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What DNA Says About Aryan Invasion Theory -2
It is possible that paleolitic Europe was IJ .

R1b is of neolithic expansion from Turkey.

As archeology proves ,the expansion of agriculture was demic in western Europe and cultural(not demic) in Russia.

For this reason R1a is older in Europe then R1b.
General book on DNA and race theory

Before the Dawn: Recovering the Lost History of Our Ancestors By Nicholas Wade

Publisher: P e n g u i n 2007 | 320 Pages | ISBN: 014303832X , 1429513772 |

Quote:Scientists are using DNA analysis to understand our prehistory: the evolution of humans; their relation to the Neanderthals, who populated Europe and the Near East; and Homo erectus, who roamed the steppes of Asia. Most importantly, geneticists can trace the movements of a little band of human ancestors, numbering perhaps no more than 150, who crossed the Red Sea from east Africa about 50,000 years ago. Within a few thousand years, their descendents, Homo sapiens, became masters of all they surveyed, the other humanoid species having become extinct. According to New York Times science reporter Wade, this DNA analysis shows that evolution isn't restricted to the distant past: Iceland has been settled for only 1,000 years, but the inhabitants have already developed distinctive genetic traits. Wade expands his survey to cover the development of language and the domestication of man's best friend. And while "race" is often a dirty word in science, one of the book's best chapters shows how racial differences can be marked genetically and why this is important, not least for the treatment of diseases. This is highly recommended for readers interested in how DNA analysis is rewriting the history of mankind.
Map that show that europeans are in majority neolithics from Turkey.

The map of R1b variance.

[Image: balaresque_2010_r1b-variance.jpg]

White skin pigmentation is due to mutations in

SLC24A5 and SLC45A2, both these mutations happened within the last 12000 years

Quote:In fact, much of the genetic evidence seems to suggest a South Asian origin for the F haplogroup. This haplogroup and its lines of descent account for perhaps 90 per cent of the male population in the world. Contrary to received wisdom, this would imply that much of the globe outside Africa was settled by outward migrations from South Asia dating back to over 50,000 years ago. Certainly, the distant origins of the modern European population seem to lie in South Asia, emphasising the crucial importance of this region in understanding the peopling of the globe.

The sepoy mag carrying a story outlining much of what has already been discussed here. Of course, the remaining agenda is to impart a materialist basis to varna.
Dhu, regarding ASI and ANI, ANI is ancestral to CEU, but ASI is absent in Europe

And some people claim that this vindicates AIT, since if it was OIT, then Europeans would have ASI
Nothing will convince the deracinated.

That is autosomal study, it correlates with well known N and M mtdna division seen in India itself.

All Euro lines (U) are derived from R branch of N originating in arc from Pakistan to Bhutan and more probably in SEA where N diversity is greatest. No M is seen Europe. Unlike mtdna, Autosomal does not show descent; only some measure of isolation and inbreeding

This division relects the peculiar initial settlement of Europe only at 40 K.

Next seyylement of Europe was a proto gypsy one of R1a1- postglacial, holocene, neolithic, delineated as such by Underhill who discovered the group and by now well accepted and unchallenged.

In all cases, these jokers try to "compare" the isolation of a founder group against the diversity of the originating group.. This is a normative monotheist mind trick where a false causality is projected by removing the time considerations and essentializing all categories.
Dhu, can you take the material from this thread and its previous version and put all the relevant matter in an organized manner? The reason is we want to get it published.
G. Subramaniam, Ramana,

Please see this comprehensive article by Dr. D. Priyadarshi:



The author also presents new evidence for indian J being much older than that of ME-- this possibility was mentioned here in passing before since Oppenheimer considered it likely but confined it only to footnote.

What is clear is that the most recent Indian expansion had components of both postglacial and Neolithic and was overwhelming. It is only European biblical prejudice which gives precedence to the ME in Neolithic. The rubric, of course, is to posit a value neutral ME as the progenitor rather than entertain the possibility of an overarching and generative dynamic emanating out of the subcontinent, ie an advance to the rear strategy.

