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Thread: The mystery of Lactase Persistence (LP) in Europeans

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    I sometimes take scientific articles to seriously, but it's probably good to reference the actual references within in the article. Thanks Angela. I can't find the reference supplied by the article that talks about 6500 year claim of LP in a Northern German ancient man. I don't know if Andrew Curry made it up or if he didn't cite his work correctly, or if it's buried in one of his listed sources. Does somebody know the actual study that the article is propagating?

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    Quote Originally Posted by ebAmerican View Post
    I sometimes take scientific articles to seriously, but it's probably good to reference the actual references within in the article. Thanks Angela. I can't find the reference supplied by the article that talks about 6500 year claim of LP in a Northern German ancient man. I don't know if Andrew Curry made it up or if he didn't cite his work correctly, or if it's buried in one of his listed sources. Does somebody know the actual study that the article is propagating?


    I tried to find a Burger et al paper where he states that a sample from 4500 B.C. in Central Europe carried the lactase persistent gene but nothing turned up.

    In fact, the only paper of his that I could find that talked about ancient Central European DNA in this context said that it didn't show up in any of those samples tested. He does state that based on some computer modeling it might have been present at low levels around 4500 B.C., but that's not quite the same thing.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1820653/

    This isn't to say that such a paper doesn't exist...it's just that I couldn't find it.

    This is Jean Manco's page on ancient autosomal results for this marker. The earliest it shows up seems to be 3300 B.C., which I suppose according to some analysts might be recent enough for an Indo-Euopean input. She's always meticulous about things like this, but I don't know how recently the page was updated.
    http://www.ancestraljourneys.org/aut....shtml#lactase

    Sorry I couldn't find anything more definitive.


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    Quote Originally Posted by martiko View Post
    Yes ! the race for meat closer to the Auroch but the mestizo who give European dairy cows. You can still see the difference today
    and it is in Europe that are created Varietal dairy with lactose intake at the time of europeanNeolithic
    That is not correct, at least for the British cattle, as I already pointed out. Some of the British dairy cattle are marked with green and some of of them are marked with red, and some of the British beef cattle are marked with green and some of them are marked with red. However, I'm not familiar enough with other European breeds of cattle to know whether red and green indicate cattle type in Germany or France or wherever.

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    1 out of 1 members found this post helpful.
    Quote Originally Posted by Greying Wanderer View Post
    @Angela

    ..................

    @Aberdeen

    "
    I feel better when I have more dairy in my diet. And although my Y haplotype is I1, I can't help but wonder how many of my indirect paternal ancestors were R1b."

    The highest rates of LP overlap with the highest rates of I1. It's not just a descended from R1b thing. It's a descended from [regions where milk was a particularly critical part of the diet in the neolithic] thing.

    http://img534.imageshack.us/img534/6959/lactose.png

    http://2.bp.blogspot.com/-lhXgXOSp_a0/UKljuK_d9AI/AAAAAAAAABM/gB_lmZj0Jqc/s1600/792px-Distribution_Haplogroup_I_Y-DNA.svg.png



    That's true, to some extent. Although there's a lot of R1b in Sweden, there's more I1. And there's little R1b in Finland and a lot of I1. But the most common Y haplotype in Finland is N, and yet Finland has a very high rate of lactase persistence. I find that interesting, but I'm not sure what it means. I'd like to know the rate of lactase persistence among folk with high rates of Y haplotype N in Siberia.

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    1 out of 1 members found this post helpful.
    @Aberdeen

    "But the most common Y haplotype in Finland is N, and yet Finland has a very high rate of lactase persistence. I find that interesting, but I'm not sure what it means."

    I think it means regions on the forward edge of the advance of agriculture where for some reason milk can partially compensate for crops not yet being adapted to the local climate select strongly for LP regardless of y DNA.

    So wherever LP started from it could exist in many populations at a low to moderate level and then have a dramatic sweep in the right conditions.

    .

    "
    That is not correct, at least for the British cattle"

    Either way the distinct Atlantic distribution is interesting.

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    Quote Originally Posted by Greying Wanderer View Post
    @Aberdeen

    "But the most common Y haplotype in Finland is N, and yet Finland has a very high rate of lactase persistence. I find that interesting, but I'm not sure what it means."

    I think it means regions on the forward edge of the advance of agriculture where for some reason milk can partially compensate for crops not yet being adapted to the local climate select strongly for LP regardless of y DNA.

    So wherever LP started from it could exist in many populations at a low to moderate level and then have a dramatic sweep in the right conditions.

    .

    "
    That is not correct, at least for the British cattle"

    Either way the distinct Atlantic distribution is interesting.
    So I guess you're assuming that once a mutation causing lactase persistence occurs, it remains, even if the amount of lactose consumption subsequently decreases. That seems likely, but I don't know how one would prove or disprove that idea.

    As far as the map is concerned, I find data to be useful only if it's accurate.

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    Quote Originally Posted by Aberdeen View Post
    So I guess you're assuming that once a mutation causing lactase persistence occurs, it remains, even if the amount of lactose consumption subsequently decreases. That seems likely, but I don't know how one would prove or disprove that idea.

    As far as the map is concerned, I find data to be useful only if it's accurate.
    Mathematically, I guess, frequency of mutation of single gene multiplied by population numbers, in function of time. Without environmental selection, the only law is the luck, the chance, randomness. One should be able to calculate time frame of complete disappearance ( or below 1% level) of LP allele.

    It's like we can't prove who is going to die in car accidents, we can't print the names of unlucky ones in advance, but we can statistically calculate number of deaths for a country to one percentile precision.
    Be wary of people who tend to glorify the past, underestimate the present, and demonize the future.

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    Aberdeen : Mt DNA H1, H3, T1 are LP.
    We can assume that many Scandinavians : H1, H3, T1 as Irish, Basque, English...

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    Quote Originally Posted by Aberdeen View Post
    So I guess you're assuming that once a mutation causing lactase persistence occurs, it remains, even if the amount of lactose consumption subsequently decreases. That seems likely, but I don't know how one would prove or disprove that idea.
    No, I'm just avoiding the argument about where LP arose as it's not relevant to the main point about the development of a cattle-centric culture with a milk-heavy diet on the forward edge of farming. LP might well have evolved and disappeared many times but we know it arose somewhere and lasted long enough for it to somehow spread to fixation in certain regions of Europe.

