Out-of-India - From Theory to Truth: Part 2

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johneeG
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Re: Out-of-India - From Theory to Truth: Part 2

Post by johneeG »

RoyG wrote:Shivji and others,

A very professional youtube video should be put together pooling together all the latest genetic, linguistic, archaeological, and historical research. I can talk to a relative of mine who made it big in the digital media industry. He currently puts together very polished advertisements for a particular US political party. It just so happens he is also interested in this debate.

It would also be much easier to circulate on twitter. Let me know what you think.
Great. All the best. :)

----
Primus wrote:
johneeG wrote:Primus' saar,
I think your scepticism is misplaced. You should be first sceptical about out of africa theory itself. out of africa was first proposed by darwin himself. At the same time, out of asia was also proposed by some German. There is no proof to support out of africa theory as far as I understand, atleast there was none when darwin proposed it. It is just assumed to be true. The whole theory is based on speculation over speculation just like AIT.

The reference to east africa as origin seems to be based on bible.

As for the sceptic version you linked, he didn't give one good point relevant to the issue. His whole scepticism seems to be based on the site's other content. In short, he would believe it if mainstream media reports it.
JohneeG Ji, wouldn't you agree though that if somebody claims in one breath that the Sun revolves around the Earth and then claims humanity came out of India, you would be skeptical? Moreover, the website that 'debunks' OOA bases its conclusions on the work of the Russian chemist who has been thoroughly discredited by his own countrymen as per the reference I posted.

Granted, Darwin first proposed a single origin for humanity but it was all speculation until 1987 when the seminal paper by Cann et al was published.

You have, with respect not yet put forward any scientific evidence that modern humans did NOT come of Africa but instead came out of India as you claim. I have already said that there may well have been waves of humans going out of India to the rest of the world AFTER they had come there from Africa originally.

The question here is whether modern, homo sapiens sapiens came out of Africa originally or there was a 'multi-regional' evolution going on simultaneously OR if, as you claim India was the cradle of this particular 'civilization'. Even Priyadarshi himself admits humans entered India from Africa and then dispersed elsewhere.

I have, in my limited search, not found any credible evidence to support an Out of India theory for humanity.

Will post some more links to support the OOA belief. As I said, the likely scenario is a 'leaky replacement model'.
- If several claims are made by one entity, then validity of each claim has to be tested independently. Rightness of one claim doesn't make other claims right and wrongness of one claim doesn't make other claims wrong. Many websites and forums have several contents especially those which are not mainstream. All sites have their own agenda. We don't have to agree or disagree with all the content of any site. We use critical analysis to separate the right from wrong.

- Out of Africa was always popular from the time of Darwin himself. Cann only 'corrobarated' it once again.

About that Russian:

Here is the translation of the site you posted:
DNA demagoguery Anatoly Klyosov

January 13, 2015. TRV number 170, c. 1-2, "Science and Society"
EV Balanovskaya, SA Borinskaya, AP Buzhilova AV Dybo, LS Klein and others.
Category: Science and Society

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Fig. O. Feigel'man

At last in late 2014 of the academic conference "ethnogenesis, ethnic and socio-political history, the genesis of the language and culture of Karachai-Balkar people" acted Doctor. chemical. Sciences Anatoly Klyosov, claiming that he created a new science that the formulas of chemical kinetics reconstructs the history of the peoples. This event caused a negative feedback scientists - anthropologists, archaeologists, historians, geneticists, linguists. Scientists are concerned not so much active propaganda A. Klyosov his pseudoscience as decreased immunity of the scientific community who has made an amateurish performance on the academic platform.
The new genealogy of a chemist

We are not surprised at the appearance of strange distortion of reality television stations issued for the achievements of science. However, the inclusion in the program of the academic conference report, treats the story of the peoples on the basis of methods of chemical kinetics contrary to the facts, firmly established by anthropologists, geneticists, linguists and historians - unacceptable event for the scientific community.

Speaker A. Klyosov known public statement in the film Mikhail Zadornov, the history of the Slavs has 9 thousand. Years and they came Scandinavians [1]. We all know that movies can distort the words of the scientist and the need to look its publication in scientific journals. But in the case of A. Klyosov is problematic. He sets out his ideas mainly on the Internet, and books that do not have the neck scientific institution. Yes, in two journals, which are called scientific. The subjects first - "Bulletin of the Russian Academy of DNA Genealogy" ("Academy" was founded by himself) - wide: articles on genetics are combined with a breakdown of Veles book and analysis of climate change on the signs of the zodiac. The second magazine (Advances in Anthropology, chief editor A. Klyosov, published Scientifc Research Publishing) is not included in base recognized scientific journals, but included in the list of suspicious titles, earning the fee for the publication of anything. [2] Before hobbies human history A. Klyosov chemistry and I have worked in this specialty scientific articles and patents. Georgian Academy of Sciences even introduced him to his part in "Biochemistry." Perhaps, like Academician Fomenko, the famous mathematician, Anatoly Klyosov announced the desire to "restore order" in an alien science.

Scientists and amateurs

Studies of the genetic diversity of humanity has been going on for almost a hundred years. Population genetics studies the gene pools of all new markers: blood groups, mitochondrial DNA, Y-chromosome, and now on the complete genome. These genetics have long been used as one of many sources, telling about human migration. Today, the analysis of their DNA has become available to everyone - it did more than a million people. Due to population genetics operating time each of them can trace their direct migration of genealogical lines (male and female) for thousands of years deep. This application is called genetics branch of Genetic Genealogy, although in Russia often called "DNA genealogy." She turned out to be a breeding ground for AA Klyosov. Using ready-made database and pulling from an extensive toolkit of population geneticists Y-chromosome (occasionally mtDNA), it adds to one of the methods of genetic dating of several formulas, usurps the term "DNA genealogy" and exploiting the ever increasing interest in genetic reconstruction of the history of peoples, announces all this "new science", and itself - its creator. [3]
As Slavs make arias

A. Klyosov uses techniques that can derive the origin of any population of any desired ancestors. Here's an example: "Eastern Slavs - the genus R1a1. Their descendants, across Europe and around the world, up to Arabia, Qatar, the United Arab Emirates - representatives of R1a1, descendants of the Slavs. Or Slav, which in this context is the same "[4]. How to prove the origin of the Slavs from the Arabs? Easy - with the help of substitution of concepts: "In DNA genealogy" Eastern Slavs "- are members of an ancient family R1a1» [4]. The genetic term "haplogroup" AA Klyosov substitute for social category of "race", putting in a biological sense. Was there a common ancestor kind of real or perceived, is entirely dependent on history and not on A. Klyosov. Therefore, rigid adherence AA Klyosov kind of biology - an attempt biologization social categories.

"Members of the genus R1a1 in the Balkans, who lived there 12 thousand. Years ago, after more than 200 generations took to the East European Plain, where 4.5 thousand. Years ago there was the ancestor of modern Russian and Ukrainian kind R1a1. Even after 500 years, 4 thousand. Years ago, they came to the southern Urals, even after 400 years, went to India, where now live about 100 million of their descendants, members of the same kind R1a1. Rod Aryans. Descendants of Slav or their next of kin "[4]. In this entertaining "history" is used several times receiving substitution of terms. First, the term "Slavs", which has very definite linguistic and ethnological values ​​arbitrarily interpreted as "ancient carriers of haplogroup R1a1", this ignores that haplogroup R1a1 were many other peoples. Then, when the settlement "kind R1a1" brought to India, biological carriers of haplogroup R1a1 carries the name of the language of the "Aryans", this ignores that the Aryan (Indo-Iranian) languages ​​are divided into a couple of thousand years before the Russian and Ukrainian. Now we have to equate the end of a long migration to its beginning - and the eastern Slavs will arias (and the Arabs - the descendants of the Slavs).

A. Klyosov Formally, of course, recognizes that a lot of people haplogroup (what did he do with that fact?). Really - you draw them a picture of migrations based on this ideology throughout the existence of it is biological haplogroup Tagged really exist ethno-political or social community.

Such rigid linking biological and social parameters goes far beyond science.
How to make humanity from the Russian Plain

These methods can be used to refute anything, such as "exit" man from Africa. "The theory of human output in Africa is currently approved only as a tool to combat racism. For science, it has nothing to do "[5], says A. Klyosov. However, even the new data is not necessary - you can use the same genetic data that the world scientific community accepts as indisputable evidence of exit person from Africa. The trick is simple: explain the maximum genetic diversity in Africa is not out migrations and migrations to [6]. No matter what the theory of "the set of inputs into Africa" ​​is required abyss assumptions: for hundreds of thousands of have to go one by one targeted migration from Eurasia to Africa, and that many of the genetic lines of obligation in Africa, though crowded, but to survive, whereas in Eurasia These lines will AA Klyosov should disappear without a trace. In the writings of A. Klyosov the hypothesis that the Russian North - the ancestral home of Homo sapiens, "160 thousand. Years ago, people lived on the Russian plain, or in the north of the Russian Plain, and hence of his relatives went to the south, to Africa, arriving there after a long migration of about 140-120 thousand. years ago, "[7]. Analysis of fantastic constructions AA Klyosov already given in the book archaeologist LS Klein [8] and anthropologists on the website "Human evolution" [9]. At the same site contains gradually updated and detailed analysis of the genetic distortions, reasoned analysis for which there is no place [15].
The master of mimicry

The creator of the "new science" demonstrates not only the pressure of aggressive, but also an excellent ability to mimic academic standards, which sometimes leads to confusion not only viewers but also scientists. For example, in an article for a scientific audience surname geneticists M. Hammer, T. Karafet, L. Zhivotovsky listed among the forerunners of his "new science" [3], and in publications designed for lovers, genetics declared trash, into which the same most scientists [10].

Mimicking in response to criticism, A. Klyosov writes: "The Slavs and Aryans belong to different epochs. It's like saying that Prince Vladimir was a Soviet. Even if we have among his descendants. In any scientific article, I do not have that Arias - are Slavs, and vice versa ". [11] In fact, just about the fact that the Slavs - this aria, A. Klyosov written several books (see. Above). A skilful populist A. Klyosov produces the expected results on the public consumption. Each AA Klyosov gives the desired interpretation of its history, while not disdaining and political conclusions. But those who are sincerely interested in the origin of its people, is unlikely to find in the constructions AA Klyosov their real ancestors.
Reformatting Sciences

"New Science", designed to "reformat views of the past," not only denies the results of genetics and anthropology, and linguistics and archeology. For example, rename the Proto-Indo-European language in Proto-Slavic (with the same success can be called Teutonic, but the audience is not the same). Language imposed tight biological context: if two people have the same haplogroup, their languages ​​are required to consist of kinship: "In DNA genealogy Aryans and Slavs (at least from one-half to three-quarters of the Slavs) are one and the same family, who had a total ancestor, and the languages ​​they are obliged to diverge from a common root "[12, p. 35]. So why now the linguistics? Tested several people in a commercial company - and soon "can be classified in a different language," according to AA Klyosov [12, p. 83].

No less decisively crushes A. Klyosov and eternal problem of archeology - the relation of ethnic communities and material culture. According to the "new science", each ethnic group is associated with "their" main haplogroup. So we just have to find for each haplogroup circuit changing the time of archaeological cultures, "Attributes Arkaima ... in fact, it refers to the expected haplogroup R1a» [11]. If the community is not appropriate, it should be invented: for carriers of haplogroup «R1b» consonance created Phantom - the ancient people "erbiny."

