The mystery of Lactase Persistence (LP) in Europeans

Tabaccus Maximus

Tabaccus Maximus
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Ethnic group
Galo-Germanic Atlantic Fringe
Y-DNA haplogroup
R1b - SRY 2627
mtDNA haplogroup
H1a
Lactase Persistence (ability to digest raw milk comfortably) appears suddenly in Europe after the late neolithic where it was virtually absent before. In Northwestern Europe today it reaches into the ninetieth percentile and in some areas is almost uniformly present. It then forms a cline that slowly descends throughout Northwest Eurasia down to zero.

One theory suggested present levels of LP in Europe came about due to the cloudy environment in which Vitamin D and Calcium may have enriched the lives of the natives and was thereby was very positively selected to its present frequency. "the calcium assimilation hypothesis"

Dienekes has posted a link to a study that examines this theory in detail which finds it lacking. (Sverrisdottir et al, 2014) http://dienekes.blogspot.com/2014/01/lactase-persistence-and-natural.html

I thought Dienekes made an interesting point on LP selection vs. LP admixture:

For example, the lactase persistence allele occurs at a non-trivial frequency in present-day inhabitants of the Americas, whereas it was zero there a few thousand years ago, with the culprit being post-1492 European colonization. The frequency change in the Americas didn't happen because of natural selection, but because a new population (Europeans) moved in.

I think what this suggests is:

1) LP is most likely not native to Europe
2) LP was brought to Europe involving a substantial population replacement by individuals already LP
3) Beneficial traits may not always be the subject of strong positive selection, otherwise we would all be tall and beautiful.

It's worth noting that the world's largest populations in Asia, S. Asia and Indo-China are nearly completely Lactose Intolerant, yet LP has probably been introduced multiple times over the millenia.
 
I won't toot my own horn too much, but here's another timely T.M. post that I wrote 2 or 3 days before this paper came out regarding the origin of R1b and its move into Europe.

Old thread, but I couldn't resist.

Here's my take... (which I have posted in other areas of this forum at different times)

1. R1b lingered in the Kazakhstani grasslands from 18-11 ybp. SPECIFICALLY, the Kazakhstani grassland and NO OTHER.
2. Within this grassland are the four corners of R1b's ancient domain.
a) NW - Bashkirostan (M269 + M73)
b) NE - The Yenesian Valley (Mal'ta and Afontova oldest R*)
c) SE - Tarim Basin (M269 + M73)
d) SW - Turkmenistan (M269 wonderland)
*It is within this region in which the generations of overhunting Mammoth and Asian Bison (Buffalo) led to a realization for the need of basic cattle management techniques and controlled breeding programs.
This would have involved culling herds of weak traits and non-producing bulls. Large bulls (with large balls - not kidding) would purposefully have been left alone.
Cows with large utters, twins, birthing ease, calf growth, good marbling and muscle growth would have been left on the field when possible. Early R1b peoples recognized these beneficial traits and attempted to maintain sustainable wild herds.
They expanded into like terrain: The plains of Anatolia (M269), Iran (M269 + R2) and Eastern Siberia (M73).


It's interesting that LP would be dated by the authors at around 13,500 ybp (or something like that).
That's about where I would put it based on a presumed developmental period of cattle management in the area noted above.


Tassili Ladies, Algeria (c. 2900 b.c.) [also likely from a population R1b-V88/H1/H3]
Tassili_ladies.jpg
 
I don't think it is a mystery. Lactase persistence was found in some Late Neolithic/Chalcolithic populations in Sweden and Spain, but its frequency increased considerably after the Indo-European migrations. The allele might have been present in various human populations globally for a very long time, but was only positively selected when people started drinking cow milk regularly. The R1b Proto-Indo-Europeans were possibly the first people in the world to domesticate cattle, and developed a lifestyle almost exclusively based on cattle herding in the Pontic Steppe. That is essentially why the selective pressure in favour of lactase persistence happened earlier and was stronger within the Neolithic and Bronze Age R1b population than anywhere else.

Naturally, the frequency of LP progressively increased century after century since the Neolithic. That is a very slow process, but today the only populations who have over 80% of lactase persistence are all found in northern and western Europe, the British Isles having the highest frequency. R1a population picked up early LP alleles from their R1b neighbours in the steppes during the Bronze Age, but even today R1a populations have slightly lower frequencies of LP than R1b populations. Scandinavia scores particularly high due to the high combined total of R1a/R1b ancestry.

The above explanation is so self-evident that I wonder why Sverrisdóttir's team of evolutionary biologists and geneticists from five countries decided to spend time and money on that question instead of testing something more useful. The only explanation is that they haven't accepted that R1b cattle herders from the Pontic Steppe invaded Europe during the Bronze Age. Why else would they only analyse Mesolithic and Neolithic samples to find an answer to the origin of lactase persistence ?

Sometimes I wish I could advise university researchers on what to research so as to avoid wasting precious time and money.
 