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    just a document (link) concerning Meso-Neolithic transition in Britain and ireland

    arheologija.ff.uni-lj.si/documenta/pdf31/31thomas.pdf‎

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    1 out of 1 members found this post helpful.
    Mongols are very interesting example of high dairy diet, and surprisingly only being around 30% lactose persistent. (if all the maps are correct).

    This is from the trip of Lieutenant-Colonel Nikolai Mikhailovich Przhevalsky in 1870:
    Milk and Meat

    "The food of the Mongols also consists of milk prepared in various ways, either as butter, curds, whey or koumiss. The curds are made from the unskimmed milk, which is gently simmered over a slow fire, and then allowed to stand for some time, after which the thick cream is skimmed off and dried, and roasted millet often added to it. The whey is prepared from sour skimmed milk, and is made into small dry lumps of cheese. Lastly, the koumiss is prepared from mares' or sheep's milk; all through the summer it is considered the greatest luxury, and Mongols are in the habit of constantly riding to visit their friends and taste the koumiss till they generally become intoxicated. They are all inclined to indulge too freely, although drunkenness is not so rife with them as it is in more civilized countries.
    "Tea and milk constitute the chief food of the Mongols all the year round, but they are equally fond of mutton. The highest praise they can bestow on any food is to say that it is ‘as good as mutton.' Sheep, like camels, are sacred; indeed all their domestic animals are emblems of some good qualities. The favorite part is the tail, which is pure fat.

    When it comes to "white foods" (anything made from milk), almost everything is heated due to the brucellosis problem within the country. The only thing that they commonly drink raw is mare's milk just taken from the mare when it is still warm. I have had it and it is quite tasty. They all want to drink the milk from a white mare for health reasons. They will drink from any mare, but the most sought after is a white mare

    Looks like they used to have diet only made of dairy and meat. Makes you think how they manage doing it without being lactose tolerant. Granted they consume most dairy as cheeses and butter, but in quantities they do one would think they should be lactose tolerant.
    One explanation is that they must have adequate bacterial flora in their digestive organs to help them deal with all the lactose, or we are missing one more gene or allele taking part in lactose digestion.

    If it is about bacterial flora, it would be a good news for people who are not LP but like eating dairy. Start with small quantities of natural products containing good bacteria. With time build up consumption and your good bacterial flora will grow together adequately.

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    Quote Originally Posted by LeBrok View Post
    Mongols are very interesting example of high dairy diet, and surprisingly only being around 30% lactose persistent. (if all the maps are correct).

    This is from the trip of Lieutenant-Colonel Nikolai Mikhailovich Przhevalsky in 1870:


    Looks like they used to have diet only made of dairy and meat. Makes you think how they manage doing it without being lactose tolerant. Granted they consume most dairy as cheeses and butter, but in quantities they do one would think they should be lactose tolerant.
    One explanation is that they must have adequate bacterial flora in their digestive organs to help them deal with all the lactose, or we are missing one more gene or allele taking part in lactose digestion.

    If it is about bacterial flora, it would be a good news for people who are not LP but like eating dairy. Start with small quantities of natural products containing good bacteria. With time build up consumption and your good bacterial flora will grow together adequately.
    As you say, if they don't have an as yet undiscovered LP gene, something else is going on, since even if each individual food might be low in lactose, the total must be pretty high. I wonder what foods would be important for development of this intestinal flora?

    On a somewhat related note, I read an article the other day about the fact that there seems to be an ever increasing number of people in the U.S. who can no longer digest dairy. The author was speculating that it might have to do with the fact that all the milk is ultra-pasteurized. I have no idea if that would have an effect, but if it does, what irony if the process that made it safer should make it indigestible for certain people.

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    Quote Originally Posted by Angela View Post
    As you say, if they don't have an as yet undiscovered LP gene, something else is going on, since even if each individual food might be low in lactose, the total must be pretty high. I wonder what foods would be important for development of this intestinal flora?

    On a somewhat related note, I read an article the other day about the fact that there seems to be an ever increasing number of people in the U.S. who can no longer digest dairy. The author was speculating that it might have to do with the fact that all the milk is ultra-pasteurized. I have no idea if that would have an effect, but if it does, what irony if the process that made it safer should make it indigestible for certain people.
    I'm thinking along same lines, plus who knows what damage the overuse of antibiotics do to our digestive system.
    Some lines of useful digesting bacteria, adapted to way of lives of our ancestors and their guts, might be gone forever. (just a thought).

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    The British Royal Society has published a paper showing that some Finns were using milk products 4500 years ago, which seems like quite an early date. The abstract and a link to the full article (free) is here.

    http://rspb.royalsocietypublishing.o...40819.abstract

    And here's a copy of the abstract.

    "The conventional ‘Neolithic package’ comprised animals and plants originally domesticated in the Near East. As farming spread on a generally northwest trajectory across Europe, early pastoralists would have been faced with the challenge of making farming viable in regions in which the organisms were poorly adapted to providing optimal yields or even surviving. Hence, it has long been debated whether Neolithic economies were ever established at the modern limits of agriculture. Here, we examine food residues in pottery, testing a hypothesis that Neolithic farming was practiced beyond the 60th parallel north. Our findings, based on diagnostic biomarker lipids and δ13C values of preserved fatty acids, reveal a transition at ca 2500 BC from the exploitation of aquatic organisms to processing of ruminant products, specifically milk, confirming farming was practiced at high latitudes. Combining this with genetic, environmental and archaeological information, we demonstrate the origins of dairying probably accompanied an incoming, genetically distinct, population successfully establishing this new subsistence ‘package’."

    However, when you read the whole article, the picture seems to be more complex. I'm too tired to study it carefully tonight, but it seems to be worth a read.

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    I think the interesting thing about this study is that it seems to disprove the idea that dairy farming is a fairly recent phenomenon in Finland. The Comb Ware sherds from 3900-3300 B.C. contained residue that indicated a hunting-fishing-foraging economy, with marine lipids being the most common. However, the Corded Ware sherds from 2500 B.C. contained traces of animal remains and, in the case of the drinking vessels, milk fats. Only one Corded Ware vessel showed traces of marine material, and it apparently had the closest proximity to the sea of all the Corded Ware sherds examined.