'Breaking India' also consolidates much of this evidence and Rajiv Malhotra has forsaken his earlier stance that Indians are obsessed with opposing the AIT.
^^^^ All that is on topic. This is not.

Quote:'Breaking India' also consolidates much of this evidence and Rajiv Malhotra has forsaken his earlier stance that Indians are obsessed with opposing the AIT.
Never knew he thought/said that before.

Well, "Indians' obsession" - as he called it then - is now his, it seems: his earlier blanket description and those it applies to ("Indians") can hardly have changed merely because he has suddenly chosen to throw in his opinion with the lot of those he so dismissively described earlier.
Yes ,it is time to accept that your language came from Ukraine,from bronze age cowboys.

You are not alone.

Turks accepted that their language came from Siberia,hungarians accepted that their language came from Ural mountains,algerians accepted that their language came from Arabia.

Personally ,I have no problem in accepting the discoveries of scientists.They studied for years,unlike us.

History is made of pain,blood,death, corruption,barbarity.
[quote name='HareKrishna' date='27 June 2011 - 09:24 AM' timestamp='1309146381' post='112051']

Yes ,it is time to accept that your language came from Ukraine,from bronze age cowboys.

You are not alone.

Turks accepted that their language came from Siberia,hungarians accepted that their language came from Ural mountains,algerians accepted that their language came from Arabia.

Personally ,I have no problem in accepting the discoveries of scientists.They studied for years,unlike us.

History is made of pain,blood,death, corruption,barbarity.


Why not from Mars.

Indian traditions are one of the oldest and there is also record of that traditions including language.

So fake history is not what Indians want
Looks like people keep an illusion that if they keep on repeating a BS for a long time, others will accept that as truth. Ancient Indian "Panchatantra" has a story about this, and we knew this kind of strategies.
[quote name='acharya' date='28 June 2011 - 01:33 AM' timestamp='1309204548' post='112054']

Why not from Mars.

Indian traditions are one of the oldest and there is also record of that traditions including language.

So fake history is not what Indians want


Yes,the end justifies the means and nationalism is more important than truth or evidence.

It doesn't matter hard evidence or lesser positive circumstantial evidence.
Evidences are not conclusive and suites the propaganda that was based on linguistics. In fact, when Indians perform the genom tests, they see different results than those used for propaganda. Take it if that suites you, otherwise it is just garbage.
There was never any evidence for the "theory".

It was, foremost, a theology to support the presence of a proto-Monotheism in India, since the absence of such would have collapsed Christianity.

The various narratives of the Indians were selectively filtered to support this proto-Monotheism.

And because Monotheism must necessarily have a singular origin as revelation, the (our) narratives were filtered as "history"; the relational clans were recast as normative Tribes (imagine calling Pandavas and Kauravas as tribes!!), and the learning potential of the narratives was denied as the narratives increasingly became a manifestation of ideology.

The Aryans needed to be ushered in to support the presence of ‘ideology’ (e.g., caste system) in Ancient India, which alone could “explain” all that was seen in India. And without ideology the Aryans could not be ushered in.

That is, the theory itself was an ideology, and was thus embraced eagerly by the colonials and by both their ordinary and communist sepoys. In broader terms, it became colonial invective in the guise of theory, as well stated by the Romanian Cioran.

A materialist basis was sought for the theory only as a secondary measure, as a vehicle for the motivated Aryan, the harbinger of Religion and Civilization.

However, as soon as the “religious” origin of the theory became clear, the theory collapsed in explanatory power. Knowledge of the colonial use of the theory was by itself not enough to collapse the theory’s explanatory power. Correspondingly, in the modern domain, Said’s critique against colonialism could be withstood but not that of Balagangadhara’s against religion

Yet the various materialist justifications remained on their own. This was taken as an improvement in the “theory”, as a shedding of unnecessary detail, and as an occam razor. This was the nihilist-socialist phase of the theory.

It would have been the coup of all time, the joker and thief being crowned king.

Yet Paramatma was on the side of the Hindus and denied the jokers even a semblance of credibility.