Sometimes I wish I could advise university researchers on what to research so as to avoid wasting precious time and money

Ha. Agreed!
 
LP mutation, or any other mutation, to be beneficial and successful (wildly spread) it need to happen in already existing environment, complementing it environment. For example, if LP happened in hunter-gatherers who never drink animal milk, it wouldn't be successful, because it is not needed. Hunter-gatherer can't know or feel he has the mutation and knowingly looks for a cow and a sheep to milk it and drink milk. Therefore, LP gene to be successful it needs to happen in already milk using society. Most likely it happened in herders of cows, sheeps or even horses. In these societies milk is ubiquitous and always given to children. Children are all lactose tolerant (unlike adults). When kids of these herders are growing up they need to stop drinking milk at certain age (10 years?) when lactose tolerant gene is turned off.
Now kids with lactose persistent gene never needed to stop enjoying milk, as there is no reason for it. This extra source of nutrients and calories gave them an edge over other populations, especially in North, where through winter, dry grass could be converted to a feed for cows and milk for people.

LP is less common in the South where growing season is much longer, and also less common for coastal/fishing communities.

Same as Maciamo, I don't see much of mystery here.

2) LP was brought to Europe involving a substantial population replacement by individuals already LP


For example, the lactase persistence allele occurs at a non-trivial frequency in present-day inhabitants of the Americas, whereas it was zero there a few thousand years ago, with the culprit being post-1492 European colonization. The frequency change in the Americas didn't happen because of natural selection, but because a new population (Europeans) moved in.
In both cases IE brought not only their dominant language but also their culture of drinking milk. Once locals learnet giving milk to children it was only matter of time for LP gene to drift into local population. No population replacement needed. Wherever there is a "fertile ground" for a gene it will start drifting in this direction. Speed of the drift might vary on other factors, scale of population mix, bottlenecking, beneficial value of a gene, the advantage it gives to people, etc.
Some none IE cultures were already limited goat and sheep milk drinkers, which could have helped embrace cow milk drinking culture. Also processing milk into cheeses and butter could have evolved in lactose intolerant societies, as a way to consume dairy products containing minute amounts of lactose, when compared to pure milk.
 
IMO, if IE folk could develop lactase persistence, so could other people, in time. And those who developed lactase persistence may have had a strong evolutionary advantage over their neighbours and relatives who did not develop lactase persistence. The Archeology News Network had a recent article about this subject. One of the comments by researchers that they quoted was this:

"Although most early European farmers would not have been lactase persistent, they would still have been able to consume fermented milk products such as yoghurt and cheese, because fermentation converts much of the lactose into fats. But in famine conditions, such as when crops fail, they are likely to have eaten all the fermented milk foods, leaving only the more high-lactose products. This would have caused the usual lactose intolerance symptoms such as diarrhea. Diarrhea in in healthy people is not usually life-threatening, but in severely malnourished individuals it certainly can be. So famine could have led to episodes of very strong natural selection favoring lactase persistence."
 
LP mutation, or any other mutation, to be beneficial and successful (wildly spread) it need to happen in already existing environment, complementing it environment. For example, if LP happened in hunter-gatherers who never drink animal milk, it wouldn't be successful, because it is not needed. Hunter-gatherer can't know or feel he has the mutation and knowingly looks for a cow and a sheep to milk it and drink milk. Therefore, LP gene to be successful it needs to happen in already milk using society. Most likely it happened in herders of cows, sheeps or even horses. In these societies milk is ubiquitous and always given to children. Children are all lactose tolerant (unlike adults). When kids of these herders are growing up they need to stop drinking milk at certain age (10 years?) when lactose tolerant gene is turned off.
Now kids with lactose persistent gene never needed to stop enjoying milk, as there is no reason for it. This extra source of nutrients and calories gave them an edge over other populations, especially in North, where through winter, dry grass could be converted to a feed for cows and milk for people.

LP is less common in the South where growing season is much longer, and also less common for coastal/fishing communities.

Same as Maciamo, I don't see much of mystery here.

In both cases IE brought not only their dominant language but also their culture of drinking milk. Once locals learnet giving milk to children it was only matter of time for LP gene to drift into local population. No population replacement needed. Wherever there is a "fertile ground" for a gene it will start drifting in this direction. Speed of the drift might vary on other factors, scale of population mix, bottlenecking, beneficial value of a gene, the advantage it gives to people, etc.
Some none IE cultures were already limited goat and sheep milk drinkers, which could have helped embrace cow milk drinking culture. Also processing milk into cheeses and butter could have evolved in lactose intolerant societies, as a way to consume dairy products containing minute amounts of lactose, when compared to pure milk.