    The paper also states that:
    "The Final ‘Neolithic’ Kiukainen culture, whose ceramic inventory shows similarities with Late Corded Ware and local hunter–fisher–forager ware (Pyheensilta Late Comb Ware), is believed to be a cultural amalgamation emerging locally during a period of climatic deterioration [20,32]. While the low number of residues recovered makes interpretation preliminary, this intriguingly appears mirrored in the pottery residues, because the fatty acid stable carbon isotope values fall along a mixing line between ruminant and non-ruminant/marine products."

    And:

    "Finally, residues from Early Metal Age pottery (ca 1200–500 BC) all derived from dairy fats. Increasing population size despite the continuing climatic deterioration of the Late Holocene is believed to have arisen from the intensification of agriculture by the later Metal Ages which overcame environmental constraints upon population size. Certainly, such a scenario of established stock-rearing would be supported by the prevalence of dairy fats in the pots."

    So, when we try to determine why lactose tolerance is so common among Finns, it seems to me that one factor is that lactose has been consumed by Finns for a very long time, contrary to what some people have assumed. Using lactose regularly promotes lactose tolerance.


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    A well readable and highly interesting essay:
    https://cuwhist.files.wordpress.com/...love-story.pdf.

    The peak distribution of lactase persistence matches an area also showing the highest diversity of cattle milk genes. Notably, this region corresponds to the land of the Neolithic farmers of the Funnel Beaker Culture from the third millennium BC suggesting a remarkable gene-culture co-evolution. (..)
    From a purely nutritional side it is therefore not clear why such an extremely strong selective advantage is conferred by the lactase persistence phenotype. However, this mutation is characteristic for cultures that share the traits of animal domestication and adult milk consumption. Pastoralist populations in Africa also display the lactase persistence phenotype (90% in Tutsi, 50% in Fulani), they likewise show haplotype homozygosity extending for > 2 Mb around the lactase gene. The changes are again point mutations in the lactase enhancer region, but they are molecularly distinct from those found in European people (G/C-14010, T/G-13915, C/G-13907) (Tishkoff et al., 2007). We have here a remarkable case for convergent adaptive evolution. Is it possible that the lactase-associated haplotype is adaptive for something else in addition to fresh milk digestion? Might it confer protection against infection like another sugar-degrading enzyme, glucose-6-phosphate dehydrogenase, against malaria? (..)
    The close contact between domesticated animals and the farmers created problems: humans were in too close contact with sick animals and trans-species infections became much more likely. The hunter met his prey only at distance and when he could touch the prey, the animal was already dead. All the mechanisms, which microbes induced in the infected host to assure their transmission like sneezing, coughing or diarrhoea are not any longer operative in the dead animal. The farmer probably also discovered quite early the value of animal dung for burning and as fertilizer on the field, which recycles animal pathogens into the human food chain. We can thus safely anticipate that the early farming society was plagued by new diseases (Diamond, 1997). Zoonosis was feeding new pathogens into the human population (Weiss, 2001).
    Notably, important human pathogens, which happen to belong to the most transmissible agents like measles and smallpox, have their closest relatives in viruses from domesticated animals. Sequence analysis revealed that measles, which today circulates exclusively in the human population, is a close relative of rinderpest virus of cattle and the Peste des petits ruminants virus of sheep and goat (all belong to the morbillivirus group of paramyxoviruses) (Griffin, 2001; Lamb and Kolakofsky, 2001). If viruses had co-evolved with their hosts during evolution, we would expect the closest relatives of measles virus in paramyxoviruses of primates. In the morbillivirus group only a Tupaiavirus is known, but the systematic attribution of tupaias (tree shrews) to the primates is disputed (some zoologists classify them with the insectivores). (..)
    The close relationship of smallpox (variola) virus (Moss, 2001) with the cowpox virus permitted one of the biggest success stories of medicine. Milkmaids who had acquired cowpox were resistant to smallpox. Based on this observation, Jenner developed modern vaccination by inoculating cowpox lesion material into humans. The very name vaccination recalls the cow (Latin vacca) and underlines again the close relationship between a human and a bovine virus. The precise origin of the vaccinia virus is not known. In fact smallpox seems to have emerged perhaps 5000 years ago presumably from wild animals like rodents (Esposito et al., 2006). Cattle are only an intermediate host. However, this does not change the argument. Rats and mice, attracted by the cereal stores of the early farmers, belong as a pest also to the undesired content list of the Neolithic package like fleas and lice. The closest existing relative of smallpox is camelpox, but this does not go against the argument either since camel bedouins also have developed lactase persistence characterizing them as members of the dairy cultures. After the eradication of smallpox, cases looking like smallpox have been traced to monkeypox, demonstrating ongoing trans-species infection and a possible reservoir independent of dairy animals.
    Another paper that I have read (unfortunately not bookmarked) notes the paucity of Mesolithic HG remains in certain entrance areas of EEF (e.g. parts of Italy, Bohemia), and speculates on an "American" scenario, whereby some early "scouts" had transmitted yet unknown diseases onto the "natives". The paper also notes that certain areas, notably Iberia, withstood Neolithic immigration for a sustained period. Since bats are a common disease reservoir, as demonstrated by SARS or Ebola, the theory was put forward that cave-dwelling HG populations had already received immunity from occasional contact with bats, and thus could withstand (some of) the EEFs infectious pressure
    In this sense, one could also speculate that HGs in the North European plain had built up resistance against certain diseases. Note that Bad Segeberg in Schleswig-Holstein has the highest European bat population today, though (migratory) birds, including geese, are also a relevant virus reservoir. So, NW Europeans might already have been immunised (probably including some genetic selection process) against certain potentially cattle-transmitted diseases - a trait new entrants from the Balkan lacked. Or, alternatively, bush and forest cleaning drove bats closer to farm-sites, where they encountered cattle (typically grazing in open forests), and spread their diseases via them to the farmers. Mesolithic HGs along the North and Baltic Sea are known to have cultivated hazelnut, so squirrels are an alternative potential disease vector. Smallpox, which are supposed to have originated from rodents, could particularly be of an issue here.

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    1 out of 1 members found this post helpful.
    Quote Originally Posted by FrankN View Post
    A well readable and highly interesting essay:
    https://cuwhist.files.wordpress.com/...love-story.pdf.



