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Author Topic: Neolithic Farmers and the Spread of Indo-European, The Case for Euphratic, etc.  (Read 13783 times)
NealtheRed
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« Reply #75 on: June 04, 2011, 05:01:42 PM »


Roukus makes the conclusion that R1b must have had a biological advantage. The only one I can think of at the approximate time would be the milk drinking gene.  


The highest concentrations of lactase persistence are in Western/Northwestern Europe, and it decreases as one moves south and east. Coincidentally or not, R1b levels match this pattern as well.

I think that such a gene was spread by nomadic pastoralists. This brings to mind an area of very high concentrations of lactase persistence - the Scottish Highlands. Folks practiced transhumance, and I believe it is still done in both the Highlands and in Ireland.
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« Reply #76 on: June 04, 2011, 05:17:14 PM »

I came across some thing about  large scale drought at about 4000 and 2200 BC covering the whole  med. I didn't get much but it was to do with the Atlantic conveyor, The dissertation of N.Africa leading to the population of the nile delta etc. Could this also caused large population movement into/out of or around in Europe or the Steppes. Possibly crop failure led to the increase of lactose persistence. Milk drinkers may have survived in greater proportions. Moved to more grass land regions and prospered.
My thinking is these kind of disasters cause 'refugees' and disperse rather than move some where on a settled mass.   
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rms2
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« Reply #77 on: June 04, 2011, 06:32:22 PM »

At the bottom of the Wikipedia article is a mention of the source, it's a 252 page dissertation, in German.

http://webdoc.sub.gwdg.de/diss/2006/schilz/schilz.pdf

Thanks! It will take me awhile to work my way through it again, but I found the stuff on lactase persistence.

Individual M9 (the "M" is for male) is the apparent R1b. On page 198 you can see the little chartlet on him. The "LAK C/C" indicates that he was homozygotic at 13910 with two Cs, meaning he was lactose intolerant. You need at least one T there to be lactase persistent. A C/T or T/T at 13910 means one is lactase persistent.

Regarding the two "R1a" individuals, M10 and M11, who were apparently father and son, as far as I can tell, they were not SNP tested (evidently no one was). The idea that they were R1a is a guess based on a 12-marker haplotype. The haplotypes of the 19 males from whom y-dna was obtainable are shown on page 93. The shared haplotype of M10 and M11 is "Y5" on that chart. It seems to me the notion that they were R1a hangs on a slender thread, i.e., that they have 19=15, 439=11, and 390=25. Someone tell me if I am missing something, but those two could just as easily be R1b, because there are plenty of R1b men who have those marker values. I don't see anything startlingly R1a about their haplotype.

Anyway, M10 and M11 also have little chartlets on page 198, where you can see that both of them have "LAK C/T" and thus were lactase persistent.

I see one individual, M18, also shown on page 198, who has a "LAK T/T" entry, but they were not able to extract any y-dna from him, although I guess they could tell he was a male, since they gave him the magic "M" designation.

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NealtheRed
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« Reply #78 on: June 04, 2011, 07:40:04 PM »

At the bottom of the Wikipedia article is a mention of the source, it's a 252 page dissertation, in German.

http://webdoc.sub.gwdg.de/diss/2006/schilz/schilz.pdf

Thanks! It will take me awhile to work my way through it again, but I found the stuff on lactase persistence.

Individual M9 (the "M" is for male) is the apparent R1b. On page 198 you can see the little chartlet on him. The "LAK C/C" indicates that he was homozygotic at 13910 with two Cs, meaning he was lactose intolerant. You need at least one T there to be lactase persistent. A C/T or T/T at 13910 means one is lactase persistent.

Regarding the two "R1a" individuals, M10 and M11, who were apparently father and son, as far as I can tell, they were not SNP tested (evidently no one was). The idea that they were R1a is a guess based on a 12-marker haplotype. The haplotypes of the 19 males from whom y-dna was obtainable are shown on page 93. The shared haplotype of M10 and M11 is "Y5" on that chart. It seems to me the notion that they were R1a hangs on a slender thread, i.e., that they have 19=15, 439=11, and 390=25. Someone tell me if I am missing something, but those two could just as easily be R1b, because there are plenty of R1b men who have those marker values. I don't see anything startlingly R1a about their haplotype.