It is unfortunate that a materialist explanation was needed in the end, yet there is no other that can smash the last vestige hope of the remnant nihilist.
[url="http://samvada.org/2011/news-digest/indian-cow-give-healthier-milk-research/"]Indian cow, buffalo breeds give healthier milk: Research[/url]

Quote:New Delhi, June 26 (PTI) Indian cow and buffalo breeds possess a rich A2 allele gene that provides a better and healthier quality of milk than foreign breeds, according to a new study.

“The A2 allele gene in Indian milk breeds of cows and buffalos are 100 per cent, while in foreign breeds, it is around 60 per cent,” scientists of the National Bureau of Animal Genetic Resources (NBAGR) have said in a report. Furthermore the frequency of this allele in Indian milk breeds is 1.0 (100 per cent), while in exotic breeds, it has been reported to be nearly 0.6 (60 per cent) or less, they added. Set up in 1984, NBAGR is an arm of the Indian Council of Agricultural Research (ICAR) and is based in Karnal, Haryana.

The finding was arrived at after screening the status of the A2 allele of the beta casein gene in indigenous cows like Red Sindhi, Sahiwal, Tharparkar, Rathi and Gir etc, NBAGR Director B K Joshi said. “The counter allele to A2 is A1, which is considered to be associated with diabetic, obesity, cardiovascular diseases etc,” added Joshi. “Although the foreign breeds of cows produce more milk than Indian varieties, but due to more concentration of A1 gene in those breeds, the milk is of low quality,” the report said, adding that the long-term use of such milk may cause several health disorders.

The scientists scanned 22 breeds of Indian cows and found that in five milk yielding Indian cows — Red Sindhi, Sahiwal, Tharparkar, Rathi and Gir — the status of the A2 allele was 100 per cent, while in other Indian breeds used for farming, its status was around 94 per cent, Joshi added. The scientists also scanned the status of this allele in the two most popular foreign breeds in India, Holstein Friesian and Jersey, in which the status of the A2 allele was 60 per cent only.
^ Relevant to thread topic.

Quote:Indian cow and buffalo breeds possess a rich A2 allele gene that provides a better and healthier quality of milk than foreign breeds, according to a new study.
A2/"Asian cows" milk being specifically 'good' for you vs "European cows" milk being 'bad' for you was already established quite some years ago. There's more research out there on this.

Reinstating one half of the stuff I snipped in the above post, because I found some links for support.

Quote:Indian cow and buffalo breeds possess a rich A2 allele gene that provides a better and healthier quality of milk than foreign breeds, according to a new study.
A2/"Asian cows" milk being specifically good for you vs "European cows" milk being bad for you was already established quite some years ago. And IIRC A1 milk is supposed to cause or exacerbate the onset of mental problems as well, not just cardiovascular disease. Don't quote me on this: only vaguely know about the matter as it was a cause of concern for my mother - she was trying to discourage us from drinking so much of the local milk (I tended to down many glasses on a good day).

Things I didn't post with the above (edited them out before posting, since I wouldn't bet on my memory over this and, being unable to confirm at that time, didn't want to get called on it):

2. "African and Asian cows" => "A2"

3. Presence of A1 in cows (mainly European) were due to 'recent' mutations

And point one is this line:

1. "IIRC A1 milk is supposed to cause or exacerbate the onset of mental problems as well, not just cardiovascular disease."

Again, I recalled autism and schizofrenia (in that order), but I wouldn't bet money on my recollection.

A simple web search gives some indicators that my memory wasn't off . The following is not an endorsement of anything (the links are certainly not verified).

a) Mentions "African and Asian cows" <-> A2.

And mentions of autism.


Quote:Shifting from A1 to A2 milk

Sunday, 23 September 2007, 4:44 pm

Press Release: Professor Keith Woodford

Media release for immediate use

Shifting from A1 to A2 milk - Infant formula a priority - let's get on with it says Woodford

NZFSA is claiming that Professor Keith Woodford presents no strong evidence in his book "Devil in the Milk" linking illness to A1 beta-casein. NZFSA says both milks are equally safe. The Authority remains in denial. Woodford's evidence is drawn from more than 100 scientific papers. It includes the following:

NZ scientists have found that countries with high A1 beta-casein intake are the same countries with high Type 1diabetes (the early onset form). The relationships are so strong that the possibility of getting them by chance is less than one in a thousand.