    Another paper that I have read (unfortunately not bookmarked) notes the paucity of Mesolithic HG remains in certain entrance areas of EEF (e.g. parts of Italy, Bohemia), and speculates on an "American" scenario, whereby some early "scouts" had transmitted yet unknown diseases onto the "natives". The paper also notes that certain areas, notably Iberia, withstood Neolithic immigration for a sustained period. Since bats are a common disease reservoir, as demonstrated by SARS or Ebola, the theory was put forward that cave-dwelling HG populations had already received immunity from occasional contact with bats, and thus could withstand (some of) the EEFs infectious pressure
    In this sense, one could also speculate that HGs in the North European plain had built up resistance against certain diseases. Note that Bad Segeberg in Schleswig-Holstein has the highest European bat population today, though (migratory) birds, including geese, are also a relevant virus reservoir. So, NW Europeans might already have been immunised (probably including some genetic selection process) against certain potentially cattle-transmitted diseases - a trait new entrants from the Balkan lacked. Or, alternatively, bush and forest cleaning drove bats closer to farm-sites, where they encountered cattle (typically grazing in open forests), and spread their diseases via them to the farmers. Mesolithic HGs along the North and Baltic Sea are known to have cultivated hazelnut, so squirrels are an alternative potential disease vector. Smallpox, which are supposed to have originated from rodents, could particularly be of an issue here.
    I don't think "American" scenario makes much sense in Europe. Europe never was disconnected and insulated from the rest of the world, the way America or Australia is. As you know yourself, in Eurasia there was always a trading network between different groups of hunter gatherers or with farmers, therefore "free flow" of new diseases between them. Surely, it didn't work as fast as in modern world but what is a decade or two, just a small delay. At least European HG were not pummeled by barrage of new diseases, as Americans were when Europeans arrived.


    There is a mystery though, if it comes to American/Europen first contact. The new diseases should have worked both ways, as Europeans were not immuned much to American strains either. But it didn't work both ways. Could it be a matter of bad luck for American Natives?

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    Quote Originally Posted by LeBrok View Post
    I don't think "American" scenario makes much sense in Europe. Europe never was disconnected and insulated from the rest of the world, the way America or Australia is. As you know yourself, in Eurasia there was always a trading network between different groups of hunter gatherers or with farmers, therefore "free flow" of new diseases between them. Surely, it didn't work as fast as in modern world but what is a decade or two, just a small delay. At least European HG were not pummeled by barrage of new diseases, as Americans were when Europeans arrived.

    There is a mystery though, if it comes to American/Europen first contact. The new diseases should have worked both ways, as Europeans were not immuned much to American strains either. But it didn't work both ways. Could it be a matter of bad luck for American Natives?
    It comes with farming, The first evidence of animal-related diseases is Tuberculosis identified in remains of 7,000 BC Greek early farmers. Farming populations gradually build up resistance, by means of an intensive selection process (so their population drops, goes up again, drops, etc.), and after some time they are immune but still carry the germs. The biggest killer of all, btw., is still today the flu (via poultry, pigs, but also cattle), but most Europeans now survive it. Native Americans didn't. And by 6,000 BC, HGs were still quite isolated, and met East Mediterranean early farmers that already had gone through 1-2 millenniums of genetically building up resistance.

    Europe had "American" moments with the plague, which seems to be endemic around the Himalaya, with the Antonine Plague (probably a henceforth unknown strain of smallpox or measles), most likely also when Malaria was imported into the Mediterranean from Sub-Saharan Africa by migrants (the Anopheles mosquito was probably already around, but it only starts transmitting after it has bitten an infected person).
    There is a nice study in German on diseases they identified in Slovakian and East German bronze-age grave fields: Lepra, Syphhillis, Borrelliose / Meningitis, 50% with chronical respiratory infections (possibly also due to the flu), and around 25% with symptoms of arsenic poisoning from working with arsenic bronze, or, especially the women, carrying arsenic bonze necklaces and earrings. Quite a lot of Vitamin B and C shortage as well (actually the first problem encountered by early farmers when they switch to a cereal-based diet, the second one is caries).

    America had few domesticized animals, little possibility to build up resistance. There's one exception - the turkey, which was found to be the host of SARS. But the SARS virus is closely related to others that are found in pheasants, cats, mice, rats, and various seagulls, so many Europeans (especially from the coast) might already have had developed some basic resistance. However, compare this to records of the first Europeans travelling to south and south-east Asia ("fewer-hell" etc.).

    Read my linked article - its all in there (well, mostly, you can in addition check out Wikipedia pages on various diseases, they typically include a section on history).

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    I found that paper again. The "Mesolithic HG disappeared already before massive settlement of EEF" is just the introduction. It's mainly about a special allele,
    http://dro.dur.ac.uk/9368/1/9368.pdf
    Though some diseases, such as tuberculosis, are observable from archaeological skeletal remains (Roberts & Buikstra 2003), most zoonoses are not so detectable, even by ancient DNA analysis (Barnes & Thomas 2006). There is, nevertheless, evidence of rapid selection for genetic resistance to one or more of these diseases during the last 7000 years or so (Wolfe et al. 2007).
    We suggest that a prime genetic candidate for this resistance is CCR5-32, a mutant allele of the CCR5 gene. Normally, this gene encodes the lymphocyte transmembrane coreceptor to which HIV can bind (Dean et al. 1996; Liu et al. 1996), enabling the virus to infect CD4 lymphocytes. In people homozygous for the CCR5-32 allele, however, the truncated CCR5 does not reach the cell surface, thus preventing access to HIV.

    The CCR5-32 allele is found in 10–15% of people of Northern European descent and is rare or absent in those of Asian or African descent (O’Brien et al. 2008). Within Europe there is a north to south gradient in its distribution with highest frequencies being found in Finnish and adjacent Russian populations, suggesting that the original mutation producing this allele took place in north-east Europe (Libert et al. 1998). Mesolithic DNA from southern Sweden dates the allele to around 7000 years ago, suggesting it originated in Mesolithic populations, and yet achieved a frequency of 17% in Swedish Neolithic populations (Liden et al. 2006).To increase in frequency so rapidly implies considerable selection pressure. The Early Neolithic was a time of unique new selection pressure; the gene-culture co-evolution of Neolithic subsistence farmers with persistent lactase production enabling lactose tolerance occurred through strong selection for the T-13910 allele that exists among most modern Europeans, but which was negligible amongst the earliest Neolithic Europeans (Burger et al. 2007; Itan et al. 2010).
    Among the diseases CCR5-32 allele may originally have conferred resistance against, HIV-1 is an unlikely candidate because it is thought to have originated in early twentieth century Central Africa (Korber et al. 2000; Vidal et al. 2000). However, CCR5-32 may also protect against pox viruses that, like HIV, gain entry to leucocytes by using chemokine receptors (Lalani et al. 1999).Galvani and Slatkin (2003) suggested that children, being immunologically naiıve, were more likely to be killed by smallpox, which selected against those without the protective CCR5-32 allele, thus increasing its frequency in populations.