Anyway, M10 and M11 also have little chartlets on page 198, where you can see that both of them have "LAK C/T" and thus were lactase persistent.

I see one individual, M18, also shown on page 198, who has a "LAK T/T" entry, but they were not able to extract any y-dna from him, although I guess they could tell he was a male, since they gave him the magic "M" designation.



Yeah, I don't see why they would designate the samples as belonging to R1a with just three STR values. Even if they were R1a, the distribution of lactase persistence clearly matches the trail of R1b in Europe.

Jean M writes on her blog that R1a-R1b populations must have been mixing for some time in order for the LP gene to become so dominant in them. Nevertheless, LP appears to have come from the Near East, and the initial spread I believe from R1b.
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rms2
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« Reply #79 on: June 04, 2011, 08:23:46 PM »

At the bottom of the Wikipedia article is a mention of the source, it's a 252 page dissertation, in German.

http://webdoc.sub.gwdg.de/diss/2006/schilz/schilz.pdf

Thanks! It will take me awhile to work my way through it again, but I found the stuff on lactase persistence.

Individual M9 (the "M" is for male) is the apparent R1b. On page 198 you can see the little chartlet on him. The "LAK C/C" indicates that he was homozygotic at 13910 with two Cs, meaning he was lactose intolerant. You need at least one T there to be lactase persistent. A C/T or T/T at 13910 means one is lactase persistent.

Regarding the two "R1a" individuals, M10 and M11, who were apparently father and son, as far as I can tell, they were not SNP tested (evidently no one was). The idea that they were R1a is a guess based on a 12-marker haplotype. The haplotypes of the 19 males from whom y-dna was obtainable are shown on page 93. The shared haplotype of M10 and M11 is "Y5" on that chart. It seems to me the notion that they were R1a hangs on a slender thread, i.e., that they have 19=15, 439=11, and 390=25. Someone tell me if I am missing something, but those two could just as easily be R1b, because there are plenty of R1b men who have those marker values. I don't see anything startlingly R1a about their haplotype.

Anyway, M10 and M11 also have little chartlets on page 198, where you can see that both of them have "LAK C/T" and thus were lactase persistent.

I see one individual, M18, also shown on page 198, who has a "LAK T/T" entry, but they were not able to extract any y-dna from him, although I guess they could tell he was a male, since they gave him the magic "M" designation.



Yeah, I don't see why they would designate the samples as belonging to R1a with just three STR values. Even if they were R1a, the distribution of lactase persistence clearly matches the trail of R1b in Europe.

Jean M writes on her blog that R1a-R1b populations must have been mixing for some time in order for the LP gene to become so dominant in them. Nevertheless, LP appears to have come from the Near East, and the initial spread I believe from R1b.

Honestly, I don't know the answer. It's complicated. It looks like lactase persistence originated in the Pontic-Caspian steppe, but right now part of the problem is proving where R1b came from.

Half of the problem is mtDNA. It could be that T-13910 had a female origin and spread more by means of the distaff side at first than otherwise.
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NealtheRed
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« Reply #80 on: June 04, 2011, 11:30:21 PM »

At the bottom of the Wikipedia article is a mention of the source, it's a 252 page dissertation, in German.

http://webdoc.sub.gwdg.de/diss/2006/schilz/schilz.pdf

Thanks! It will take me awhile to work my way through it again, but I found the stuff on lactase persistence.

Individual M9 (the "M" is for male) is the apparent R1b. On page 198 you can see the little chartlet on him. The "LAK C/C" indicates that he was homozygotic at 13910 with two Cs, meaning he was lactose intolerant. You need at least one T there to be lactase persistent. A C/T or T/T at 13910 means one is lactase persistent.