Especially densely fantasies chemist genealogist full of his books. One - in collaboration with the inventor of the "rusantropa" (Pithecanthropus and contemporary at the same time ancestors of the Russian) AA Tyunyaevym, which the RAN Commission to Combat Pseudoscience describes the three most famous pseudo-scientists. Another book - co-authored by amateur authors from Vladivostok, many years proving that the Great are the oldest people in the world. She, like other non-scientific "achievements" AA Klyosov, advertises humorist M. Zadornov. The scientific world of his DNA genealogy rejects. It does not help even the State Prize received for achievements in chemistry. Do not save and claimed at different sites rank of professor at Harvard. Query to Harvard shows that AA Klyosov was once a «visiting professor» (position, to put it mildly, does not correspond to the Russian "Professor"). And because AA Klyosov has to announce the entire list: "Let's be honest, even though I do not like to rattle regalia. But they - an objective reality. You are comparing someone? I - Academician of the World Academy, initiated by Einstein, academician of the National Academy, winner of various awards, including the USSR State Prize for Science and Technology, the author of hundreds of jobs, most of which he wrote, without co-authors, an author of over twenty books on different languages, doctors and professors to thirty years of age, and who you are to me (implicitly) competes? Some N? (Names omitted for ethical reasons. - Ed.) That is so mad that I called "pseudoscientist"? Who do not understand the basics of what they say? Which is a complete crap, mediocrity? "[11]. Such lists of relevant plans and New Vasyukovskogo scale [13] in the "priorities DNA genealogy" includes, among other things, to achieve a "decision of the Government of the Russian Federation to support the new direction of DNA genealogy at the level of Federation" [11].
Hazardous phantoms

To sum up: the "new science" AA Klyosov de facto is not a scientific concept and can not therefore be the subject of scientific debate. This parascientific concept, unfortunately, is not harmless. Signs of language and culture is not transmitted as haplogroups or color, these are two different mechanisms. Phantoms A. Klyosov in which biological mixed with social - populist tool for managing hazardous and hidden forces. Its packaging in fashionable pseudo-scientific form flattering layman their accessibility and attract readers, the national political ambitions which does not meet the scientific world. In an effort to gain notoriety not only on the internet, A. Klyosov straightforwardly seeks political issues of the day, including a Ukrainian and a map [14], based prove to be popular, if not the science, the teleideologiey and TV propaganda. Dilettantism on television the scientific community can only comment, but amateurism on the academic podium invalid.

EV Balanovskaya (geneticist, Doctor. Biol. Sciences, prof.)
SA Borinskaya (geneticist, Doctor. Biol. Sciences)
AP Buzhilova (anthropologist, corresponding member. Russian Academy of Sciences)
V. Volkov (genealogy)
MM Gerasimov (anthropologist, PhD. Ist. Sciences)
EZ Godin (anthropologist Doctor. Biol. Sciences, prof.)
NA Dubova (anthropologist Doctor. Ist. Sciences)
AV Dybo (linguist, Corresponding Member. Russian Academy of Sciences)
LM Yepiskoposyan (geneticist, Doctor. Biol. Sciences, prof.)
A. Kassian (linguist, PhD. Filol. Sciences)
VF Kashibadze (anthropologist Doctor. Biol. Sciences)
LS Klein (archaeologist, doctor. Ist. Sciences, prof.)
AG Kozintsev (anthropologist Doctor. Ist. Sciences. Prof.)
OL Kurbatov (geneticist, Doctor. Biol. Sciences)
NV Markina (science journalist, PhD. Biol. Sciences)
DV Pezhemskiy (anthropologist, PhD. Biol. Sciences)
IV Carriers (anthropologist Doctor. Biol. Sciences)
A. Sokolov (editor of the portal "Human evolution")
EY Tetushkin (geneticist, PhD. Biol. Sciences)
VI Khartanovich (anthropologist, PhD. Ist. Sciences)
JK Net (anthropologist Doctor. Ist. Sciences)
VA Shnirelman (ethnologist, doctor. Ist. Sciences)
Yu Yusupov (ethnologist, PhD. Ist. Sciences)
LT Yablonsky (archaeologist, doctor. Ist. Sciences, prof.)
Link

Here is the wiki page of Anatoly Klyosov
Anatole A. Klyosov is a US scientist (since 1990) born in the Kaliningrad region of Russia on 20 November 1946. He is now living in Newton, Massachusetts. He is known for his work in physical chemistry, enzyme catalysis, biomedical sciences, industrial biochemistry,[1][2] and mathematical/statistical/ computer application on DNA genealogy studies. In Russia, he held one of the top scientific recognitions, being awarded the USSR State Prize in Science and Technology (1984).[3]
From 2000 to 2013, he was senior Vice President and then (from 2006) Chief Scientist of Pro-Pharmaceuticals and then Galectin Therapeutics, a public company in the Boston area, from 1996 to 2000, he was vice president of research and development for Kadant Composites, Inc., a subsidiary of Kadant, Inc., where he directed a laboratory specializing in biochemistry, microbiology and polymer engineering. From 1990 to 1998, Dr. Klyosov was visiting professor of biochemistry at the Center for Biochemical and Biophysical Sciences at Harvard Medical School. From 1981 to 1990, he was professor and head of the Carbohydrates Research Laboratory at the A.N. Bach Institute of Biochemistry, USSR Academy of Sciences.[7] Currently he is Emeritus Founder and Chief Scientist of Galectin Therapeutics and a member of Scientific Advisory Board. MIR International is his Massachusetts consulting company which he owns since October 1991, currently specializing in composite materials and DNA genealogy (two separate divisions). He is a fellow of the World Academy of Art and Science[8] (since 1989), and Foreign Member of the National Academy of Sciences of Georgia[9] (since 2014).
Wiki Link

Wikipedia is as mainstream as anyone can get. He has received some state award from Russia. He was a professor in Harvard. So, he is clearly a well-respected academician who has written a paper along with someone else saying that Non-africans don't have african genes. I don't see what exactly was debunked by this bunch who are attacking their compatriot because he is opposing their pet theories. This is similar to how any attempts to undistort the Indian history are met by a bunch of commie historians acting as roadblocks.

Anyway, as for the Out of Africa theory itself:

This is a really long but quite exhaustive article on this whole issue. It doesn't matter whether you agree or disagree with it. But, it explains how the whole thing came to be.
The Demise of Mitochondrial Eve
Brad Harrub, Ph.D. and Bert Thompson, Ph.D.
© 2003 Apologetics Press, Inc.
All Rights Reserved.
Reproduced by Permission from Apologetics Press

On the first day of 1987, a scientific “discovery” seized the attention of the popular press. The original scientific article that caused all the commotion—“Mitochondrial DNA and Human Evolution”—appeared in the January 1, 1987 issue of Nature, and was authored by Rebecca Cann, Mark Stoneking, and Allan C. Wilson (see Cann, et al., 1987). These three scientists announced that they had “proven” that all modern human beings can trace their ancestry back to a single woman who lived 200,000 years ago in Africa. This one woman was nicknamed “Eve” (a.k.a., “mitochondrial Eve”)—much to the media’s delight. An article in the January 26, 1987 issue of Time magazine bore the headline, “Everyone’s Genealogical Mother: Biologists Speculate that ‘Eve’ Lived in Sub-Saharan Africa” (Lemonick, 1987). A year later, that “speculation” became a major Newsweek production titled, “The Search for Adam and Eve” (Tierney, et al., 1988). The provocative front cover presented a snake, tree, and a nude African couple in a “Garden of Eden” type setting. The biblical-story imagery was reinforced by showing the woman offering an apple to the man.

A word of explanation is in order. For decades, evolutionists had been trying to determine the specific geographical origin of humans—whether we all came from one specific locale, or whether there were many small pockets of people placed around the globe. When they set out to determine the specific geographical origin of humans, a curious piece of data came to light. As they considered various human populations, Africans seemed to show much more genetic variation than non-Africans (i.e., Asians, Europeans, Native Americans, Pacific Islanders, et al.). According to molecular biologists, this increased variability is the result of African populations being older, thus, having had more time to accumulate mutations and diverge from one another. This assumption led some researchers to postulate that Africa was the ancient “cradle of civilization” from which all of humanity had emerged.

The genetic material (DNA) in a cell’s nucleus controls the functions of the cell, bringing in nutrients from the body and making hormones, proteins, and other chemicals. Outside the nucleus is an area known as the cytoplasmic matrix (generally referred to simply as the cytoplasm), which contains, among other things, tiny bean-shaped organelles known as mitochondria. These often are described as the “energy factories” of the cell.

Mitochondria contain their own DNA, which they use to make certain proteins; the DNA in the nucleus oversees production of the rest of the proteins necessary for life and its functions. However, mitochondrial DNA (mtDNA) was thought to be special for two reasons. First, it is short and relatively simple in comparison to the DNA found within the nucleus, containing only thirty-seven genes instead of the 70,000+ genes located in the nuclear DNA. This makes it relatively easy to analyze. Second, unlike nuclear DNA, which each person inherits in a jumbled form from both parents, mitochondrial DNA was thought to be passed on only through the mother’s line (more about this later). Working from the assumption that mtDNA is passed to the progeny only by the mother, Dr. Cann and her coworkers believed that each new cell should contain copies of only the egg’s mitochondria. In trying to draw the human family tree, therefore, researchers took a special interest in these minute strands of genetic code. What they really were interested in, of course, was the variations in mitochondrial DNA from one group of people to another.

Although our mtDNA should be, in theory at least, the same as our mother’s mtDNA, small changes (or mutations) in the genetic code can, and do, arise. On rare occasions, mutations are serious enough to do harm. More frequently, however, the mutations have no effect on the proper functioning of either the DNA or the mitochondria. In such cases, the mutational changes will be preserved and carried on to succeeding generations.

Theoretically, if scientists could look farther and farther into the past, they would find that the number of women who contributed the modern varieties of mitochondrial DNA gets less and less until, finally, we arrive at one “original” mother. She, then, would be the only woman out of all the women living in her day to have a daughter in every generation till the present. Coming forward in time, we would see that the mtDNA varieties found within her female contemporaries were gradually eliminated as their daughters did not have children, had only sons, or had daughters who did not have daughters. This does not mean, of course, that we would look like this putative ancestral mother; rather, it means only that we would have gotten our mitochondrial DNA from her.

To find this woman, researchers compared the different varieties of mtDNA in the human family. Since mtDNA occurs in fairly small quantities, and since the researchers wanted as large a sample as possible from each person, they decided to use human placentas as their source of the mtDNA. So, Rebecca Cann and her colleagues selected 145 pregnant women and two cell lines representing the five major geographic regions: 20 Africans, 34 Asians, 46 Caucasians, 21 aboriginal Australians, and 26 aboriginal New Guineans (Cann, et al., 1987, 325:32). All placentas from the first three groups came from babies born in American hospitals. Only two of the 20 Africans were born in Africa.

After analyzing a portion of the mtDNA in the cells of each placenta, they found that the differences “grouped” the samples by region. In other words, Asians were more like each other than they were like Europeans, people from New Guinea were more like each other than they were like people from Australia, and so on.

Next, they saw two major branches from in their computer-generated tree of recent human evolution. Seven African individuals formed one distinct branch, which started lower on the trunk than the other four. This was because the differences among these individuals were much greater than the differences between other individuals and other groups. More differences mean more mutations, and hence more time to accumulate those changes. If the Africans have more differences, then their lineage must be older than all the others. The second major branch bore the non-African groups and, significantly, a scattering of the remaining thirteen Africans in the sample. To the researchers, the presence of Africans among non-Africans meant an African common ancestor for the non-African branches, which, likewise, meant an African common ancestor for both branches. The nickname “Eve” stuck to this hypothetical common ancestral mother, and later, then, fired the media’s imagination.