    If diseases such as smallpox had been brought to Europe via Neolithic spread, it would be ironic if LBK populations gained CCR5-32 frequency through intermarriage with certain north European Mesolithic groups, who were already carriers of the CCR5-32 allele (Liden et al. 2006). This could explain the relative survival of some Mesolithic groups while others, lacking both CCR5-32 and the more general resistance of Neolithic groups, perished.
    A nice and short overview on farming and health is here:
    http://riversong.wordpress.com/healt...d-agriculture/


    And a good Wikipedia article: http://en.wikipedia.org/wiki/Social_history_of_viruses

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    1 out of 1 members found this post helpful.
    Quote Originally Posted by FrankN View Post
    It comes with farming, The first evidence of animal-related diseases is Tuberculosis identified in remains of 7,000 BC Greek early farmers. Farming populations gradually build up resistance, by means of an intensive selection process (so their population drops, goes up again, drops, etc.), and after some time they are immune but still carry the germs. The biggest killer of all, btw., is still today the flu (via poultry, pigs, but also cattle), but most Europeans now survive it. Native Americans didn't. And by 6,000 BC, HGs were still quite isolated, and met East Mediterranean early farmers that already had gone through 1-2 millenniums of genetically building up resistance.
    I heard that few times but I don't really buy it. Domesticated animals, especially at the beginning of farming, were exactly the same as their wild cousins. HG had contact with them all the time and if unlucky they caught infections from them. They were actually infested with parasites all the time; hookworms, brainworms, flatworm, etc. Wild boar was always the favorite food of HG of central europe. I'm sure they didn't need to wait till Neolithic to catch the flu.

    Europe had "American" moments with the plague, which seems to be endemic around the Himalaya, with the Antonine Plague (probably a henceforth unknown strain of smallpox or measles), most likely also when Malaria was imported into the Mediterranean from Sub-Saharan Africa by migrants (the Anopheles mosquito was probably already around, but it only starts transmitting after it has bitten an infected person).
    There is a nice study in German on diseases they identified in Slovakian and East German bronze-age grave fields: Lepra, Syphhillis, Borrelliose / Meningitis, 50% with chronical respiratory infections (possibly also due to the flu), and around 25% with symptoms of arsenic poisoning from working with arsenic bronze, or, especially the women, carrying arsenic bonze necklaces and earrings. Quite a lot of Vitamin B and C shortage as well (actually the first problem encountered by early farmers when they switch to a cereal-based diet, the second one is caries).
    I agree, no matter what continent people live on, from time to time a nasty sickness comes and can kills most of the population.

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    Quote Originally Posted by LeBrok View Post
    I heard that few times but I don't really buy it. Domesticated animals, especially at the beginning of farming, were exactly the same as their wild cousins. HG had contact with them all the time and if unlucky they caught infections from them. They were actually infested with parasites all the time; hookworms, brainworms, flatworm, etc. Wild boar was always the favorite food of HG of central europe. I'm sure they didn't need to wait till Neolithic to catch the flu.
    Influenza is actually a highly interesting case. It spreads from mammals by aerosols (sneezing), so infection risks from domesticized (living) animals are much higher than from (dead) hunting prey. Mammal viruses can survive outside the body, but on skin at 20°C for only five minutes. Thus, the risk of a south European HG of catching the flu from hunted boar (anyway only the third common prey, far behind Aurochs and deer) is minimal. An Anatolian pig or poultry farmer, OTOH, should have had quite an exposure, especially as poultry feces are also infective and may stay so for several days. Another issue here is that swine is susceptive to both bird and mammal flu, which makes it the perfect vessel for turning one variant into the other one. As such, by the time of spreading to the Central Mediterranean early farmers should already have had quite some infection history.

    Survival of mammal influenza viruses outside the body depends on four factors:
    1. Temperature: The cooler, the better. At 0°, the virus can survive up to 30 day, in ice permanently. It is killed at around 60°C.
    2. Humidity: The dryer, the better. In aerosols at 21°C, it can survive over one hour below 40% humidity, less than half an hour at 70% humidity.
    3. UV radiation: Though I haven't read details, higher levels of UV radiation also appear to reduce survival times.
    4. Medium/ surface: In sweetwater (22°) it can survive more than 4 days, 2-4 days on smooth surfaces (plastics, steel), 8-12 hours on textiles or paper, and only 5 minutes on skin (that may also be temperature-related, though).

    For these reasons, flu epidemics mostly occur during late autumn/ winter in moderate to cold climate zones. Vitamin D, production of which is stimulated by sunlight, seems to protect against influenza, and may be another factor for seasonal variation in infection.

    The main virus reservoir appear to be birds, especially waterfowl and gulls, from where it may have spread to other fowl (chicken, turkey etc.). Alternatively, deer and horses are considered (German research from 1980 found antibodies against a specific strain in wild deer, which predate corresponding human and swine infections later that year). Seals and bats appear to have similar recombination abilities as swine/boar. Aside from the aforementioned, relevant secondary hosts include whales, reindeer, sheep, goat, camels, dogs/ wolves, bears, ferrets / polecats, marten, minks, raccoons, possibly also squirrels.
    http://www.nytimes.com/2012/07/31/sc...reat.html?_r=0
    As such, I agree that north Eurasian HGs most likely had caught the flu, and developed some immunity from it, already before the entrance of early farmers. Climate is one factor here, the other one is the reliance on seal, deer, reindeer and wild horses as hunting prey. Moreover, North Eurasian HGs may have picked up flu viruses from seal-infected brackish water (Baltic Sea!), or from ice (igloo construction etc.). Domestication of wolves/ dogs as hunting or traction animals should also be considered. In fact, north Eurasian HGs' exposition, immunity and transmission potential should have been substantially higher than that of EEFs.