Regarding the two "R1a" individuals, M10 and M11, who were apparently father and son, as far as I can tell, they were not SNP tested (evidently no one was). The idea that they were R1a is a guess based on a 12-marker haplotype. The haplotypes of the 19 males from whom y-dna was obtainable are shown on page 93. The shared haplotype of M10 and M11 is "Y5" on that chart. It seems to me the notion that they were R1a hangs on a slender thread, i.e., that they have 19=15, 439=11, and 390=25. Someone tell me if I am missing something, but those two could just as easily be R1b, because there are plenty of R1b men who have those marker values. I don't see anything startlingly R1a about their haplotype.

Anyway, M10 and M11 also have little chartlets on page 198, where you can see that both of them have "LAK C/T" and thus were lactase persistent.

I see one individual, M18, also shown on page 198, who has a "LAK T/T" entry, but they were not able to extract any y-dna from him, although I guess they could tell he was a male, since they gave him the magic "M" designation.



Yeah, I don't see why they would designate the samples as belonging to R1a with just three STR values. Even if they were R1a, the distribution of lactase persistence clearly matches the trail of R1b in Europe.

Jean M writes on her blog that R1a-R1b populations must have been mixing for some time in order for the LP gene to become so dominant in them. Nevertheless, LP appears to have come from the Near East, and the initial spread I believe from R1b.

Honestly, I don't know the answer. It's complicated. It looks like lactase persistence originated in the Pontic-Caspian steppe, but right now part of the problem is proving where R1b came from.

Half of the problem is mtDNA. It could be that T-13910 had a female origin and spread more by means of the distaff side at first than otherwise.

Interesting you mention the female component to this. That explains LP's emergence in both R1b and R1a populations.

Yet I still think R1b tribes introduced it.
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rms2
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« Reply #81 on: June 05, 2011, 06:36:26 AM »

The thing about the T 13910 allele is that it spreads easily (like warm butter). All that is required is for one parent to give down a T, and - voila! - you're a milk drinker.

It is certainly widespread in R1b populations now, but just how it started and spread to the northwest is a mystery. Some connection to R1b would seem to make sense, but who knows, really?

FTDNA should add a test for 13910 to its Factoid menu. I think it would sell. It could also be interesting to collect the data on C/C, C/T, and T/T.
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« Reply #82 on: June 05, 2011, 06:42:03 AM »


. . .

Jean M writes on her blog that R1a-R1b populations must have been mixing for some time in order for the LP gene to become so dominant in them. Nevertheless, LP appears to have come from the Near East, and the initial spread I believe from R1b.

If you think about it, lactase persistence is far less dominant in predominantly R1a populations than it is in predominantly R1b populations.

Eastern Europe is less lactase persistent than western Europe, especially northwestern Europe.

I don't think lactase persistence is prevalent in India, although I could be wrong about that.
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rms2
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« Reply #83 on: June 05, 2011, 06:51:45 AM »


. . .

Jean M writes on her blog that R1a-R1b populations must have been mixing for some time in order for the LP gene to become so dominant in them. Nevertheless, LP appears to have come from the Near East, and the initial spread I believe from R1b.

If you think about it, lactase persistence is far less dominant in predominantly R1a populations than it is in predominantly R1b populations.

Eastern Europe is less lactase persistent than western Europe, especially northwestern Europe.

I don't think lactase persistence is prevalent in India, although I could be wrong about that.

Here is an article on lactase persistence in India:

Frequency of lactose malabsorption among healthy southern and northern Indian populations by genetic analysis and lactose hydrogen breath and tolerance tests.

Quote
Results: Volunteers from southern and northern India were comparable in age and [gender - WFN won't allow the s-x word]. The LTT result was abnormal in 88.2% of southern Indians and in 66.2% of northern Indians (P = 0.001). The lactose HBT result was abnormal in 78.9% of southern Indians and in 57.1% of northern Indians (P = 0.003). The CC genotype was present in 86.8% and 67.5% (P = 0.002), the CT genotype was present in 13.2% and 26.0% (P = 0.036), and the TT genotype was present in 0% and 6.5% (P = 0.03) of southern and northern Indians, respectively. The frequency of symptoms after the lactose load (47.4% compared with 15.6%; P < 0.001) and peak concentrations of breath hydrogen (88.5 ± 71.9 compared with 55.4 ± 61.9 ppm; P = 0.003), both of which might indicate the degree of lactase deficiency, were higher in southern than in northern Indians.

