also, in practice, humans may be the only animal for which the knowledge base for PCR MHC typing is complete. This patent from late 2004:
http://www.wipo.int/pctdb/en/wo.jsp?IA=GB2004003906&wo=2005028672&DISPLAY=DESC
says a bunch of stuff about how sheep and cattle MHCs weren’t fully charecterised at that time. To really examine whether cryptic, near-avirulent TTs exist, you would want to look in many taxa not just one. That patent also has various references on the development of sequence based MHC typing in man and animals.
They find extraneous MHC molecules all the time, I think: main mechanisms are thought to be maternal-fetal microchimerism (look it up) and transfusions. But since male microchimerism is fairly common in women without sons, other routes such as sexual intercourse have been suggested.
The maternal transfer route could end up selecting for a symbiote, rather like the maternally transmitted bacteria that exist in many insects with specialized diets.
The emmdees are not thinking about this in terms of tvt or parasite evolution.
Late to the conversation…
First off, IMO, this is a MUST BUY book for all readers of this blog. I’ll buy it for the proposed Indo-European explanation alone!
Secondly, I’ve been thinking about a possible candidate for a TVT like disease in humans – I think it would have to infect Europeans primarily, especially Northern Europeans, and be possible spread by sexual means, as some infection. What I found was this article on Multiple Sclerosis, which meets all my criteria?!
Abstract:
The worldwide distribution of multiple sclerosis (MS) can be described within three zones of frequency: high, medium, and low. The disease has a predilection for white races and for women. Migration studies show that changing residence changes MS risk. Studies of persons moving from high- to low-risk areas indicate that in the high-risk areas, MS is acquired by about age 15. Moves from low- to high-risk areas suggest that susceptibility is limited to persons between about ages 11 and 45. MS on the Faroe Islands has occurred as four successive epidemics beginning in 1943. The disease appears to have been introduced by British troops who occupied the islands for 5 years from 1940, and it has remained geographically localized within the Faroes for half a century. What was introduced must have been an infection, called the primary MS affection (PMSA), that was spread to and from successive cohorts of Faroese. In this concept, PMSA is a single widespread systemic infectious disease (perhaps asymptomatic) that only seldom leads to clinical neurologic MS. PMSA is also characterized by a need for prolonged exposure, limited age of susceptibility, and prolonged incubation. I believe that clinical MS is the rare late outcome of a specific, but unknown, infectious disease of adolescence and young adulthood and that this infection could well be caused by a thus-far-unidentified (retro)virus.
What do you think Greg?
One way to look at microchimerism would be to just type your mom, then screen you for her other allele (the one you didn’t inherit in the proper sense). If you did that, amoebic neanderthals would slip right by. But here’s at least one paper where MHC microchimerism was apparently sought without looking only for the maternal alleles; they screened for many or all the alleles of the locus. Eight of the microchimeric subjects’ mothers were typed, and all the micrografts turned out to match maternal alleles. Thus, if people carry TTs, it would seem that the TT cells must be a lot less concentrated in the blood than these maternal micrografts are. Or maybe people with TTs are just rarer.
.oxfordjournals.org/cgi/content/full/40/11/1279
However, I just realized that TT MHC loci could be severely mutated. In that case, how would you ever detect the TTs? You would have to look for polymorphisms in some housekeeping gene under strong purifying selection, I guess. The MHCs might be under purifying selection themselves in TTs, since one of the functions of NK cells is supposed to be to zap any cell not expressing MHCs. But in that blog post of Ian York’s that I linked to above (it’s an awesome pathobio blog by the way), he says CTVT expresses very little MHC, and that the same is true of many normal tumors. In principle, any tumor might have some other way of avoiding lysis by NK cells, and then it wouldn’t need MHC.
HLA Cw analysis was performed with 12 µg extracted DNA by a sequence-specific primer method according to Artlett et al. [12]; each sample was tested once. The method used 23 polymerase chain reaction (PCR) reactions, which analysed 17 HLA Cw alleles. Ethidium bromide staining following electrophoresis in 1% agarose gels identified the resulting PCR products. The two intense bands of the PCR products were assigned as the inherited genotype, whereas a weaker third band was classified as the microchimeric allele.
[...]
The mothers of eight JIIM patients with evidence of microchimeric Cw alleles were also HLA Cw-typed, and the additional allele present in the patients was confirmed to be identical to a maternal Cw allele in all cases tested (Table 2Go).
http://rheumatology
pconroy
For what it’s worth you can’t get Multiple Sclerosis unless you’ve been infected with Epstein Barr Virus.
Glandular fever link offers hope of vaccine for MS
The findings add weight to theories that EBV plays a role in triggering MS. Previous studies have shown that people who have never been infected with EBV do not develop MS, and a study last year found the brains of MS patients had abnormally high numbers of EBV-infected cells.