Having concluded that the African group was the oldest, Dr. Cann and her colleagues wanted to find out just how old the group might be. To do this, they used what is known as a “molecular clock” that, in this case, was based on mutations in the mtDNA. The rate at which the clock ticked was determined from the accumulation of changes over a given period of time. As we note below in our discussion of the so-called molecular clock, if the assumption was made that there was one mutation every 1,000 years, and if scientists found a difference of 10 mutations between us and our ancient hypothetical ancestor, they then could infer that that ancestor lived 10,000 years ago.

The researchers looked in two places for their figures. First, they compared mtDNA from humans with that from chimpanzees, and then used paleontology and additional molecular data to determine the age of the supposed common ancestor. This (and similar calculations on other species) revealed a mutation rate in the range of 2% to 4% per million years. Second, they compared the groups in their study that were close geographically, and took the age of the common ancestor from estimated times of settlement as indicated by anthropology and archaeology. Again, 2% to 4% every million years seemed reasonable to them.

Since the common mitochondrial ancestor diverged from all others by 0.57%, she must have lived sometime between approximately 140,000 (0.57 ÷ 4 × 1,000,000) and 290,000 (0.57 ÷ 2 × 1,000,000) years ago. The figure of 200,000 was chosen as a suitable round number.

The results obtained from analysis of mitochondrial DNA eventually led to what is known in evolutionary circles as the “Out of Africa” theory. This is the idea that the descendants of mitochondrial Eve were the only ones to colonize Africa and the rest of the world, supplanting all other hominid populations in the process. Many (though not all) evolutionists claim that such an interpretation is in accord with archaeological, paleontological, and other genetic data (see Stringer and Andrews, 1988; for an opposing viewpoint, see the written debate in the April 1992 issue of Scientific American).

While many evolutionists have accepted the mitochondrial DNA tree, they differ widely in their views regarding both the source of the nuclear DNA and the “humanity” of Eve. Some believe that Eve contributed all the nuclear DNA, in addition to the mitochondrial DNA. Some believe she was an “archaic” Homo sapiens, while others believe she was fully human. The exact interpretation is hotly debated because mitochondrial DNA is “something of a passenger in the genetic processes that lead to the formation of new species: it therefore neither contributes to the formation of a new species nor reveals anything about what actually happened” (Lewin, 1987, 238:24).
The Demise of Mitochondrial Eve

Things change rapidly in science. What is popular one day, is not the next. Theories come, and theories go. And so it is with mitochondrial Eve. She once was in vogue as “the woman of the moment,” so to speak. Now, she has become virtually the “crazy aunt in the attic” that no one wants to admit even exists.

But it was not forbidden fruit that caused her demise this time around. The “passing” of one of evolution’s most familiar icons is due to new scientific facts that have surfaced since her introduction in 1987. If humans received mitochondrial DNA only from their mothers, then researchers could “map” a family tree using that information. And, if the mutations affecting mtDNA had indeed occurred at constant rates, then the mtDNA could serve as a molecular clock for timing evolutionary events and reconstructing the evolutionary history of extant species. It is the “ifs” in these two sentences that are the problem.

Mitochondrial Eve is alleged to have lived in Africa at the beginning of the Upper Pleistocene period (between 100,000 and 200,000 years ago). She has been described as the most-recent common ancestor of all humans on Earth today, with respect to matrilineal descent. The validity of these assertions, however, is dependent upon two critically important assumptions: (1) that mtDNA is, in fact, derived exclusively from the mother; and (2) that the mutation rates associated with mtDNA have remained constant over time. However, we now know that both of these assumptions are wrong!

First, let us examine the assumption that mtDNA is derived solely from the mother. In response to a paper that appeared in Science in 1999, anthropologist Henry Harpending of the University of Utah lamented: “There is a cottage industry of making gene trees in anthropology and then interpreting them. This paper will invalidate most of that” (as quoted in Strauss, 1999, 286:2436). Just as women thought they were getting their fair shake in science, the tables turned. As one study noted:

Women have struggled to gain equality in society, but biologists have long thought that females wield absolute power in a sphere far from the public eye: in the mitochondria, cellular organelles whose DNA is thought to pass intact from mother to child with no paternal influence. On page 2524 however, a study by Philip Awadalla of the University of Edinburgh and Adam Eyre-Walker and John Maynard Smith of the University of Sussex in Brighton, U.K. finds signs of mixing between maternal and paternal mitochondrial DNA (mtDNA) in humans and chimpanzees. Because biologists have used mtDNA as a tool to trace human ancestry and relationships, the finding has implications for everything from the identification of bodies to the existence of a “mitochondrial Eve” 200,000 years ago (Strauss, 286:2436, emphasis added).

One year later, researchers made this startling admission:

Mitochondrial DNA (mtDNA) is generally assumed to be inherited exclusively from the mother…. Several recent papers, however, have suggested that elements of mtDNA may sometimes be inherited from the father. This hypothesis is based on evidence that mtDNA may undergo recombination. If this does occur, maternal mtDNA in the egg must cross over with homologous sequences in a different DNA molecule; paternal mtDNA seems the most likely candidate…. If mtDNA can recombine, irrespective of the mechanism, there are important implications for mtDNA evolution and for phylogenetic studies that use mtDNA (Morris and Mightowlers, 2000, 355:1290, emphasis added).

In 2002, a study was conducted that concluded:

Nevertheless, even a single validated example of paternal mtDNA transmission suggests that the interpretation of inheritance patterns in other kindreds thought to have mitochondrial disease should not be based on the dogmatic assumption of absolute maternal inheritance of mtDNA…. The unusual case described by Schwartz and Vissing is more than a mere curiosity (Williams, 2002, 347:611, emphasis added).

And now we know that these are more than small “fractional” amounts of mtDNA coming from fathers. The August 2002 issue of the New England Journal of Medicine contained the results of one study, which concluded:

Mammalian mitochondrial DNA (mtDNA) is thought to be strictly maternally inherited…. Very small amounts of paternally inherited mtDNA have been detected by the polymerase chain reaction (PCR) in mice after several generations of interspecific backcrosses…. We report the case of a 28-year-old man with mitochondrial myopathy due to a novel 2-bp mtDNA deletion…. We determined that the mtDNA harboring the mutation was paternal in origin and accounted for 90 percent of the patient’s muscle mtDNA (Schwartz and Vissing, 2002, 347:576, emphasis added).

Ninety percent! And all this time, evolutionists have been selectively shaping our family tree using what was alleged to be only maternal mtDNA!

As scientists have begun to comprehend the fact, and significance, of the “death” of mitochondrial Eve, many have found themselves searching for alternatives that can help them maintain their current beliefs regarding human origins. But this recombination ability in mtDNA makes the entire discussion a moot point. As Strauss noted:

Such recombination could be a blow for researchers who have used mtDNA to trace human evolutionary history and migrations. They have assumed that the mtDNA descends only through the mother, so they could draw a single evolutionary tree of maternal descent—all the way back to an African “mitochondrial Eve,” for example. But “with recombination there is no single tree,” notes Harpending. Instead, different parts of the molecule have different histories. Thus, “there’s not one woman to whom we can trace our mitochondria,” says Eyre-Walker (1999, 286:2436, emphasis added).

Our thoughts on the matter exactly.
The Molecular Clock—Dating Mitochondrial Ancestors

Second, let us examine the assumption that the mutations affecting mtDNA did indeed occur at constant rates. The researchers who made the initial announcement about Eve not only gave a location for this amazing female, but also proposed the time period during which she was supposed to have lived. However, in order for the mtDNA theory to be of any practical use, those scientists had to assume that random mutations in the DNA occurred at documented, steady rates. For example, if they speculated that there was one mutation every 1,000 years, and they found a difference of 10 mutations between us and our ancient hypothetical ancestor, they then could infer that that ancestor lived 10,000 years ago. Scientists—who used this concept to determine the age of mitochondrial Eve—refer to this proposed mutation rate as a “molecular clock.” One group of researchers described the process as follows:

The hypothesis of the molecular clock of evolution emerged from early observations that the number of amino acid replacements in a given protein appeared to change linearly with time. Indeed, if proteins (and genes) evolve at constant rates they could serve as molecular clocks for timing evolutionary events and reconstructing the evolutionary history of extant species (Rodriguez-Trelles, et al., 2001, 98:11405, parenthetical item in orig.).

It sounds good in theory, but the actual facts tell an entirely different story. As these same researchers went on to admit:

The neutrality theory predicts that the rate of neutral molecular evolution is constant over time, and thus that there is a molecular clock for timing evolutionary events. It has been observed that the variance of the rate of evolution is generally larger than expected according to the neutrality theory, which has raised the question of how reliable the molecular clock is or, indeed, whether there is a molecular clock at all…. The observations are inconsistent with the predictions made by various subsidiary hypotheses proposed to account for the overdispersion of the molecular clock (98:11405, emphasis added).

Another study that was published in 2002 pointed out a built-in, natural bias for older ages that result from use of the molecular clock. The researchers who carried out the study noted:

There is presently a conflict between fossil- and molecular-based evolutionary time scales. Molecular approaches for dating the branches of the tree of life frequently lead to substantially deeper times of divergence than those inferred by paleontologists…. Here we show that molecular time estimates suffer from a methodological handicap, namely that they are asymmetrically bounded random variables, constrained by a nonelastic boundary at the lower end, but not at the higher end of the distribution. This introduces a bias toward an overestimation of time since divergence, which becomes greater as the length of the molecular sequence and the rate of evolution decrease…. Despite the booming amount of sequence information, molecular timing of evolutionary events has continued to yield conspicuously deeper dates than indicated by the stratigraphic data. Increasingly, the discrepancies between molecular and paleontological estimates are ascribed to deficiencies of the fossil record, while sequence-based time tables gain credit. Yet, we have identified a fundamental flaw of molecular dating methods, which leads to dates that are systematically biased towards substantial overestimation of evolutionary times (Rodriguez-Trelles, et al., 2002, 98:8112,8114, emphasis added).

Until approximately 1997, we did not have good empirical measures of mutation rates in humans. However, that situation greatly improved when geneticists were able to analyze DNA from individuals with well-established family trees going back several generations. One study found that mutation rates in mitochondrial DNA were eighteen times higher than previous estimates (see Parsons, et al., 1997).

Science writer Ann Gibbons authored an article for the January 2, 1998 issue of Science titled “Calibrating the Mitochondrial Clock,” the subheading of which read as follows: “Mitochondrial DNA appears to mutate much faster than expected, prompting new DNA forensics procedures and raising troubling questions about the dating of evolutionary events.” In that article, she discussed the new data which showed that the mutation rates used to obtain mitochondrial Eve’s age no longer could be considered valid, and concluded:

Regardless of the cause, evolutionists are most concerned about the effect of a faster mutation rate. For example, researchers have calculated that “mitochondrial Eve”—the woman whose mtDNA was ancestral to that in all living people—lived 100,000 to 200,000 years ago in Africa. Using the new clock, she would be a mere 6,000 years old (1998: 279:29, emphasis added).

Gibbons quickly went on to note, of course, that “no one thinks that’s the case,” (279:29). She concluded her article by discussing the fact that many test results are (to use her exact word) “inconclusive.” She then noted: “And, for now, so are some of the evolutionary results gained by using the mtDNA clock” (279:29).

We now know that the two key assumptions behind the data used to establish the existence of “mitochondrial Eve” are not just flawed, but wrong. The assumption that mitochondrial DNA is passed down only by the mother is completely incorrect (it also can be passed on by the father). And, the mutation rates used so calibrate the so-called “molecular clock” are now known to have been in error. (To use the words of Rodriguez-Trelles and his coworkers, the method contains a “fundamental flaw.”)