    The human defence against influenza is based on various antibodies that are produced in plasma cells, but also included in the mother milk to provide the infant with basic protection as long as its own immune system is still building up. In 2012, a specific antibody (FI16) that effectively blocks the cell entry of all the 16 influenza strains currently known has been isolated from a human blood donor. Another such antibody, CR6261, protective against 50% of influenza strains including the "Spanish Flu", was in 2010 successfully tested on ferrets. The distribution of the European polecat, from which ferrets were domesticated, may give an indication where that antibody originated genetically (see Wikipedia map below). I tend to say that we can exclude EEF and steppe populations from the list. No detail is given on the individuals from whom the antibodies were extracted, but both finds were reported by a Dutch research team. Details are included in the following report - maybe someone who is more into the details of genetics than I am can extract further information (responsible SNPs, etc.) from it.
    http://www.ncbi.nlm.nih.gov/pmc/arti...e.0003942.s001


    Now, let's get back to the OT. Lactose tolerance enables adult humans to take up antibodies from other mammals' milk. For influenza, cow milk is not an issue, but reindeer, horse and goat milk could be relevant. Nevertheless, drinking cow milk could enhance protection against other, cow based diseases such as pox and measles.
    Moreover, mother milk, and afterwards (to the extent it can be digested) cow milk include the highest concentration of sialic acids found in human food. Sialic acids have multiple functions in the human body, including stimulating brain growth and supporting neural transmission. They are also making up the outer part of cell membranes. Many infective organisms, including influenza viruses, but also Botulinum, Tetanus and Cholera toxins, bond themselves to those sialic acids in order to be able to release the toxine and virus RNA, respectively, into the host cell. Influenza viruses later on release a special enzyme, neuramidase, to cleave that bond in order for the replicated viruses being released and allowed to spread further.
    The mechanism is used by a number of popular flu medicaments such as Tamiflu, which essentially flood the body with synthetic sialic acids. This makes it more difficult for influenza viruses to identify cells - instead they bond to the free-floating sialic acids, and can be neutralised by lymphocytes. Moreover, the presence of free-floating sialic acids is inhibiting release of fresh viruses from the cells they are bond to. For its comparatively high sialic acid content, intake of fresh milk has essentially the same effect. One litre of fresh cow milk contains 220-300 mg of sialic acids, the bio-active content of Tamiflu (which is re-synthesized in the liver) is around 60 mg per capsule. The benefit isn't restricted to fresh milk - certain milk products, e.g. paneer, also include substantial amounts of sialic acids, while the content decreases substantially in yoghurt, cheese and especially butter (the sialic acids appear to concentrate in the whey).
    Note that not all of the 43 types of sialic acids are beneficiary. One variant, N-Glycolylneuraminic acid (Neu5GC), has been demonstrated to cause immune response and promote cancer cell growth, though most humans appear to have developed antibodies which allow for a limited intake and digestion (150 mg/day on a single occasion, no further tests done due to ethical / health considerations). Neu5GC is especially found in red meat, eggs, and goat milk and cheese, but also present in cow milk (1% of total sialic acid content). Thus, technically, flu protection comparable to one Tamiflu capsule can also be obtained by eating 450g of pork, 750g of beef fat, a kilo of lean beef, or 800g chicken meat per day. Aside from the fact that the first three possibilities should significantly increase cancer risk, consuming a quarter litre of cow milk daily might be the most easily achievable way for EEF to enhance their flu resistance.
    http://en.wikipedia.org/wiki/Sialic_acids
    http://www.ijabpt.com/pdf/57048-V.M.Biju%20(1).pdf
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC218710/


    Bottom lines & conclusions:
    1. For climatic and nutritional reasons (seal, reindeer), North Eurasian populations are likely to have been earliest and most intensively affected by influenza;
    2. The resulting process of genetic adaptation may among others have promoted lactose tolerance, which substantially increases influenza resistance. Rather than cow-herders, reindeer herders could have been the first group that effectively benefitted from the new genetic trait. Given that reindeer are also affected by small pox, it is probably no coincidence that pox resistance (CCR5-32 allele, see my previous post) has the highest prevalence in Finnish and adjacent Russian populations.
    3. Lactose tolerance became widespread when cattle-based farming reached northern Europe with the Funnelbeaker culture.
    4. Influenza prevalence in already reasonably resistant (pre-) Funnelbeaker populations should have promoted substantial influenza epidemics in less-resistant cultures further south, especially during the epi-Rössen and epi-Lengyel (Schöningen) phase (4,100-3,800 BC) when the contact intensified. These should primarily have been equestrian / maritime strains (H7N7, H3N3, H3N8) yet mostly unknown to central European farmers. The latter may of course have "paid back" with swine flu (H1N1, H3N2), but since the H1N1 strain also occurs with deer, Funnelbeaker people might have been already prepared.

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    Quote Originally Posted by FrankN View Post
    Influenza is actually a highly interesting case. It spreads from mammals by aerosols (sneezing), so infection risks from domesticized (living) animals are much higher than from (dead) hunting prey. Mammal viruses can survive outside the body, but on skin at 20°C for only five minutes. Thus, the risk of a south European HG of catching the flu from hunted boar (anyway only the third common prey, far behind Aurochs and deer) is minimal. An Anatolian pig or poultry farmer, OTOH, should have had quite an exposure, especially as poultry feces are also infective and may stay so for several days. Another issue here is that swine is susceptive to both bird and mammal flu, which makes it the perfect vessel for turning one variant into the other one. As such, by the time of spreading to the Central Mediterranean early farmers should already have had quite some infection history.
    There is no doubt that catching flu from killed animals is minimal, however it still can occur occasionally from bodily fluids during butchering. Giving thousands of years of hunting wild boar and wild birds and catching occasional flu gave HG some immunity to this pathogen.

    For these reasons, flu epidemics mostly occur during late autumn/ winter in moderate to cold climate zones. Vitamin D, production of which is stimulated by sunlight, seems to protect against influenza, and may be another factor for seasonal variation in infection.
    Since taking vitamin D supplements I can attest to fewer flu cases and if infected having much milder symptoms.

    As such, I agree that north Eurasian HGs most likely had caught the flu, and developed some immunity from it, already before the entrance of early farmers. Climate is one factor here, the other one is the reliance on seal, deer, reindeer and wild horses as hunting prey. Moreover, North Eurasian HGs may have picked up flu viruses from seal-infected brackish water (Baltic Sea!), or from ice (igloo construction etc.). Domestication of wolves/ dogs as hunting or traction animals should also be considered. In fact, north Eurasian HGs' exposition, immunity and transmission potential should have been substantially higher than that of EEFs.
    My take on this would be that EEF could have brought intensity and faster mutation of pathogens due to much higher population density and closeness and interaction of various domesticated animals. Although these new strains affected them and surrounding HGs equally, HGs might have not been exposed to all of them (living far away), later paying higher consequences being attacked by completely (for them) new strains, unlike EEF.