Conclusion: The frequency and degree of LM is higher in southern than in northern Indian healthy populations because of genetic differences in these populations
.


You can see that India is not particularly lactase persistent, even in the mostly R1a North, although it is more lactase persistent in the North than in the South.
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« Reply #84 on: June 05, 2011, 07:36:33 AM »

Here is an interesting abstract of an article:

Comparison of lactase persistence polymorphism in ancient and present-day Hungarian populations.

Quote
Abstract

The prevalence of adult-type hypolactasia varies ethnically and geographically among populations. A C/T–13910 single nucleotide polymorphism (SNP) upstream of the lactase gene is known to be associated with lactase non-persistence in Europeans. The aim of this study was to determine the prevalence of lactase persistent and non-persistent genotypes in current Hungarian-speaking populations and in ancient bone samples of classical conquerors and commoners from the 10th–11th centuries from the Carpathian basin; 181 present-day Hungarian, 65 present-day Sekler, and 23 ancient samples were successfully genotyped for the C/T-13910 SNP by the dCAPS PCR-RFLP method. Additional mitochondrial DNA testing was also carried out. In ancient Hungarians, the T-13910 allele was present only in 11% of the population, and exclusively in commoners of European mitochondrial haplogroups who may have been of pre-Hungarian indigenous ancestry. This is despite animal domestication and dairy products having been introduced into the Carpathian basin early in the Neolithic Age. This anomaly may be explained by the Hungarian use of fermented milk products, their greater consumption of ruminant meat than milk, cultural differences, or by their having other lactase-regulating genetic polymorphisms than C/T-13910. The low prevalence of lactase persistence provides additional information on the Asian origin of Hungarians. Present-day Hungarians have been assimilated with the surrounding European populations, since they do not differ significantly from the neighboring populations in their possession of mtDNA and C/T-13910 variants. Am J Phys Anthropol, 2011. © 2011 Wiley-Liss, Inc.

Interesting that the nomadic, conquering Magyars out of the Eurasian steppe were not lactase persistent. Lactase persistence in ancient Hungary was connected with the native population.

Unfortunately, I can't get the whole article to read.
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« Reply #85 on: June 05, 2011, 07:56:14 AM »

Sorry to be turning this thread into the lactase persistence corner, but here is a really interesting article:

Lactase persistence genotypes and malaria susceptibility in Fulani of Mali

Quote
Results

Among 79 Dogon only one heterozygote of the lactase enhancer polymorphism was detected, whereas all others were homozygous for the ancestral C allele. Among the Fulani, the main European polymorphism at locus C/T-13910 was by far the most common polymorphism, with an allele frequency of 37%. Three other single-nucleotide polymorphisms were found with allele frequencies of 3.7%, 1.9% and 0.6% each. The novel DNA polymorphism T/C-13906 was seen in six heterozygous Fulani. Among the Fulani with lactase non-persistence CC genotypes at the C/T-13910 locus, 24% had malaria parasites detectable by microscopy compared to 18% for lactase persistent genotypes (P = 0.29). Pooling the lactase enhancer polymorphisms to a common presumptive genotype gave 28% microscopy positives for non-persistent and 17% for others (P = 0.11)
.

What is interesting is that the Chadic-speaking Fulani have a fairly high frequency of R-V88 (downstream of P25 but not P297), as well as lactase persistence on the European allele, T-13910.

Hmmm . . .
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Maliclavelli
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« Reply #86 on: June 05, 2011, 08:25:25 AM »

What is interesting is that the Chadic-speaking Fulani have a fairly high frequency of R-V88 (downstream of P297 but not M269), as well as lactase persistence on the European allele, T-13910.
Hmmm . . .

upstream
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NealtheRed
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« Reply #87 on: June 05, 2011, 09:26:23 AM »

Here is an interesting abstract of an article:

Comparison of lactase persistence polymorphism in ancient and present-day Hungarian populations.