Philip Awadalla and his coworkers noted in Science: “Many inferences about the pattern and tempo of human evolution and mtDNA evolution have been based on the assumption of clonal inheritance. There inferences will now have to be reconsidered” (1999, 286:2525). However, rather than merely “reconsidering” their theory and attempting to revamp it accordingly, evolutionists need to admit, honestly and forthrightly, that “mitochondrial Eve,” as it turns out, has existed only in their minds, not in the facts of the real world. Science works by analyzing the data and forming hypotheses based on those data. Science is not supposed to massage the data until they fit a certain preconceived hypothesis. All of the conclusions that have been drawn from research on mitochondrial Eve via the molecular clock must now be discarded as unreliable. A funeral and interment are in order for mitochondrial Eve.


References

Awadalla Philip, Adam Eyre-Walker, and John Maynard Smith (1999), “Linkage Disequilibrium and Recombination in Hominid Mitochondrial DNA,” Science, 286:2524-2525, December 24.

Cann, Rebecca L., Mark Stoneking, and Allan C. Wilson (1987), “Mitochondrial DNA and Human Evolution,” Nature, 325:31-36, January 1.

Gibbons, Ann (1998), “Calibrating the Mitochondrial Clock,” Science, 279:28-29, January 2.

Lemonick, Michael D. (1987), “Everyone’s Genealogical Mother,” Time, p. 66, January 26.

Lewin, Roger (1987), “The Unmasking of Mitochondrial Eve,” Science, 238:24-26, October 2.

Morris, Andrew A. M., and Robert N. Lightowlers (2000), “Can Paternal mtDNA be Inherited?,” The Lancet, 355:1290-1291, April 15.

Parsons, Thomas J., et al. (1997), “A High Observed Substitution Rate in the Human Mitochondrial DNA Control Region,” Nature Genetics, 15:363.

Rodriguez-Trelles, Francisco, Rosa Tarrio, and Francisco J. Ayala (2001), “Erratic Overdispersion of Three molecular Clocks: GPDH, SOD, and XDH,” Proceedings of the National Academy of Sciences, 98:11405-11410, September 25.

Rodriguez-Trelles, Francisco, Rosa Tarrio, and Francisco J. Ayala (2002), “A Methodological Bias Toward Overestimation of Molecular Evolutionary Time Scales,” Proceedings of the National Academy of Sciences, 99:8112-8115, June 11.

Schwartz, Marianne and John Vissing (2002), “Paternal Inheritance of Mitochondrial DNA,” New England Journal of Medicine, 347:576-580, August 22.

Strauss, Evelyn (1999), “mtDNA Shows Signs of Paternal Influence,” Science, 286:2436, December 24.

Stringer, C.B. and P. Andrews (1988), “Genetic and Fossil Evidence for the Origin of Modern Humans,” Science, 239:1263-1268, March 11.

Tierney, John, Lynda Wright, and Karen Springen (1988), “The Search for Adam and Eve,” Newsweek, pp. 46-52, January 11.

Williams, R. Sanders (2002), “Another Surprise from the Mitochondrial Genome,” New England Journal of Medicine, 347:609-611, August 22.
Link

This is an anti-evolution site. But, this article itself seems to be pretty rigorously researched with references and all.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by johneeG »

shiv wrote:
johneeG wrote:
The reference to east africa as origin seems to be based on bible.
This is unlikely.

Old testament - from which Christianity arose says that God made man. Not evolution in Africa. Later Noah (of Noah's ark) had 3 sons Ham, Shem and Japheth.

Ham apparently saw his father Noah naked (presumably he was fkcuing) and Noah got so angry that he cursed his son Ham and said all Ham's descendants would be slaves.

Christianity has considered Africans and blacks as "Ham-ites" - sons of Ham - fit only to be slaves. The descendants of Noah's sone Shem became "Shemites" - or Semites - i.e. Arabs and Jews. European Christians are descendants of Japheth - considered as the most superior people. In fact European Christian Orientalists (Germans, British, French) were extremely upset when they found very ancient ruins in Iraq/Syria that were older than their bible. That is why they were so thrilled when the "found" Sanskrit - which was older than those ruins. They then claimed Sanskrit as theirs or a descendant language of the European Christians. I have academic references for all this and they will appear in my book.

So the idea that out of Africa came from the bible is wrong.

I was referring to this:
Cush (Bible)
From Wikipedia, the free encyclopedia

Kush, also spelled Cush (/kʊʃ, kʌʃ/; Biblical: כּוּשׁ Kûš), was, according to the Bible, the eldest son of Ham, who was a son of Noah. He was the brother of Mizraim (Egypt), Canaan (land of Canaan), and Phut, and the father of the Biblical character Nimrod mentioned in the "Table of Nations" in the Genesis 10:6 and I Chronicles 1:8. Cush is traditionally considered the eponymous ancestor of the people of the "land of Cush," an ancient territory that is believed to have been located on either side or both sides of the Red Sea. As such, "Cush" is alternately identified in Scripture with the kingdom of Kush, ancient Aethiopia, and/or the Arabian peninsula.[1]
Link
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Re: Out-of-India - From Theory to Truth: Part 2

Post by JE Menon »

http://arstechnica.com/science/2016/01/ ... s-genomes/

Something which may be useful to be aware of - another line of argument perpetuating subtly the AIT bull.

Don't know which the original study they are referring to is, and who the researchers are.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by member_29325 »

JEM boss, a bit coincidental that all these guys are now mentioning the Gupta regime all of a sudden --seems to be based off the same source like this earlier one from archeology today posted in previous page. 1500 years is hardly a blip in evolutionary time scales -- will try to get the original arch today article and dig through the references.

link to arch today article
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Re: Out-of-India - From Theory to Truth: Part 2

Post by member_29218 »

johneeG wrote:


- Out of Africa was always popular from the time of Darwin himself. Cann only 'corrobarated' it once again.
JohneeG Ji, I doubt if the OOA theory was 'popular' from Darwin's time. In fact, the 'multiregional' theory was more commonly accepted and promoted since that conformed with the Western view of superior racial attributes being genetic in origin.
About that Russian:

Here is the translation of the site you posted:
DNA demagoguery Anatoly Klyosov

................ Anatoly Klyosov, ............treats the story of the peoples on the basis of methods of chemical kinetics contrary to the facts firmly established by anthropologists, geneticists, linguists and historians.


A. Klyosov uses techniques that can derive the origin of any population of any desired ancestors.


The creator of the "new science" demonstrates not only the pressure of aggressive, but also an excellent ability to mimic academic standards, which sometimes leads to confusion not only viewers but also scientists.

To sum up: the "new science" AA Klyosov de facto is not a scientific concept and can not therefore be the subject of scientific debate. This parascientific concept, unfortunately, is not harmless.

EV Balanovskaya (geneticist, Doctor. Biol. Sciences, prof.)
SA Borinskaya (geneticist, Doctor. Biol. Sciences)
AP Buzhilova (anthropologist, corresponding member. Russian Academy of Sciences)
V. Volkov (genealogy)
MM Gerasimov (anthropologist, PhD. Ist. Sciences)
EZ Godin (anthropologist Doctor. Biol. Sciences, prof.)
NA Dubova (anthropologist Doctor. Ist. Sciences)
AV Dybo (linguist, Corresponding Member. Russian Academy of Sciences)
LM Yepiskoposyan (geneticist, Doctor. Biol. Sciences, prof.)
A. Kassian (linguist, PhD. Filol. Sciences)
VF Kashibadze (anthropologist Doctor. Biol. Sciences)
LS Klein (archaeologist, doctor. Ist. Sciences, prof.)
AG Kozintsev (anthropologist Doctor. Ist. Sciences. Prof.)
OL Kurbatov (geneticist, Doctor. Biol. Sciences)
NV Markina (science journalist, PhD. Biol. Sciences)
DV Pezhemskiy (anthropologist, PhD. Biol. Sciences)
IV Carriers (anthropologist Doctor. Biol. Sciences)
A. Sokolov (editor of the portal "Human evolution")
EY Tetushkin (geneticist, PhD. Biol. Sciences)
VI Khartanovich (anthropologist, PhD. Ist. Sciences)
JK Net (anthropologist Doctor. Ist. Sciences)
VA Shnirelman (ethnologist, doctor. Ist. Sciences)
Yu Yusupov (ethnologist, PhD. Ist. Sciences)
LT Yablonsky (archaeologist, doctor. Ist. Sciences, prof.)

Here is the wiki page of Anatoly Klyosov

Wikipedia is as mainstream as anyone can get. He has received some state award from Russia. He was a professor in Harvard. So, he is clearly a well-respected academician who has written a paper along with someone else saying that Non-africans don't have african genes. I don't see what exactly was debunked by this bunch who are attacking their compatriot because he is opposing their pet theories. This is similar to how any attempts to undistort the Indian history are met by a bunch of commie historians acting as roadblocks.

About Wiki: I don't think anybody believes Wikipedia is absolute proof of anything, it's a freely editable site. I made corrections to a webpage a few days ago and today I find that somebody has reverted to the old stuff. A lot of information on Wiki is agenda driven. The only good thing is that it is a repository of general information that is useful at times and the citations often are valuable. However, it is by no means a factual database especially when something controversial is presented. It is not in that sense a peer-reviewed and respected journal (although that is another story - for some other time).

I deleted most of the material from the Russian site, leaving only the comments of the scientists - bolded by me in one instance, and the list of their names.

I believe their credentials are equally impressive and not being from Harvard does not diminish their opinion in any way.

About Klyosov: Just because he is at Harvard does not make his word gospel. Plenty of academicians from such universities can write garbage. I do not believe his paper on the origins of Humanity was approved or vetted by Harvard, his other work in chemistry may have been. If you are a Professor of Neurology at Columbia and choose to write an article in an obscure journal or website about the genetic make up of the Bantu claiming some new scientific method that you have developed, it would not be surprising if geneticists do not agree with you. Just because you are a recognized expert and authority in one field does not mean that whatever you say about anything is equally authentic.
Anyway, as for the Out of Africa theory itself:

This is a really long but quite exhaustive article on this whole issue. It doesn't matter whether you agree or disagree with it. But, it explains how the whole thing came to be.
The Demise of Mitochondrial Eve
Brad Harrub, Ph.D. and Bert Thompson, Ph.D.
© 2003 Apologetics Press, Inc.
All Rights Reserved.
Reproduced by Permission from Apologetics Press

This is an anti-evolution site. But, this article itself seems to be pretty rigorously researched with references and all.
To help you along, I will quote another article by the same guys in which they spew the same nonsense and come to a different conclusion:


CONCLUSION

One of the best arguments against evolution is the complexity, intricacy, ingenuity, beauty, and design of the molecules in living systems. Michael Denton affirmed:

Molecular biology has shown that even the simplest of all living systems on earth today, bacterial cells, are exceedingly complex objects. Although the tiniest bacterial cells are incredibly small, weighing less than 10-12gms, each is in effect a veritable microminiaturized factory containing thousands of exquisitely designed pieces of intricate molecular machinery, made up altogether of one hundred thousand million atoms, far more complicated than any machine built in the non-living world (1985, p. 250).

How can blind chance account for the information stored in the molecular structure of DNA? And how can “slight modifications” account for the complex highway of molecular motors? The reality is, they cannot. Centuries ago, Greek philosopher Democritus stated that everything that exists in the Universe is the end result of chance and necessity. Today, even with all of our advanced knowledge of the molecular world around us, many people remain dedicated to such an idea. As G.K. Chesterton once remarked: “When men stop believing in God, they do not believe in nothing; they believe in anything.”
Notice they do not argue about the Out of Africa facts but instead focus mainly on the mtDNA and 'Eve' which is to be expected since their entire existence is threatened if this African Eve is real and therefore the Biblical one is false. They base their entire argument on two 'facts'

1. mtDNA is flawed and 2. The rate of mutations within are also flawed.