    1. For climatic and nutritional reasons (seal, reindeer), North Eurasian populations are likely to have been earliest and most intensively affected by influenza;
    2. The resulting process of genetic adaptation may among others have promoted lactose tolerance, which substantially increases influenza resistance. Rather than cow-herders, reindeer herders could have been the first group that effectively benefitted from the new genetic trait. Given that reindeer are also affected by small pox, it is probably no coincidence that pox resistance (CCR5-32 allele, see my previous post) has the highest prevalence in Finnish and adjacent Russian populations.
    Good thinking. Flue could have accelerated faster spreading of lactose persistent gene.

    Influenza prevalence in already reasonably resistant (pre-) Funnelbeaker populations should have promoted substantial influenza epidemics in less-resistant cultures further south, especially during the epi-Rössen and epi-Lengyel (Schöningen) phase (4,100-3,800 BC) when the contact intensified. These should primarily have been equestrian / maritime strains (H7N7, H3N3, H3N8) yet mostly unknown to central European farmers. The latter may of course have "paid back" with swine flu (H1N1, H3N2), but since the H1N1 strain also occurs with deer, Funnelbeaker people might have been already prepared.
    Interesting thought. EEF and HG would have been attacked by same strains with different intensity according to genetic immunity of both groups. The most important questions would be how often both groups were decimated by really bad cases of flu? Once in generation, once in 100 years or even more rarely?

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    1 out of 1 members found this post helpful.
    Thanks for your extensive reply, LeBrok. A few comments:
    Quote Originally Posted by LeBrok View Post
    There is no doubt that catching flu from killed animals is minimal, however it still can occur occasionally from bodily fluids during butchering. Giving thousands of years of hunting wild boar and wild birds and catching occasional flu gave HG some immunity to this pathogen.
    Direct human infection from birds is rare, though there have been a few cases reported from workers on large chicken farms and chicken slaughterhouses, but none of the European cases spread that flu further to other humans. Conversion from bird to human flu in general needs a mammal vessel. So far, pigs, seals and bats are proven to have acted as such a vessel, dogs at least seem to have the potential, and I personally think more research on rodents, especially squirrels, is required in this respect.

    It's not clear whether pig/boar were original hosts, or only became so with the spread of agriculture. Equestrian flu isn't well researched, but the one and only study that I have seen, from Germany in 1980, had 11 out of 20 deer samples showing antibodies to in total 3 different flu strains, one of which later spread to humans (via horses?). HGs catching the flu when butchering deer is of course a possibility, but when the deer is already dead, and outside temperatures are above freezing, the risk is rather minimal. I think the main issue for HGs in warmer climates is caves (cool, dry, no sunlight) and bats (which also aren't well researched for their flu reservoir and transmission potential). And, in fact, cave-dwelling Mesolithic Europeans appear to have been quite resilient to the spread of EEFs (and their diseases?) - Iberia / SW France is a point in case here.

    My take on this would be that EEF could have brought intensity and faster mutation of pathogens due to much higher population density and closeness and interaction of various domesticated animals. Although these new strains affected them and surrounding HGs equally, HGs might have not been exposed to all of them (living far away), later paying higher consequences being attacked by completely (for them) new strains, unlike EEF.

    EEF and HG would have been attacked by same strains with different intensity according to genetic immunity of both groups. The most important questions would be how often both groups were decimated by really bad cases of flu? Once in generation, once in 100 years or even more rarely?
    I will comment on this in more detail I the thread related to the recent Brotherton study on Neolithic population exchange in the Elbe-Saale region, which actually inspired me to look deeper into the possible effect of diseases on the haplogroup composition.
    http://www.eupedia.com/forum/threads...l=1#post435557

    However, here my current line of thinking as concerns NHG:
    From 5,500 BC on, the Baltic Sea became flooded from the west, around 4,500 BC the former sweetwater lake had turned brackish. Seals immigrated from the North Sea and quickly became the main food source along the SW Baltic coast (25-40 % of all animal bones, second only to deer). Given that seals are potent flu conversion vessels, and flu viruses can survive much longer in brackish than in saltwater, Ertebolle culture HGs should have gained substantial exposition to new strains [Under a "out of Doggerland" scenario, one might assume that Ertebolle populations had already gained substantial seal flu resistance much earlier,.]
    Hazelnut was cultivated around Ertebolle settlements, as food, but also as the branches were used for various devices such as fish traps. This should have increased exposition to (flu-bearing) rodents. The same applies to attested rasp- and blackberry cultivation, and flu-bearing bats. Several late Ertebolle settlements on the Danish isles show substantial shares (~30%) of bones of fur-bearing animals (another known source of flu infections), apparently hunted for their pelts. Dogs typically make up for 1-4% of all mammal bones. Dog burials together with their "master" are known from some Ertebolle sites (Skateholm), quite common in Funnelbeaker graves, and the tradition appears to have continued uninterruptedly to early Medieval Saxon graves. As such it is fair to assume that the Ertebolle culture had already domesticized dogs. Genetic analysis of excavated pig bones shows that from 4,700 BC on, the Ertebolle culture did not any more rely exclusively on boar, but had imported domesticated pigs (Anatolian DNA) from the south, and was most likely raising them systematically. In short, latest by the mid-5th milennium BC the Ertebolle culture had assembled an impressive package of substantial exposition to almost all known influenza hosts.
    http://www.nature.com/ncomms/2013/13...comms3348.html
    http://etheses.whiterose.ac.uk/1712/5/chapter_4.pdf

    Flu infections are difficult to trace from the Ertebolle archaeological record, as most sites were only used for a limited period before they became submerged by the rising Baltic Sea. Nevertheless, Scandinavia witnessed at least two periods of volcanic winters around 4,500-4350 BC, and it would be a miracle if those hadn't caused flu epidemics. A rapid cooling sets in in Scandinavia around 4,100 BC, contemporarily with the transition to the Funnelbeaker culture, which is described as quick in the south (Mecklenburg/ Holstein), abrupt in the north (Jutland), but as subtle blend-over in Southern Sweden. Demic expansion is genetically proven, but there is no evidence of violent conflict associated to it. Did a (swine) flu epidemic pave the way for EEF on the Cimbrian peninsula, but not make it across the Öresund?