The frequency of the hypolactosie in the different
ethnic groups the following is : KETTER-THILL european medical analize laboratory

http://www.llam.lu/fileadmin/media/newsletter/Lactoselow.pdf

DIGESTION of the LACTOSE

>
Basques
0,3%
>
Hollandais
1%
>
Su?dois
2%
>
Scandinaves
5%
>
Anglais
5-15%
>
Suisses
10%
>
Allemands
15%
>
Autrichiens
15%
>
Espagnols
15%
>
Fran?ais du nord
17%
>
Italiens du centre
19%
>
Portugais
35%
>
Italiens du sud
41%
>
Mexicains
55%
>
Fran?ais du sud
65%
>
Grecs
66%
>
Juifs
60-85%
>
Siciliens
71%
>
Sud Am?ricains
65-75%
>
Libanais
78%
>
Asiatiques
80%
>
Africains
89%
>
Chinois
95%

a haphazard accident is it, if both people having the best tolerance in lactose bovine are both bigger consumer of cheese?
And Chinese those who use it not.
Really it confirms the link of high tolerance in lactose and R1b.
 
Milk-Comsumption-per-Capita.png

1000px-Lactase_Intolerance_world_map.png
 


attention! it is question on lactose of the bovine and does not concern other dairy products.
And it is on this foundation that the Swiss laboratory with fact of studies for producers' business companies of dairy products.
And fact is to note that the tolerance in lactose bovine is proportional to the intensity of R1b, if you notice results.

I thinks that the milk and the cattle were also important in the success of the quick growth of the demography of R1b or can be more than bronze, horse or agriculture.
 
attention! it is question on lactose of the bovine and does not concern other dairy products.
Are you sure if lactose persistence matters if it is bovine, goat or human milk?


And it is on this foundation that the Swiss laboratory with fact of studies for producers' business companies of dairy products.
Can you rephrase?

And fact is to note that the tolerance in lactose bovine is proportional to the intensity of R1b, if you notice results.
Well, let's say that it correlates well enough to make LP of R1b origin quite plausible. However the "model" breaks down for Eastern Europe where milk consumption is high with little R1b.
 
So I guess that if lactase persistence correlates with R1b, and if we can estimate the countries with the highest lactase persistence based on per capital milk consumption, R1b must reach its greatest levels in countries like Sweden and Greece. Nope, not even close.
 
So I guess that if lactase persistence correlates with R1b, and if we can estimate the countries with the highest lactase persistence based on per capital milk consumption, R1b must reach its greatest levels in countries like Sweden and Greece. Nope, not even close.
What I meant was this: It is possible that lactose persistence gene came with R1b IE invaders, but since then it drifted to populations where it was mostly beneficial for, slowly losing its correlation with the haplogroup of its origin.
 
What I meant was this: It is possible that lactose persistence gene came with R1b IE invaders, but since then it drifted to populations where it was mostly beneficial for, slowly losing its correlation with the haplogroup of its origin.

I understood what you meant, but I'm not sure why you think Neolithic Europeans who owned cattle wouldn't have already developed a considerable degree of lactase persistence before IE invaders (regardless of haplotype) arrived on the scene.
 
Funnelbeaker were a cattle-culture (that used beakers with funnels hint hint)

http://en.wikipedia.org/wiki/Funnelbeaker_culture

Funnelbeaker extent

http://www.geocities.ws/reginheim/funnelbeakerculture.gif

Lactose Tolerant

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

I understood what you meant, but I'm not sure why you think Neolithic Europeans who owned cattle wouldn't have already developed a considerable degree of lactase persistence before IE invaders (regardless of haplotype) arrived on the scene.


I would say that Funnelbeaker and Corded Ware cultures are the main suspects too.
 
I suspect the reason there's a higher rate of lactase persistence in northern Europeans is because back in the days before refrigeration and scientific testing, it was safer to drink raw milk in colder, more northerly climates than in southern Europe. Although the terrain would also affect lactase persistence rates by determining how easy it was to raise cattle, so you might not have as high a rate of lactase persistence in Finland as in Britain, par example. But I suspect that people in southern Europe learned that it was safer to process raw milk into cheese, butter and yogurt, rather than drinking it in its raw state.

The further north you go, the fewer pathogens you find in food, generally. Inuit people here in Canada who catch wild birds sometimes eat them raw and suffer no ill effects. Try that with supermarket chicken and you'll get very sick.
 
So I guess that if lactase persistence correlates with R1b, and if we can estimate the countries with the highest lactase persistence based on per capital milk consumption, R1b must reach its greatest levels in countries like Sweden and Greece. Nope, not even close.

the highest levels are in the Basque, Dutch and English and they become much weaker leaving towards the east of the Europe and more particularly the east south.

These results concern the contemporary period and are based on medical studies and no cultural studies.
 
hese studies are made by a subsidiary of Luxembourg of Swiss laboratory for the professionals of health and for milk industry, it is therefore studies expensive and concerning the actual populations. It concern taurines lactose.
the group "Cerba European Lab"
http://www.cerba-european-lab.com/
 
the highest levels are in the Basque, Dutch and English and they become much weaker leaving towards the east of the Europe and more particularly the east south.

These results concern the contemporary period and are based on medical studies and no cultural studies.

I'm doubtful about such results, as they don't correlate very well with milk consumption patterns.
 

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