Thus, the whole origin of Humans out of Africa thing is wrong. They do not talk about whole genome sequencing, the SNP analysis and the literally hundreds of papers supporting the OOA concept.

In a response to their original article, Cann et al do talk about the 'molecular clock' and admit that the exact time scale is unclear. They also confirm their own methodology as far as the mtDNA is concerned. I will see if I can attach that here.

FWIW, here's a critique of the Apologetics

The site has a sleek design, having recently been revamped. Despite this, it still contains obvious bias and reversal of scientific method, the site is also a good place where one can practice one's knowledge of logical fallacies. The site's most popular ones are: the false dichotomy, non sequitur, argument from design, argument from authority and the typical straw man.
Also, not that it impacts on scientific argument, but perhaps just adds one more nail........
He said one minister told him, “He didn't molest Methodists. He didn't molest Baptists. He didn't molest atheists. And we intend to keep it in the church.” (The minister who allegedly made that statement declined to comment.)
So, to sum it up, you have quoted two sources to refute the long-held OOA theory, both are of dubious status and certainly not mainstream.

Here is an image of the correspondence in Nature from the original authors of the article in 1987:

Image

Image



I will, with respect, continue to believe that modern humanity came out of Africa.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by ramana »

JE Menon wrote:http://arstechnica.com/science/2016/01/ ... s-genomes/

Something which may be useful to be aware of - another line of argument perpetuating subtly the AIT bull.

Don't know which the original study they are referring to is, and who the researchers are.

JEM and Others try this:

http://www.pnas.org/content/early/2016/ ... 3.full.pdf

Three authors study on which the Hindu had an article.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by member_29218 »

^^^

The study is interesting but as always, when driven by an agenda, the conclusions are often far beyond the scope of the original work.

Any research starts off with a hypothesis - you set off to prove or disprove an established fact, or propose a new idea and present your materials, methods and results with a conclusion as to whether your hypothesis was confirmed or not.

In this instance they tested a bunch of samples and concluded that there were several 'ancestral' populations and of course the 'evil caste system' can even be seen in our genetic markers! Next they will say that being poor is programmed into our genes - not a far cry from bubba who is beating a woman over the head with a club lamenting he can't help it, it's his genes making him do it!

What is left out from the paper completely is the religious profile of the subjects. It would be interesting to note if the differences in caste are also present in different faiths. Given the history of conquests and large scale interbreeding that went on in Northern India it may not be surprising. OTOH, it may not paint a pretty picture politically speaking. This way it is much better and can get maximum media coverage.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by ramana »

Cell Biology:

http://www.cell.com/current-biology/ful ... 16)00087-7

Single major Dispersal of non-Africans and Late Glacial Population Turnovre in Europe.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Virendra »

Article in ToI today - '70 Generations ago, caste stopped people intermixing.'
http://m.timesofindia.com/india/70-gene ... 859632.cms
Excerpts :
Study by National Institute of Biomedical Genomics, Kalyani West Bengal, traces indian origin to five ancestral groups.
All ancestral populations arrived over 10000 yrs ago. Except Andaman, all ancestral groups intermingled until 1600 yrs ago.
Caste system originated 1500 BCE or earlier. Got entrenched over centuries. Its impact on genetic material is evident around 1600 yrs ago.

Image
Last edited by Virendra on 05 Feb 2016 11:32, edited 2 times in total.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by ramana »

Virendera, See the 4th post I made above.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Prem Kumar »

An interesting paper (by Basu, Roy & Majumder). Couple of thoughts, comparing this to the 2013 Priya Moorjani paper:

1) This paper says admixing happened till about 1600 YBP. Priya Moorjani said admixing happened between 4200 YBP to 1900 YBP

2) Reich has claimed that this paper uses 22.5 years per generation. According to him, the "standard" supposedly is 29 years. If the latter number is used, 70 generations translate to 2030 years, which takes the "admixture stoppage date" close to the Priya Moorjani date. Reich might just be griping because, in the last para, the latest paper says that Reich's study wasn't comprehensive enough!

3) What this paper states (& Priya Moorjani only hinted at) is that there were admixtures from the very early ASI/ANI dates itself. So, its not like suddenly very recently, ANIs woke up to flirt with ASI girls

4) What Priya Moorjani warned in her paper is that the 4200 YBP - 1900 YBP admixture is not to be confused with any mythical Aryan invasion. This was purely Indians-having-sex-with-Indians

5) Genetics papers should stop quoting Linguists if they want to be taken seriously. A paragraph in this latest paper casually mentions that the Rig Veda is dated to be between 1500 - 1000 BC! WTF :roll:

6) I don't trust this Reich character, even though Priya seems to have been his student. I am convinced he is an AIT-Nazi. His comment is always sought out on papers which don't involve him and he tries to give an AIT-ish spin to the results
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Re: Out-of-India - From Theory to Truth: Part 2

Post by RoyG »

Ramanaji,

>10000 ya arrival of whites is very close to the dates given in the 2015 and 2012 papers posted by Shiv and me.

This is where the R-Z93 (R1a1a1b2) becomes relevant. It is the most ancient and found in Punjab itself.

They then branched outward and into Central Asia and then Europe and Siberia (Whether this was a 1st or 2nd loop is still questionable. Not sure if R1a breakdown can tell us anything about it)

It's all coming together nicely now.

Coupled with Jati/Varna solidification starting sometime around 6th Century during the fag end of Gupta rule (most likely Skandagupta) we can conclude that varna/jati is indeed non-vedic in origin and AIT/AMT discredited.

Not sure what can keep AIT/AMT afloat now. Genetics seems like to have officially finished it.

SHIVJI, we need that book lol. Maybe we can generate a very logical timeline and migration track to simplify things.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by ramana »

Am waiting for a few more comments from biologists.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by shiv »

Primus wrote:^^^

The study is interesting but as always, when driven by an agenda, the conclusions are often far beyond the scope of the original work.

Any research starts off with a hypothesis - you set off to prove or disprove an established fact, or propose a new idea and present your materials, methods and results with a conclusion as to whether your hypothesis was confirmed or not.

In this instance they tested a bunch of samples and concluded that there were several 'ancestral' populations and of course the 'evil caste system' can even be seen in our genetic markers! Next they will say that being poor is programmed into our genes - not a far cry from bubba who is beating a woman over the head with a club lamenting he can't help it, it's his genes making him do it!

What is left out from the paper completely is the religious profile of the subjects. It would be interesting to note if the differences in caste are also present in different faiths. Given the history of conquests and large scale interbreeding that went on in Northern India it may not be surprising. OTOH, it may not paint a pretty picture politically speaking. This way it is much better and can get maximum media coverage.
Once again - because I like the expression, I would like to point out that there is an old Latin legal term for this which I had heard my grandfather use : "petitio principii" - when the premise is the same as the conclusion

http://philosophy.lander.edu/logic/circular.html
Petitio Principii: (circular reasoning, circular argument, begging the question) in general, the fallacy of assuming as a premiss a statement which has the same meaning as the conclusion.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by vanand »

Virendra wrote:Article in ToI today - '70 Generations ago, caste stopped people intermixing.'
http://m.timesofindia.com/india/70-gene ... 859632.cms
Excerpts :
Study by National Institute of Biomedical Genomics, Kalyani West Bengal, traces indian origin to five ancestral groups.
All ancestral populations arrived over 10000 yrs ago. Except Andaman, all ancestral groups intermingled until 1600 yrs ago.
Caste system originated 1500 BCE or earlier. Got entrenched over centuries. Its impact on genetic material is evident around 1600 yrs ago.

Image
Virendra Ji I am not well versed in DNA, but what I heard from my learned friends circle that there are some P.hd thesis done on this in Madras university and Madurai Kamarajar university. posting below few link which might be helpful in support on route 2 migration

Link1

Link2

Link3
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Virendra »

When they're showing global migrations of Pleistocene era, it would make more sense to include variations of sea level.
It is confusing for a mango reader to look at the present day map of South East Asia, and co-relate it with migrations thousands of decades ago when the landmass i.e. the canvas of migration (example-Sunda) was completely different.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Murugan »

Hope Doctor and NO will like this
Murugan wrote:Dmitri Mendeleev was born today on 8th Feb 1834

He used sanskrit number and Panini's principles in his research.

Wiki:
For his predicted eight elements, he used the prefixes of eka, dvi, and tri (Sanskrit one, two, three) in their naming. Mendeleev questioned some of the currently accepted atomic weights (they could be measured only with a relatively low accuracy at that time), pointing out that they did not correspond to those suggested by his Periodic Law. He noted that tellurium has a higher atomic weight than iodine, but he placed them in the right order, incorrectly predicting that the accepted atomic weights at the time were at fault. He was puzzled about where to put the known lanthanides, and predicted the existence of another row to the table which were the actinides which were some of the heaviest in atomic mass. Some people dismissed Mendeleev for predicting that there would be more elements, but he was proven to be correct when Ga (gallium) and Ge (germanium) were found in 1875 and 1886 respectively, fitting perfectly into the two missing spaces.[26]

By giving Sanskrit names to his "missing" elements, Mendeleev showed his appreciation and debt to the Sanskrit grammarians of ancient India, who had created sophisticated theories of language based on their discovery of the two-dimensional patterns in basic sounds. Mendeleev was a friend and colleague of the Sanskritist Böhtlingk, who was preparing the second edition of his book on Pāṇini[27] at about this time, and Mendeleev wished to honor Pāṇini with his nomenclature.[28]

Noting that there are striking similarities between the periodic table and the introductory Śiva Sūtras in Pāṇini's grammar, Prof. Kiparsky says:

"The analogies between the two systems are striking. Just as Panini found that the phonological patterning of sounds in the language is a function of their articulatory properties, so Mendeleev found that the chemical properties of elements are a function of their atomic weights. Like Panini, Mendeleev arrived at his discovery through a search for the "grammar" of the elements...[29]"

The original draft made by Mendeleev would be found years later and published under the name Tentative System of Elements
https://en.wikipedia.org/wiki/Dmitri_Mendeleev
Lalmohan
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Lalmohan »

Virendra wrote:When they're showing global migrations of Pleistocene era, it would make more sense to include variations of sea level.
It is confusing for a mango reader to look at the present day map of South East Asia, and co-relate it with migrations thousands of decades ago when the landmass i.e. the canvas of migration (example-Sunda) was completely different.
the sea level piece is really crucial imho
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Re: Out-of-India - From Theory to Truth: Part 2

Post by johneeG »

Virendra wrote:Article in ToI today - '70 Generations ago, caste stopped people intermixing.'
http://m.timesofindia.com/india/70-gene ... 859632.cms
Excerpts :
Study by National Institute of Biomedical Genomics, Kalyani West Bengal, traces indian origin to five ancestral groups.
All ancestral populations arrived over 10000 yrs ago. Except Andaman, all ancestral groups intermingled until 1600 yrs ago.
Caste system originated 1500 BCE or earlier. Got entrenched over centuries. Its impact on genetic material is evident around 1600 yrs ago.

Image
It seems that there is some disagreement about what constitutes a 'generation'. This study takes a peculiar 22.5 yrs as one generation. Then, 70 generations would be around 1575 yrs i.e. 440 CE. This is the time of Guptha rule. So, basically, it seems like this study wanted to prove that this happened during Guptha rule, so they used a peculiar number like 22.5 yrs for a generation. They could have easily used any other relevant number of years for a generation and the result would have been quite different.