Japanese and German scientists have independently shown that beta-casomorphin7, which Woodford call's the 'milk devil', is only released from A1 beta casein and not A2. This milk devil is undeniably a strong narcotic. American scientists have shown when it is injected into rats it causes bizarre behaviour.

NZ scientists have shown that almost 50% of mice fed A1 beta-casein get diabetes whereas there is close to zero incidence amongst those fed A2. The only counter evidence is a trial where the industry researchers who supplied the diets never confessed publicly to major diet contamination. (The 'milk devil' protein fragment was accidentally added to the A2 diet. The documentation is in Woodford's book.)

Canadian scientists have shown that rats fed A1 beta casein have much higher diabetes than those fed A2.

Finnish scientists found that genetically susceptible children were five time more likely to get diabetes on a high milk diet (and hence high A1 beta-casein) than those on a lower milk diet.

Italian scientists found that diabetics have much higher antibodies to beta casein than non diabetics. German scientists have shown that in diabetics the high antibodies are specifically to A1 beta casein.

Two groups of NZ scientists have shown that deaths from heart disease are much higher in countries where there is high intake of A1 beta-casein. There is less than a one in one thousand probability of getting these results by chance. Also, the Masai people of Kenya have a huge intake of milk but no heart disease (or Type 1 diabetes) But then their milk is A2. Similarly for the Tibetan Highlanders. And on the Island of Guernsey, where the milk is A2, both diseases are very rare.

Australian scientists found that rabbits fed A1 beta-casein develop arterial plaque in a period of weeks whereas those fed A2 do not.

French scientists found that the milk devil oxidizes LDL (an early indicator of heart risk). And Czech Republic scientists have shown that infants fed formula milk have up to 10 times the antibodies to oxidised LDL compared to those who are breastfed.

American, British and Norwegian scientists have all shown that autistic children typically (but not always) excrete this milk devil in their urine. This means it is getting through from the intestines to the blood. Most normal people seem to excrete it out the backend. But American scientists have shown that once in the blood it passes easily into the brain.

There are several trials in America, and Norway showing how autistic children have reduced autistic symptoms if access to beta-casein is removed. Given that it is an opiate, the children often go through withdrawal symptoms.

There is lots more evidence in Woodford's book

In NZ we already have about 900,000 pure A2 cows - perhaps even more. We can breed the rest of the herd across to A2. The existing A2 cows are more than enough to supply all milk products for NZ and Australia. But of course Australia also has its A2 cows - probably about half a million.

[color="#FF0000"]A1 beta casein is mainly a problem of the developed world. Indigenous Asian and African cows are A2. The A2 version of the gene also predominates in southern Europe. Goats, camels, yaks, and almost all sheep are A2. Human milk is of the A2 type.[/color]

A2 is an opportunity which the industry has turned into a threat by pretending there is no issue.

There are solutions. As well as breeding out the gene we can use the A1 milk for particular products such as butter (no risk) whey powders (no risk), and cheese (probably low risk).

Infant formula is the most urgent priority to shift to A2.

"Let's get on and do it!" says Woodford


b ) autism and schizofrenia mentioned:


Quote:Devil in the Milk

Kicking it a bit old school tonight as I've spent the last week or so coming up to speed with the issues around A1 vs. A2 milk - issues that are probably the best part of 4-5 years old.

For the uninitiated, A1 & A2 refer to a type of protein contained within milk, specifically, the beta casein protein. It would seem all mammalian milk contains these beta caseins. Human milk, goats milk, sheeps milk, and some cows milk, is all A2. However, due to a mutation, many cows also produce A1 casein. It is this A1 casein that is the likely culprit for peoples reactions to milk and it is the compound that New Zealand agricultural scientist Keith Woodford gained notoriety for when he published his book "Devil in the Milk."