Quote
Abstract

The prevalence of adult-type hypolactasia varies ethnically and geographically among populations. A C/T–13910 single nucleotide polymorphism (SNP) upstream of the lactase gene is known to be associated with lactase non-persistence in Europeans. The aim of this study was to determine the prevalence of lactase persistent and non-persistent genotypes in current Hungarian-speaking populations and in ancient bone samples of classical conquerors and commoners from the 10th–11th centuries from the Carpathian basin; 181 present-day Hungarian, 65 present-day Sekler, and 23 ancient samples were successfully genotyped for the C/T-13910 SNP by the dCAPS PCR-RFLP method. Additional mitochondrial DNA testing was also carried out. In ancient Hungarians, the T-13910 allele was present only in 11% of the population, and exclusively in commoners of European mitochondrial haplogroups who may have been of pre-Hungarian indigenous ancestry. This is despite animal domestication and dairy products having been introduced into the Carpathian basin early in the Neolithic Age. This anomaly may be explained by the Hungarian use of fermented milk products, their greater consumption of ruminant meat than milk, cultural differences, or by their having other lactase-regulating genetic polymorphisms than C/T-13910. The low prevalence of lactase persistence provides additional information on the Asian origin of Hungarians. Present-day Hungarians have been assimilated with the surrounding European populations, since they do not differ significantly from the neighboring populations in their possession of mtDNA and C/T-13910 variants. Am J Phys Anthropol, 2011. © 2011 Wiley-Liss, Inc.

Interesting that the nomadic, conquering Magyars out of the Eurasian steppe were not lactase persistent. Lactase persistence in ancient Hungary was connected with the native population.

Unfortunately, I can't get the whole article to read.

Yes, I perused this article before and wondered about the decreasing cline of LP as one moves east in Europe. Hungarians particularly have a high concentration of R1a1, and no doubt much of it comes with the Magyars (non-IE speaking, by the way).

However, some of the highest levels of LP can be found amongst populations like the Dutch or the Irish and Scots.
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alan trowel hands.
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« Reply #88 on: June 05, 2011, 04:01:38 PM »

One thing that the British Isles, Holland and Scandinavia have in common is that traces of milk on their pots have been noted from the very inception of their Neolithic periods.  That is not true of a lot of the other countries, including the whole Med. and much of central Europe.

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« Reply #89 on: June 05, 2011, 08:31:10 PM »

One thing that the British Isles, Holland and Scandinavia have in common is that traces of milk on their pots have been noted from the very inception of their Neolithic periods.  That is not true of a lot of the other countries, including the whole Med. and much of central Europe.



Do you know if there were any cultural links or common antecedents between the British Neolithic and the Funnelbeaker culture who had lactose persistence?
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« Reply #90 on: June 06, 2011, 01:23:55 AM »

Do we know that these people were drinking the raw milk?
Or were they collecting it to make butter? and or cheese?
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« Reply #91 on: June 06, 2011, 08:42:03 AM »

News on BBC to day about Neolithic states that there was a technological building and if I picked it up correct population explosion within a few generations in Britain. I didn't hear any thing about invasion or migration but I only caught some of it. This appears to have happened some time after the start of the Neolithic. It's probably the same thing JeaMn has been talking about for ages But they made it sound new.
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« Reply #92 on: June 06, 2011, 09:39:23 AM »

I think this is the relevant link http://www.bbc.co.uk/news/science-environment-13647544
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« Reply #93 on: June 06, 2011, 03:37:15 PM »

Yeah I read that article about the Neolithic.  It slightly contradicts another recent study of early Neolithic dates that suggested a simultaneous entry into south-central England and south-east Scotland.  I understand the guys of it is there was a short pioneer phase for 200 years restricted to lowland England where presumably some adaptation happened before they expanded into the rest of the isles suddenly in 2 or 3 generations.  The time difference of 2-300 years would barely be detectable using variance etc so I am not sure this makes much difference.
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« Reply #94 on: June 06, 2011, 07:23:33 PM »

What is interesting is that the Chadic-speaking Fulani have a fairly high frequency of R-V88 (downstream of P297 but not M269), as well as lactase persistence on the European allele, T-13910.
Hmmm . . .

upstream

I apologize. V88 is downstream of P25 but parallel to P297.