If they assumed that 20 yrs is one generation, then it would be about 1400 yrs back for 70 generations i.e. 615 CE
If they assumed that 25 yrs is one generation, then it would be about 1750 yrs back for 70 generations i.e. 265 CE.
If they assumed that 28 yrs is one generation, then it would be about 1960 yrs back for 70 generations i.e. 55 CE
If they assumed that 30 yrs is one generation, then it would be about 2100 yrs back for 70 generations i.e. 85 BCE
If they assumed that 32 yrs is one generation, then it would be about 2240 yrs back for 70 generations i.e. 225 BCE
If they assumed that 35 yrs is one generation, then it would be about 2450 yrs back for 70 generations i.e. 435 BCE

But, the most curious thing for me was the the precise estimation of 70 generations. I wondered how this precise estimation of 70 generations was reached.

I think the following article provides an answer to this. Its a very long and technical article but I am posting it because it seems to explain how the whole thing works.

Population Genetics Made Simple
David A. Plaisted
----------------------------------------

In order to understand discussions about evolution, even from a creationist viewpoint, it is helpful to have some background in population genetics. We give a brief survey of some of the points of population genetics most relevant for this purpose.

The characteristics of organisms are determined by their genetic material (DNA), and random mutations (changes) in the DNA can result in slight changes in organisms. As these accumulate, there can be changes in organisms, resulting in evolution. Population genetics attempts to analyze this process mathematically.

About 90 percent of DNA is thought to be non-functional, and mutations there generally have no effect. The remaining 10 percent is functional, and has an influence on the properties of an organism, as it is used to direct the synthesis of proteins that guide the metabolism of the organism. Mutations to this 10 percent can be neutral, beneficial, or harmful. Probably less than half of the mutations to this 10 percent of DNA are neutral. Of the remainder, 999/1000 are harmful or fatal and the remainder may be beneficial. (Remine, The Biotic Message, page 221.) This model is actually not realistic, because it does not take into account the interactions between various mutations. Nor does it distinguish major mutations, which change the shape of proteins, from minor mutations, which do not. Furthermore, it does not consider that the beneficial mutations observed are generally only of a restricted kind that cannot explain evolution. However, we consider the model in some detail anyway, because it is so widely used. In addition, population genetics can help to explain the rapid adaptation of organisms to their environment by changes in frequency of existing genetic material (alleles) even without mutations.

Harmful mutations result in organisms less likely to survive, and so these mutations tend to be eliminated from the population (group of organisms in a species). Beneficial mutations also tend to be eliminated by chance, but less often, and tend to be preserved. As these accumulate, the species can gradually adapt to its environment. Neutral mutations are generally eliminated, curiously, but sometimes can spread to the whole population. We then say that the mutation has fixed in the population. The rate of evolution is the rate at which mutations fix in the population. These can be either beneficial or neutral mutations.

If the offspring have on the average one harmful mutation each, then the population will degenerate; this is called "error catastrophe." This puts a bound on how many non-neutral mutations can occur per generation. It cannot be much more than about one per generation, and in fact, it must be significantly less, since most non-neutral mutations are harmful.

Rates of evolution are computed using the likelihood that various mutations will be passed on to offspring. If for each individual having a mutation, two of its offspring also have it, then the mutation will rapidly spread through the population. If less than one offspring has it, the mutation will tend to be eliminated. Often one speaks in terms of the difference (ratio) between this number of offspring for individuals with or without the mutation. If this "selective advantage" is .01, then that means that the chance this mutation will be passed on to an offspring is about 1.01 times higher than the chance that DNA without this mutation will be passed on to an offspring. The value of .01 is considered to be high. Note that in this case, after k generations, the frequency of this mutation in the population should increase by a ratio of (1.01)k. Different mutations in the same individual have a multiplier effect. So if an individual has two mutations with selective advantages of s and t, respectively, then this individual will have about (1+s)*(1+t) offspring per parent. Thus their combined effect is a selective advantage of (1+s)*(1+t) - 1. For small s and t, that is, much less than one, this expression is about equal to s + t, so we can often think of selective advantages as additive.

There seem to be many different uses of terminology in population genetics. What I call selective advantage, Spetner refers to as the selective value. Others call this the selective coefficient. ReMine uses the term selective value for something else.

For the sake of illustration, assume that the selective advantage of every beneficial mutation is 1, meaning that it doubles in frequency each generation. Suppose in some population, there are 1000 beneficial mutations. Each one will double its frequency each generation, so in about 10 generations each will multiply its frequency by about 1000 and in 30 generations, each will multiply its frequency by about a billion. Thus all these mutations can rapidly spread throughout the population, and the rate of evolution will be larger for a larger population, since there will be more beneficial mutations. Actually, after 30 generations, each individual will have only about 500 mutations, since the individuals originally in the population continue to reproduce themselves, too.

Those who are not interested in a detailed discussion of the technicalities of population genetics and Haldane's dilemma may want to skip down to the section More about Rates of Evolution now. The reason that we discuss Haldane's dilemma is that it is sometimes used by creationists to argue against evolution. However, we believe that only valid arguments should be used to support creationism, and so Haldane's dilemma is not appropriate. Furthermore, it is sometimes convenient from a creationist viewpoint to argue for rapid evolution, which Haldane's dilemma prohibits.

Problems with the Standard Analysis
There is a problem with the above analysis of mutations spreading through a population. The selective advantages of mutations are assumed to be independent, meaning roughly that the number of copies of DNA passed on from an individual with several mutations is the product of the number passed on for each individual mutation. This would imply that an individual with 1000 beneficial mutations will pass on 21000 times more copies of its DNA to the next generation than an individual with none. This is unrealistic. It is probably more realistic to assume that the most fit individual will only have a selective advantage of 1 (or some small value) over an individual without any mutations. I'm not sure what the effect of this is on the analysis, but it seems to slow down evolution very significantly, as we will show.

Also of interest is the fact that that as the population evolves, the average fitness of the population will increase, so each individual will not have such an advantage over others as it might have had in the beginning. As competition increases, the effect of beneficial mutations will be less pronounced. We can assume that the number of offspring of all individuals will be reduced by the same factor, so that the average individual will have about one offspring per parent and a selective advantage of zero. All individuals will be penalized to the same extent by this, so it will not affect the changes in frequency of mutations with time. This is intended to keep the size of the population roughly constant, also.

Suppose there are 1000 beneficial mutations spreading through a population, doubling each generation, that is, having a selective advantage of 1. Suppose each has a frequency of 1/2, that is, each mutation occurs in half of the individuals in the species. Then the average number of mutations per individual is 500. Most individuals will have a few more or a few less than 500 mutations, but not many will have other numbers. An astronomically small number of individuals will have more than 750 mutations, for example. The curious fact is, however, that the astronomically small number of individuals having way more than 500 mutations contribute a considerable fraction to the speed of evolution, since an individual with k beneficial mutations has proportional to 2k copies of its DNA passed on to the next generation, on the average. So if we restrict these individuals with many beneficial mutations to have at most two offspring, then the speed of evolution will be drastically reduced.

It is useful to have some background in probability theory in order to discuss population genetics. Suppose in a population there are n mutations altogether spreading through the population and on the average m mutations per individual. These mutations will be distributed more or less randomly, because of the effect of recombination (crossing over) during sexual reproduction. Later we will consider the case of asexual reproduction. The number of mutations per individual for organisms with sexual reproduction will be distributed as a binomial, or, normal, distribution, due to the randomizing effect of crossing over. The standard deviation of the number of mutations per individual will be at most 1/2 sqrt(m). This means that only about .31 of the population will have a number of mutations differing from m by more than 1/2 sqrt(m). Only about .046 of the population will have a number of mutations differing from m by more than sqrt(m). The normal distribution with mean zero and standard deviation one is proportional to e - x * x / 2 , where e is about 2.718.

For the case of 1000 mutations with a selective advantage of 1 each, assume that each individual has on the average 500 of them. The square root of 500 is about 23, so the standard deviation is about 11.5. This means that .31 of the population will have more than 511.5 mutations or less than 488.5 mutations, so about .16 of the population will have more than 511.5 mutations. About .023 of the population will have more than 523 mutations. Recall our assumption that competition means the average individual (with 500 beneficial mutations) will have on the average one child per parent surviving (and thus a selective advantage of zero). The individuals with 511.5 mutations will have 211.5 times this many children, or, over 2,000 children per parent! The individuals with 523 mutations will have over 8 million children per parent! Clearly these numbers are ridiculous and something is seriously wrong. These are not just extreme cases, because over two percent of the population will have 523 mutations or more. However, it turns out that the largest contribution to the speed of evolution comes from individuals having 667 mutations! Though there are very few of them, each has an astronomical number of children to make up for it.

For an average of 500 mutations per individual, since the standard deviation is about 11.5, an individual with 667 mutations is about 14.5 standard deviations away from the average. The number of such individuals relative to the number of individuals with 500 mutations is e - 14.5 * 14.5 / 2 , or, e - 105 , which is about 2.5 * 10 - 46. Even though less than one in 10 45 individuals has this many mutations for every individual with 500 mutations, each such individual has 2 167 or about 10 50 times as many offspring per parent to make up for it. In any reasonable sized population, it is doubtful that even one such prolific individual would be found. On the other hand, if each of these mutations had a selective advantage of .01, the greatest contribution to evolution would come from individuals with 502 or 503 mutations each.

One obvious problem with 1000 mutations with selective advantages of 1 is that the size of the population is increasing, since one individual has 8 million offspring, and nearly half of the population has many more than two offspring per parent. This is so even though the average individual has one offspring per parent (thus two altogether). The next generation would have (3/2)1000 or about 10 176 times as many individuals. However, we are assuming that competition reduces the absolute number of offspring so that the size of the population is maintained. This has the curious effect that an individual with an average number of beneficial mutations may at times have a very small number of offspring (much less than one) and a negative selective advantage. In our case, an individual with 500 beneficial mutations would have 10150 offspring per parent in the absence of competition, but with competition it would be reduced to 10-26 offspring per parent.

We now look at this in another way. Suppose that there are 1000 beneficial mutations spreading through a population. Let's give each mutation a selective advantage of 1/1000. This means that even an individual with all 1000 beneficial mutations will have a selective advantage of (1 + 1/1000)1000 - 1, which is 2.718 - 1, not unreasonable. (It's useful to know that for large n, (1 + 1/n)n is about 2.718 and (1 - 1/n)n is about 1/2.718.) Then each mutation will increase its frequency by a factor of 2.718 in 1000 generations, and will increase its frequency by a factor of about a million in 14,000 generations. Thus if the population is about a million, we get 1000 beneficial mutations fixing in 14,000 generations, or, about one per 14 generations. Now, if we just had one beneficial mutation spreading through the population with a selective advantage of 2.718 - 1, then it would spread through the population in 14 generations, giving the same rate of evolution. So the end result is that we do not get any gain by having mutations spreading through the population in parallel, and we cannot obtain rates of evolution faster than would be obtained by single mutations with selective advantages of about 1 (assuming that no individual has a selective advantage of more than about 1.) This means that large populations cannot lead to significantly increased rates of evolution, unless some individuals have tremendously high selective advantages. The only advantage of a large population is that if there are say 100 mutations with selective advantages of .01, they can spread through the population in parallel, leading to a rate of evolution similar to that of one mutation with a selective advantage of about 1.

Now, if we assume 20 beneficial mutations spreading through the population, each with a selective advantage of 1, and on the average 10 mutations per individual, then we obtain that the largest contribution to the speed of evolution comes from those individuals having 13 beneficial mutations. Each such individual has 8 times as many children per parent as the average. For 12 beneficial mutations, with an average of 6 per individual, the largest contribution to evolution comes from individuals having 4 times as many surviving children as the average individual. Even this seems implausible.