Book overview:

This groundbreaking work is the first internationally published book to examine the link between a protein in the milk we drink and a range of serious illnesses, including heart disease, Type 1 diabetes, autism, and schizophrenia. These health problems are linked to a tiny protein fragment that is formed when we digest A1 beta-casein, a milk protein produced by many cows in the United States and northern European countries. Milk that contains A1 beta-casein is commonly known as A1 milk; milk that does not is called A2. All milk was once A2, until a genetic mutation occurred some thousands of years ago in some European cattle. A2 milk remains high in herds in much of Asia, Africa, and parts of Southern Europe. A1 milk is common in the United States, New Zealand,

Australia, and Europe. In Devil in the Milk, Keith Woodford brings together the evidence published in more than 100 scientific papers. He examines the population studies that look at the link between consumption of A1 milk and the incidence of heart disease and Type 1 diabetes; he explains the science that underpins the A1/A2 hypothesis; and he examines the research undertaken with animals and humans. The evidence is compelling: We should be switching to A2 milk. A2 milk from selected cows is now marketed in parts of the U.S., and it is possible to convert a herd of cows producing A1 milk to cows producing A2 milk. This is an amazing story, one that is not just about the health issues surrounding A1 milk, but also about how scientific evidence can be molded and withheld by vested interests, and how consumer choices are influenced by the interests of corporate business.

From what I have read, I would rate the books author, Keith Woodford, in the same category as outspoken anti-gluten campaigner, Dr Rodney Ford (both are good Christchurch lads) in terms of both being a bit ahead of the game and being relatively lone voices in the warnings they have sounded (Ford on gluten & Woodford on A1 beta casein). I am hopeful that both will be able to sit back at some point in the future, thumb their noses at the establishment, and have a smugness that goes with knowing that they were right all along.

Keith runs his own blog site (keithwoodford.wordpress.com) where I have been catching up on his updates on this issue. Prior to doing this, I was under the impression that nothing much had happened in recent years since the initial publishing of his book... WRONG! Thanks for playing...

There is a good interview here from Dec 2009 that gives an excellent overview of the topic and where Keith slots into this picture.

There’s a devil in the milk, says agricultural scientist Keith Woodford, and it has little to do with production methods. Woodford’s startling thesis, backed up by a pile of research, is that a mutation many years ago created an aberrant protein in some European cows, called A1 cows to set them aside from all other cows, which are called A2. As a result, the milk from these cows has been linked to a host of maladies, including Type 1 diabetes, autism and heart disease. Still virtually unknown in this country, the A1-A2 question is prominent enough in New Zealand, where Woodford lives and works, to have spurred public controversy and the creation of a successful company that markets only A2 milk, the a2 Corporation. For growing numbers of Americans who have noticed that milk seems to attack their systems even though they are lactosetolerant, Woodford’s work, collected in his book, Devil in the Milk, offers vital illumination.

Clearly, Keith hasn't made much headway in terms of the political and economic forces that would rather this issue go away. For a good summary of these issues and the politics that has driven this debate away from the public eye, read Keith's recently published update (May 2010) to his "Devil in the Milk" book here.

Since ‘Devil in the Milk’ was first published in September 2007, the story has moved on considerably. The purpose of this update is to summarise the main events, recognising that it will continue to be an ongoing story, and only time will allow some events to be seen in their appropriate context. Essentially, there are three parts to the ongoing story. The first is about the politics of milk and health, how information is communicated, and market responses. The second is about what is happening ‘behind the scenes’ to Australian and New Zealand dairy herds. The third is about the new science.

All are important to an overall understanding.

Some (older) videos for those who don't like reading or for those who want to see how this issue gets dealt with at an official level:
Rest at link.

c) The following indicates that Europe's A1-milk producing cows developed afterwards. (Mutation. Etc.)