    Aside from swine import, there are other indications of regular contact between the Ertebolle culture and LBK/ Rössen further south, The oldest "Ertebolle"-pottery found (Schlamersdorf near Bad Segeberg) dates to around 5,000 BC, has apparently been produced in the Rhineland, and corresponds date-wise to the earliest imported amber found there. Flint adzes and, less frequently, axes were imported from the Harz and Silesia during the 5th millennium BC, a few copper items (Slovakia) have also been found at Ertebolle sites. There has also been cultural interchange between SW Sweden and the Narva culture in Lithuania and Latvia, e.g. Swedish flint sickles apparently produced for export across the Baltic Sea during the 5th millennium BC. Locally produced Ertebolle ceramic has several parallels to Narva culture ceramic, both in ornamental design and in function (blubber lamps). Moreover, cereal imprints have occasionally (5 times) been found on Ertebolle sherds, interpreted as signs of grain import across the Baltic Sea.
    http://what-when-how.com/ancient-eur...-70004000-b-c/

    Whether these contacts were intensive enough to disseminate "northern" influenza strains to EEF further south may be debated. Aside from humans, boar may have served as transmission channel. Domesticized pigs were commonly left grazing in open oak forests, and there is genetic evidence of substantial incorporation of European boar DNA into the originally Anatolian swine gene pool. In any case, interaction intensified during the Funnelbeaker period. Around 4,000-3,700 BC, Central Europe experienced a cold and dry phase, during which EEF should at latest have gotten the flu. The Brotherton study documents a massive genetic break around this period in the Elbe-Saale region: mtDNA H subclades of near eastern origin, which dominate the LBK and Rössen samples, get extinct, to be later replaced by subclades that are today mainly West Atlantic (H3, H4) or (south-)east European (H2, H5, H6, H10).
    Another study comes to the same result with respect to mtDNA U5 EEF: Outside the basal clade, only one out of nine early Neolithic sub-clades made it to the late Neolithic. Obviously, NHG (Funnelbeaker) U5b wasn't concerned, otherwise they wouldn't have become the dominating mtDNA haplogroup in the Elbe-Saale region during the late third millennium BC Bernburg culture (though U5b may have had other health issues, which subsequently affected its frequency).

    Coming back to the OT: The Funnelbeaker itself, and associated ceramic innovations such as the first jugs, point to a drink-based culture. Aside from fresh milk, beer might of course also be considered, but cattle herding appears to have predated systematic cereal production by several centuries. As one paper puts it:
    http://www.uni-kiel.de/ufg/bereiche/...89_mueller.pdf
    A combination of flat-based Gatersleben elements [Elbe-Saale] and funnel-necked Michelsberg types [Rhine-Weser] should have resulted in funnel beakers
    Add to this the world's most renowned dairy cow breed, the Holstein-Frisian, and the area where lactose tolerance matured (though not necessarily originated) becomes clear. Holstein Frisians have "only" been bred systematically for some two millennia, but they represent a combination of the original Anatolian/ LBK cattle )mtDNA T3), with Italian / Alpine Aurochs (mtDNA T*) crossed in via Bavarian breeds. Their yDNA is exclusively Anatolian Y1.
    http://www.pnas.org/content/103/21/8113.full#T1

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    1 out of 1 members found this post helpful.
    Quote Originally Posted by FrankN View Post
    Thanks for your extensive reply, LeBrok. A few comments:
    Lol, if mine is extensive your's has to be called colossal and exhaustive. I wish I had more time to indulge in my hobby these days.
    Your posts are always full of knowledge, well written and easy to follow, and I read them with great interest.

    Forgive me if I don't elaborate on all points from lack of time.


    Dog burials together with their "master" are known from some Ertebolle sites (Skateholm), quite common in Funnelbeaker graves, and the tradition appears to have continued uninterruptedly to early Medieval Saxon graves. As such it is fair to assume that the Ertebolle culture had already domesticized dogs.
    According to newest finds on dogs, their domestication can go back as far as 30 thousand years in Europe.
    http://www.eupedia.com/forum/threads...-ago-in-Europe



    Whether these contacts were intensive enough to disseminate "northern" influenza strains to EEF further south may be debated. Aside from humans, boar may have served as transmission channel. Domesticized pigs were commonly left grazing in open oak forests, and there is genetic evidence of substantial incorporation of European boar DNA into the originally Anatolian swine gene pool. In any case, interaction intensified during the Funnelbeaker period. Around 4,000-3,700 BC, Central Europe experienced a cold and dry phase, during which EEF should at latest have gotten the flu. The Brotherton study documents a massive genetic break around this period in the Elbe-Saale region: mtDNA H subclades of near eastern origin, which dominate the LBK and Rössen samples, get extinct, to be later replaced by subclades that are today mainly West Atlantic (H3, H4) or (south-)east European (H2, H5, H6, H10).
    Another study comes to the same result with respect to mtDNA U5 EEF: Outside the basal clade, only one out of nine early Neolithic sub-clades made it to the late Neolithic. Obviously, NHG (Funnelbeaker) U5b wasn't concerned, otherwise they wouldn't have become the dominating mtDNA haplogroup in the Elbe-Saale region during the late third millennium BC Bernburg culture (though U5b may have had other health issues, which subsequently affected its frequency).
    Mitochondria is an energy generator of every cell. Therefore I have a feeling that changeover of MtDNA in the cold phase in Europe went towards MtDNA which could produce more heat in the body. Other words, some MtDNA which came with farmers from Near East didn't survive when European climate turned cold. To forefront came many native ones found among local HGs.
    It is just my supposition based on own observation of people around. Some like winter but sweat profusely in summer. Some love summer and freeze terribly in winter. (adjusted for body size) And I think it has a lot to do with mitochondria.

    Add to this the world's most renowned dairy cow breed, the Holstein-Frisian, and the area where lactose tolerance matured (though not necessarily originated) becomes clear. Holstein Frisians have "only" been bred systematically for some two millennia, but they represent a combination of the original Anatolian/ LBK cattle )mtDNA T3), with Italian / Alpine Aurochs (mtDNA T*) crossed in via Bavarian breeds. Their yDNA is exclusively Anatolian Y1.
    http://www.pnas.org/content/103/21/8113.full#T1
    Cool map. Did they say something how they compare autosomally?

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