These results do not depend on the large selective advantages of 1. If we assume 10,000,000 mutations spreading through a population, each with a selective advantage of .01, and an average of 5,000,000 mutations per individual, then we still obtain that over 2 percent of the population has 8 million times as many children as average. For 200,000 mutations with a selective advantage of .01, and an average of 100,000 per individual, half of the speed of evolution comes from individuals with 8 or more times as many children as average. For 120,000 mutations and similar assumptions, half of the speed comes from individuals with 4 or more times as many (surviving) children as average. However, it is true that smaller selective advantages per mutation make the number of mutations to get a given selective advantage larger and tend to reduce the selective advantage of typical individuals with respect to the average.
to be contd in the next post...
Last edited by johneeG on 08 Feb 2016 20:04, edited 1 time in total.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by johneeG »

Rates of Evolution under Reasonable Assumptions
Not all the beneficial mutations are preserved, it turns out. The number that are preserved (fix) is twice the selective advantage. If a mutation has a selective advantage of .01, then the chance that it will fix (reach a frequency near 1) is .02. Thus, even most of the beneficial mutations are lost, but the number that are saved is higher for mutations having a greater selective advantage.

We can get some increase in the rate of evolution by "pipelining" mutations. Suppose there is a population of 1,000,000. Suppose there are 50 beneficial mutations per generation and therefore 50,000 harmful ones per generation. We assume that these beneficial mutations have selective advantages of .01 at most, which seems typical. Then all but one of them will be eliminated from the population, on the average. This remaining mutation will double its frequency in about 70 generations (since 1.01^70 is about 2) and will spread through the population in about 1400 generations (since 2^20 is about a million). At this time each individual will have an average of half of a mutation, and it will take 2800 generations total to complete the spread. During this time, other mutations will be entering the population and also spreading. Thus we will obtain one mutation fixing in the population per generation, in the long run. Each individual will have on the average one mutation that has spread to .99 of the population, one that has spread to (.99)2 of the population, et cetera, for an average of about 100 mutations altogether. This will give the average individual a selective advantage of about 1, which is not unreasonable. The standard deviation in the number of mutations will be about 5, so most individuals will have only a small selective advantage over the average individual. This shows that we can reach a speed of about one mutation per generation under reasonable assumptions. The actual rate is about half a mutation per generation, because we also need to consider the original individuals in the population that continue to reproduce, slowing down the process.

We now perform the analysis in another way, which permits a faster rate of evolution than one mutation every two generations. The preceding analysis assumes that the selective advantage of an individual is not larger than about 1. Instead, we can assume that the selective advantage of an individual relative to the average individual is not larger than about 1. That is, we can assume that no individual has more than about twice as many offpsring as the typical individual. Since the typical individual probably has one offspring per parent, this is reasonable. Even with this reasonable assumption, we can get faster rates of evolution. Suppose, for example, that 100 mutations fix per generation and have a selective advantage of .01. These mutations increase their frequency in the popululation by 1.01 each generation. The number of mutations in a typical individual at equilibrium that have not yet fixed will be 100(.99 + .992 + .993 + ... ) which is (summing the geometric series) 100*100 or 10,000. The standard deviation is 50, so the selective advantage of a typical individual with 50 extra beneficial mutations is only .5 over an average individual, consistent with our assumption. A typical individual with a selective advantage of .5 would have only 1.5 times as many children per parent as an average individual. But we obtain a rate of evolution of 100 mutations per generation. The population size to permit this must have 5000 beneficial mutations per generation (since only 1/50 of them fix). With 1000 harmful mutations to a beneficial one, this is 5 million harmful mutations per generation. The population size would probably have to be substantially larger than 5 million to prevent error catastrophe.

Suppose now that 1000 mutations fix per generation and have a selective advantage of .002. (We cannot use .01 again for the selective advantage, or else the selective advantages of typical individuals would be too high.) The number of mutations in a typical individual at equilibrium that have not yet fixed will be 1000(1/(1+s) + 1/(1+s)2 + 1/(1+s)3+ ...) for s = .002, which is (summing the geometric series) 1000*500 or 500,000. The standard deviation is about 350, so the selective advantage of a typical individual with 350 extra beneficial mutations is only 350*.002 or .7 over an average individual. This is consistent with our hypothesis that a typical individual should not have too great an advantage over an average individual. This time we obtain a rate of evolution of 1000 mutations per generation (though the fitness advantage of each mutation is less). The population size to permit this must have 250,000 beneficial mutations per generation (since only 2*s or 1/250 of the beneficial mutations fix). With 1000 harmful mutations to a beneficial one, this is 250,000,000 harmful mutations per generation. The population size would probably have to be substantially larger than 250 million to prevent error catastrophe.

Haldane's Dilemma and Problems with it
There is a result called Haldane's Dilemma which says that each substitution of a mutation for non-mutated DNA has a cost of about 30. This means that for each substitution, 30 individuals must die without leaving any descendents. For a population of size N, 30N individuals must die in order for a substitution to spread to the whole population. This cost must be paid by surviving individuals, who must replenish the population lost in this way. If the maximum selective advantage is 1, this would mean at most one beneficial mutation to fix in the population per 30/1 = 30 generations, regardless of the size of the population. For higher vertebrates, Haldane computed a maximum rate of one beneficial mutation fixing in the population per 300 generations. In fact, there are more costs that must be paid, so the true rate of evolution would have to be slower than this. Haldane's Dilemma implies that the assumed rates of evolution for the primates and higher vertebrates are not possible, and therefore challenges the theory of evolution. For more information about this difficult to understand subject, see The Biotic Message.

Haldane's Dilemma seems to contradict our previous result about obtaining 100 (or even 1000) mutations fixing per generation under reasonable assumptions. We are not sure where the disagreement is, but perhaps our assumptions are different. In any event, there does not seem to be anything preventing high rates of evolution, even assuming the maximum relative selective advantage is about 1.

We now present another seeming paradox, in which we obtain a rate of evolution apparently faster than Haldane's Dilemma allows. This material is fairly technical, and may not be of interest to the average reader. Let us assume the maximum selective advantage of any individual in a population is 1. The "cost" of substitution is paid by individuals having more than one descendent per parent. We placed an upper bound of 1 on the selective advantage of any individual, and used this as an upper bound on how these costs can be paid. However, many individuals will have a selective advantage of less than 1, meaning that the rate at which costs can be paid will be much less than one per individual. We recall that the sum of the selective advantages of the mutations in an average individual in the population cannot be larger than 1. We also assume that mutations have selective advantages of at most .01. Let m be the average number of beneficial mutations in an individual in the population, and suppose for illustration that m is about 10,000. The standard deviation of the number of beneficial mutations would be at most on the order of one-half the square root of m, or, 50, since we have something approximating a binomial or a normal distribution. Therefore, very few individuals would have more than m+100 mutations. A typical individual would have mutations with a combined selective advantage of at most 1. This means that the average mutation would have a selective advantage of at most 1/10,000. Thus 50 mutations would have a combined selective advantage of at most about .005. The selective advantage such individuals would have over an average individual would be very small (about .005). As a result, it would appear that very few individuals would be able to pay the maximum cost corresponding to a selective advantage of 1. The astronomically small number of individuals with many beneficial mutations would not be able to pay the cost, either, because of the upper bound of 1 on selective advantage. So it would appear that we could get only about .005 substitutions per individual in this generation, by Haldane's result.

However, of the half of the population with at least 10,000 beneficial mutations, a typical individual would have on the average about 50 extra beneficial ones. Individuals in this half of the population will produce about 1/200 extra offspring every generation, since they have a selective advantage of about .005 over an average individual. Since we are dealing with half of the population, we obtain 1/400 of the population produced from such individuals in one generation. A typical new offspring will have an extra 50 beneficial mutations, and will replace an individual having typically 50 mutations less than average, a net gain of 100 beneficial mutations per offspring. Thus we obtain a number of substitutions equal to 100 * 1/400 or 1/4 of the population in one generation, even though only 1/200 of the population is being generated each generation. This contradicts the idea that each substitution requires one birth in the population.

Even if there are 100 mutations with combined selective advantages of .01 in an average individual, we obtain a standard deviation of about 5 at most, giving a selective advantage of only .05 over an average individual. Reasoning as above, we generate 1/40 of the population from such individuals, and each such birth replaces an individual having about 10 less beneficial mutations, resulting in about 1/4 of the population receiving an additional beneficial mutation in one generation. Thus one can get more than one substitution per offspring, a seeming contradiction to Haldane's dilemma.

Recall also that we obtained a maximum rate of evolution of one mutation per two generations under reasonable assumptions in our above analysis using pipelining. This is much higher than one mutation every 30 generations, which is the maximum possible according to Haldane's analysis under the assumption that the maximum selective advantage of any individual is at most 1. It could be that our assumtions are different, or maybe there is a flaw in Haldane's analysis. We are not considering the extra cost of recessive mutations, but this should not make much difference, according to ReMine.

There is a way, however, that we can get a bound very similar to Haldane's, and that is if we assume that the most fit individual in a population has only a limited advantage over an average individual. Suppose we assume that the most fit individual (the one with all the beneficial mutations currently spreading through the population) has a selective advantage of at most 1 over an average individual. Then we can get at most about one mutation every 20 generations. For example, if there is just one mutation spreading with a selective advantage of 1, then in 20 generations it can increase its frequency by a factor of about a million, and thus spread through a reasonable sized population. This gives one mutation per 20 generations. If we assume there are 10 mutations with selective advantages of 1/10 each, then an individual with all of them has a selective advantage of about 1.718. In 10 generations, these mutations can increase their frequency by a factor of about 2.718, and in 14 such increases, they can increase their frequency by about a million. In this way we obtain 10 mutations in 140 generations, or about 14 mutations per generation. The result is about the same for say 100 mutations with a selective advantage of .01 each. Of course, 1.718 is larger than our bound of 1, explaining the increased speed. If we assume, as Haldane did, that the maximum selective advantage of an individual with all beneficial mutations is about 1/10, then we obtain a maximum of one mutation every 200 generations, not far from Haldane's bound.

A problem with this analysis is that different mutations do not combine in a multiplicative way. If we assume that a tall monkey has a selective advantage of 1, a handsome monkey has a selective advantage of 1, a muscular monkey has a selective advantage of 1, and a smart monkey has a selective advantage of 1, then it is not correct to assume that a tall, handsome, muscular, smart monkey has a selective advantage of 15. Probably it only means that all of his children will survive, and so if half of the average monkey's children die, the exceptional monkey will still only have a selective advantage of 1. If we have a population in which most of the evolution is occurring due to individuals with a selective advantage of 1 or less, then we still get more rapid rates of evolution than Haldane allows if we bound the selective advantage in this way to 1.

More about Rates of Evolution
In the article "Rates of Evolution," I calculate that there must be a beneficial mutation every 7 to 10 years if evolution is true. In terms of pure numbers of mutations, this rate does not seem to cause a problem for the theory of evolution. But if Haldane's reasoning is true, this rate of evolution would cause a problem for higher vertebrates; for higher vertebrates, Haldane's estimate of 300 generations leads to generation times of at most 1/30 of a year, which is impractically small. However, as stated above, I believe Haldane's bound is incorrect.

On the other hand, there are a number of other applications of population genetics that cause severe problems for the theory of evolution. We now consider these, beginning with a discussion of small populations. We then discuss error catastrophe and the fact that the high rate of mutation for humans should lead to rapid degeneration of the human genetic material. We also show that the human race must be young, since such deterioration is not yet observed. Finally, we discuss the ape-human gap, and show that if the human race is not degenerating, then this gap would take at least 100 million years to cross, and more probably a billion years, just counting numbers of mutations needed and not considering the problems of creating new structures for speech and thought.