Age of A1 milk cows:


Quote:A1 and A2 milk cows

There are distinct differences in milk produced by different breeds of dairy cow. A2 cows are descended from ancient breeds more than 5000 years ago. A1 cows are “newer” breeds that have been around for the last 5000 years & have experienced a mutation of a particular amino acid in a protein called beta casein which has a chain of 229 amino acids. A2 cows produce this protein with a proline at position 67, whereas an A1 cow has a mutated proline amino acid which converts to a histidine. The proline has a strong bond to another small protein called BCM 7; which keeps the potentially toxic BCM 7 from being released. But the mutated protein histidine, only weakly holds onto BCM 7 – and then it’s released into the tract of animals & humans who drink it. This is a likely cause of increased phlegm production in digestive & respiratory tract, which can worsen upper respiratory problems – among other problems. The book “The Devil In The Milk: Ilness, Health & the Politics of A1 & A2 Milk” goes into much more detail.

Older breeds such as the Jersey, Guernsey, Asian and African cows are primarily A2 as are goats and sheep. Herds in much of Asia, Africa and parts of S. Europe still produce A2 milk. Black & white breeds like Holstein or Friesians are A1 cows. They’re the most popular breeds in North America, New Zealand, Australia and the rest of Europe.
As tempted as I am to ask pertinent questions/make a remark at this point: note how I don't.

d) More on mutation and age etc


Quote:Keith Woodford, Devil in the Milk author, correctly states that [color="#FF0000"]all European cattle breeds are relatively recent[/color] and the dairy breeds originally all belonged to beta-casein group A2. The point mutations that resulted in subgroups A1, B, and C (not just A1) all include an alteration of proline to histidine at the 67th amino acid in the 209 amino acid chain that is bovine beta-casein. These cows are referred to in shorthand as A1 in the text. These subgroups, but not A2 or A3, would be classified as “bad” according to the theoretical ability to be cleaved and form beta-casomorphine-7, BCM7. Both A2 and A3 gene polymorphisms would then be considered “good” and are called A2.

Lumping these subgroups together, it is unclear that the Jersey, ranging from 50 to 57% “good”, is superior to the Holstein, ranging from 35 to 57% good across 9 studies on 3 continents (see Graph 1). This is because Jerseys range from 33 to 36% B beta-casein and this number must be added to the A1 group to determine what percent have the mutation of concern.

Ranking of European dairy breeds from “bad” to “good” based on a large California study directly comparing American cattle breeds, would be first Holstein, then Milking Shorthorn tied with Jersey, then Brown Swiss and finally Guernsey (see Graph 2). There is a mixture of types within each breed that is consistent across herds and studies. Because of this, Woodford in his book recommends testing of individual animals. If one were to bet on a breed with the “best” beta-casein type it would be the Guernsey with 96% “good” genotype.

Please see our complete “A1-A2: The Devil’s in the Details” Powerpoint presentation located HERE for more on this subject.
(Again, note no comments.)

There may be better links out there, I just picked the first that came by.

There are other reasons - more pressing than "health" - as to why you don't want to be drinking western milk obtained by farms employing certain... dubious practices. (That's only if you care about the kind of four-footed animals that go Moo.) Their ethical standards in this are beyond anything most Hindus will be capable of abiding by. Not all farms, certainly. (Some are against it.) But there exists a practice that is becoming more prevalent now in the milking process/lifecycle in certain western countries (it's common/pioneered in America, I have been told) that is considered profitable and which one could reasonably describe as inhumane.
Husky, please don't delete your comments.

It is a sad misfortune that our best people are so careful with their words, and the "populace" have endure the never ending rants of the 4M.

It is also likely that A1 was not a new mutation in the A2 wild type, but rather the wild type present in the Euro aurochs or at least a very old mutation in Europe, and that the A2 allele was a secondary introgression into europe. Such introgression is non-controversial for indic origin zebu in the case of India-to-Africa; we are only too familiar why such would not be considered in the case of Europe.

Since diabetes is a survival trait (a starvation state wherein slow metabolism is maximized), it is very likely that A1 was selected in the euro auroch. Of course, such elementaries elude those for whom creationism is culture - much more occam razory to posit a single population; In this particular case, it was not possible to posit the bovine version of aboriginal (ie normatized) ANI in Europe and ASI in India, since the "mix" is in Europe itself. Thankfully, this autosomal has "survival value" and the direction of introgression is therefore clear.

At any rate, even if this not a case is allele introgression, the (dde-domesticated) A1 mutation's circumscribed distribution also precludes a euro origin for A2.

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