But it is not upstream of P297, because that would make P297 downstream of V88, in other words, a descendant of V88, which it is not.

I have edited my original message to correct the error.
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« Reply #95 on: June 06, 2011, 07:45:17 PM »

An interesting thing about the Fulani is that, while they have a frequency of R-V88 of about 54%, on the mtDNA side their lineages are mostly African.

A 2006 study did find about 8.1% Eurasian mtDNA among them, however.

http://mathildasanthropologyblog.wordpress.com/2008/05/12/the-mtdna-of-fulani-nomads/

So, did they begin to acquire their relatively high (37%) level of lactase persistence from a female ancestor or a male ancestor?

Male seems more likely, given the higher frequency of y-dna R-V88 than of Eurasian mtDNA lineages.
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« Reply #96 on: June 07, 2011, 12:13:16 AM »

Don't forget that I hypothesized that R-V88 had migrated to North Africa from Italy (or Spain) via sea and not via Middle East and that Fulvio Cruciani promised  by a letter to investigate this hypothesis. But as I and the most part of Italians are lactose intolerant and mostly hg. R, probably this mutation has nothing to do with ancient R, perhaps with some subclade of it in Central Europe or other.
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« Reply #97 on: June 07, 2011, 06:56:14 AM »

Cruciani et al did not say that R1b-V88 migrated to Africa from Italy or Spain. There is no evidence of any such thing. They envisaged a Neolithic migration of V88 from the Levant to North Africa and then south via the Sahara.  
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« Reply #98 on: June 07, 2011, 07:00:27 AM »

The lactase persistence found in African pastoralists come from different mutations than those common in Europeans. There is a small patch of 13910T in Sub-Saharan Africa however.  Is that in the Fulani? I quote from myself:

There have been at least six separate mutations which cause the lactase switch-off to fail. Lactase-persistence genes of East African origin are 13907G and 14010C. A compound allele (13915G and 3712C) found in Saudis and East Africans probably originated in the Middle East. A rarer lactase-persistence allele (13913C) was discovered in two cases in Italy, and subsequently reported in Cameroon, Sudan, Ethiopia, and the Bedouin population in Saudi Arabia. The dominant mutation in Western Eurasia and South Asia is 13910T (rs4988235(T)). This allele is found within different haplotype backgrounds i.e. the stretches of DNA code either side of it. One of these is common, as we shall see, but the others (which originate from the same ancestral haplotype) are found only in populations living on the Pontic-Caspian steppe. So the allele probably originated in that area. The 22018A (rs182549(C)) mutation was first recognised in Finns. While it generally correlates with 13910T in Europeans, it can appear as an independent cause of lactase-persistence, for example in Pakistanis and notably in the Kazaks of Northern China.

The haplotype containing these two alleles (13910T and 22018A) is common in Northern European-derived populations (77% in European Americans). It is also largely identical over nearly 1 cM. Such lengthy stretches of DNA indicate recent origin; older DNA has had more time to be broken up by recombination each generation. The haplotype could not have risen quickly to such high frequency without the aid of natural selection. Todd Bersaglieri and colleagues calculated that strong selection occurred within the past 5,000–10,000 years, consistent with an advantage to lactase persistence in the setting of dairy farming. Even more recent estimates (1,625–3,188 years ago) were obtained for a Scandinavian population, suggesting stronger and more recent selection there.

See the original for references and a map of the distribution of 13910T: Indo-European genetics: LP
« Last Edit: June 07, 2011, 07:03:01 AM by Jean M » Logged
rms2
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« Reply #99 on: June 07, 2011, 07:38:48 AM »

The study of the Fulani I cited a few posts back shows their lactase persistence comes from the European or Eurasian T-13910 allele and not the other, African varieties.

Could their relatively high (37%) level of LP be connected to their high frequency of R-V88? Maybe not, but it is an interesting question.
« Last Edit: June 07, 2011, 07:42:36 AM by rms2 » Logged

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