We first discuss small populations, taking some material from ReMine's book, The Biotic Message. We note that the maximum possible rate of non-neutral mutation is less than one per generation, due to error catastrophe. This rate leads to at most about 1/1000 beneficial mutations per individual per generation. These mutations will probably have a selective advantage of at most .01, implying that at most 1/50 of them fix in the population. Thus we can get at most 1/50,000 mutations fixing in the population per generation per individual. Thus in a population of 100,000 individuals, we can expect at most two beneficial mutations to fix in the population per generation. In a population of a million, we might expect 20 beneficial mutations to fix per generation. However, Haldane's analysis implies that this rate does not continue to increase as the population becomes larger and larger. In fact, a more reasonable estimate is about .015 lethal mutations per generation, leading to .000015 beneficial mutations per individual per generation at most. At most 1/50 of these would fix, leading to at most about .0000003 fixing per individual per generation. This would be 0.3 mutations per generation fixing in a population of a million. We see right away that we cannot expect rapid evolution in small populations, as assumed in the theory of punctuated equilibrium. Haldane's reasoning (if it were true) would imply that even this rate is too high, and moreover, we cannot expect bursts of evolution, even in large populations.

We now discuss the subject of error catastrophe in humans. In humans, it is estimated that there are about 30 mutations per individual per generation, thus three in the functional part of the DNA. This implies that on the average there are about 3/2000 beneficial mutations per individual per generation and about 1.5 harmful mutations. ReMine notes that this rate of mutation should lead to error catastrophe in the human race, which is a puzzle for the theory of evolution.

To be precise about the human situation, there are about 3.5 * 10 9 base pairs in the human genome, and each person has two copies of these, one from the father and one from the mother. The rate of mutation in humans is believed to be about 1 * 10 -8 per base pair per generation, or, 35 mutations per generation per individual. We can assume that 9/10 of these occur in the non-functional part of the DNA, and that of the remainder, possibly half are neutral, leading to about 1.75 harmful or fatal mutations per generation. Now, the typical individual will have mutations from both parents, and therefore will have about 3.5 harmful mutations per generation. Let's divide a generation into n small time intervals; then the chance of a harmful mutation during 1/n of a generation is 3.5/n, and the chance to avoid a harmful mutation during this small time interval is 1 - 3.5/n. Thus the chance to avoid any harmful mutations during the entire generation is (1 - 3.5/n)n, which is about (1/2.718)3.5, or, 0.0302084. This means one child free of defects per 33.1 children. In order to have two children free of defects on the average, to avoid error catastrophe, the typical female would need 66 conceptions! ReMine obtains a figure of 16.3 conceptions assuming only 3 percent of the DNA is functional. Both are unrealistically large. The consequence is that humans are experiencing error catastrophe, that is, instead of evolving, we are degenerating. This implies that at one time humans were much more advanced than we now are. This is consistent with a creationist view that the human race was created with so much vitality that it could endure the degeration resulting from harmful mutations.

It is important in this respect to understand what a harmful mutation is. It must be a mutation that hinders the organism in a way that the organism is not able to compensate for. Since populations are generally stable over long time periods, this means that an organism with a harmful mutation will typically have less than one surviving offspring.

Equilibrium is the state at which the frequencies of occurrences of various mutations are fixed over time. After sufficient time, any population with constant rates of mutation should reach equilibrium. When the population reaches equilibrium, harmful mutations will be entering and leaving the population at the same rate. This means that a mutation that is only slightly harmful will spread to much of the population, but a mutation that is very harmful will spread to a small percent of the population. But both mutations will cause a number of deaths per generation equal to their frequency of occurrence in the population. So the chance that a fertilized egg will survive is less than or equal to the chance that it has no new harmful mutations, when the population is at equilibrium. Thus if there is a small chance that an offspring will be free of new defects, then there is a small chance that it will survive, when the population is at equilibrium. So at equilibrium we should expect that only about one in 33 fertilized human eggs will survive, based on the above calculations.

It is also important to understand that only essential genes will persist in a population as functioning genes for long periods of time. Inessential genes will suffer mutations that destroy their function, and since the organism is able to compensate, such mutations will accumulate over time until the gene is non functional in the whole population. This means that evolution eventually eliminates all redundancy, and only the genes that an organism really needs to survive will be maintained. So all species will eventually be living on the edge of extinction, in a sense.

One way to understand how the human race can endure a high rate of mutation is to realize that many mutations are recessive. They are only expressed (fully) when both copies of the gene have the mutation. Mutations to enzymes tend to be recessive, because an organism with one gene generating functioning enzymes can still survive, though possibly with some degradation. Mutations to structures of an organism tend to be dominant. Now, recessive mutations tend to accumulate until there are enough of them to be expressed. Assuming 10-8 point mutations per base pair per generation, a recessive mutation would accumulate until it reaches equilibrium, when the numbers of mutations entering and leaving the population are equal. Assuming the mutation were fatal, this would happen when about 1/10,000 of the individuals had a mutation at this base pair, since the probability of expression would be the square of 1/10,000, or 1/100,000,000, the same as the probability of the mutation occurring. It would take on the order of 10,000 generations to reach equilibrium (actually, somewhat longer). Now, there may be about 3*108 functional base pairs in the human genome. It would be reasonable to assume that half of these were for enzymes, which might mean about 108 recessive fatal mutations. When each reached equilibrium, a typical individual would have about 10,000 recessive mutations. Each child would then on the average have one of them expressed. This would be essentially the same as if there were one fatal mutation per generation at the start; the cost to the population is the same, but recessive mutations take longer to reach the full cost.

The fact that we have not reached the point where 66 conceptions per couple are needed means that the cost of the harmful mutations has not yet been realized. This seems to imply that many of these mutations are recessive, and also that the human race has not been around for very long (under 10,000 generations). However, these recessive harmful mutations, even when not fully expressed, may render the human organism more inefficient in various ways, and may make us increasingly susceptible to disease and degeneration of various kinds. It is possible that a better life style would reduce the rate of harmful mutations to an acceptable amount.

Actually, it is more realistic to look at the picture in terms of genes rather than base pairs. If both copies of a gene in an individual have a harmful mutation, then this will probably be expressed in the individual, even if these mutations are different. There are estimated to be about 100,000 genes in human beings, and typical rates of mutation are about one in 25,000 as observed in the population. The square root of this is about one in 160, meaning that equilibrium should be reached for recessive mutations in about 160 generations. The fact that we have not yet reached equilibrium suggests that the human race is not much more than about 200 generations (6000 years) old.

Another possibility is that a very small portion of the genome comprises the functional DNA, perhaps under one percent. ReMine mentions that some biologists have come to this conclusion due to reasoning such as the above. This would seem surprising, but there is no way we can absolutely rule it out at present. This seems to contradict Maynard Smith (cited in ReMine, The Biotic Message, page 250), who estimates that 9 to 27 percent of the human genome codes for protein. It will be interesting to see what the human genome project reveals.

In general, one can compute the time it takes for a population to reach equilibrium in the following way, assuming that the population begins perfect (with no or very few harmful mutations). Suppose f is the frequency with which a mutation occurs per generation, and m is the fraction of the population that has the mutation. Suppose s is its selective disadvantage (which will be a negative number). Now, if the mutation is dominant, then it will reach equilibrium when the probability of expression equals f, so that -ms = f. Thus if its selective disadvantage is -1/1000, it will reach equilibrium when its frequency of appearance in the population is about 1000 times its frequency of occurrence. This will happen in slightly over 1000 generations, since the frequency of appearance in the population will initially increase by f per generation, but will slow down as m approaches -f/s. In general, it will take somewhat over -1/s generations to reach equilibrium. If the mutation is recessive, the probability of expression is m2, and the fraction of the population that will die from this is -s*m2. Equilibrium will occur when -s*m2 = f. Thus m = sqrt(-f/s) at equilibrium. The frequency of occurrence will increase by f each generation and converge to sqrt(-f/s), which will take somewhat over sqrt(-f/s)/f generations, or, sqrt(-1/fs) generations.

A detailed calculation shows that if a mutation is recessive and fatal (when expressed), and occurs on the average once per generation, as assumed above, in sqrt(1/f) generations, its frequency in the population will be over .75, which implies that over half of all fertilized eggs must die due to this mutation. Even this close of an approach to equilibrium would imply too high a death rate for humans in 160 generations. It could be that the mutation rate has increased recently, or else many harmful mutations are only slightly harmful. These will take longer to reach equilibrium.

For example, harmful mutations with f = -.01 will take 10 times longer to reach equilibrium and harmful mutations with f = -.0001 will take 100 times longer to reach equilibrium. If most harmful mutations have f about -0.1, then they will take about 3 times as long to reach equilibrium. If we assume that the high mutation rate began about the time of Abraham, 4000 years ago, then there would be about 130 generations since then. Equilibrium would take 3 * 160 or 480 generations, so we would be about a fourth of the way to equilibrium, meaning that for recessive mutations only about 1/16 of the equilibrium rate would be expressed today. This might be tolerable. But in a few thousand years, the death rate would become unacceptably high.

We also note that mutations on small genes take longer to reach equilibrium. A gene having half the average size will probably have half the average rate of mutation. This means that if the gene is recessive, the frequency of mutated alleles of this gene at equilibrium will be about .707 of the average for all genes. It will also take about 1.414 times as long to reach equilibrium as an average gene. So in the early stages of approach to equilibrium, genetic disease from this gene will be about a fourth the frequency of an average gene. For a gene 1/4 average size, the frequency of genetic disease will be about 1/16 that of a gene of average size in these early stages, and mutations to this gene will take twice as long as mutations to an average size gene to reach equilibrium. The fact that these smaller genes take so much longer to reach equilibrium could also explain why the rate of genetic disease at present is relatively small.

Another possibility is that the human genome has many more than 100,000 genes and a lot of redundancy. In this case, equilibrium would take a lot longer to reach, which could explain why genetic defects are so rare today. However, at equilibrium, degeneration would occur even faster due to the larger number of genes.

Redundant genes take longer to reach equilibrium. Assuming a mutation rate per gene of 1/25,000 and assuming triple redundancy, at equilibrium each gene would have a frequency of about 1/30 in the population (the cube root of 1/25,000). This is assuming a mutation which is fatal when expressed. To reach equilibrium would require about 25,000/30 or about 900 generations. After 900 generations, the population would be at least .75 of the way to equilibrium (probably significantly more), and after 1800 generations, almost all the way. 900 generations is about 27000 years. If there are triple redundant genes and they have not reached equilibrium, then the age of the human race must be less than about 27,000 years and more than 160 generations (48,000 years) to account for those recessive genes that have reached equilibrium.

There is an interesting anomaly having to do with cystic fibrosis which is recessive and has a frequency of about one in 2500 births among Caucasians. This seems to imply that the frequency of the mutations in the population is about 1/50. This illness is caused by a number of mutations, including the loss of a single amino acid, but this is still a huge frequency, difficult to explain on the basis of frequency of occurrence of mutations. About 70 percent of the cases of CF are due to the deletion of a single amino acid in the gene. The frequency of this mutation might then be (7/10)*(1/50) or about 1/70. One explanation offered by biologists for the large frequency of these mutations is that this disease may have a heterozygote advantage. Another possibility from a creationist viewpoint is that there was once a severe population bottleneck and one of the humans at that time had this mutation. So it could be that one of the first Caucasians had this gene. Then we can compute how long it would take to come to its current frequency in the population, which is about one in 70. Starting out with a frequency of one in 8, how long would it take to reduce to one in 9? The chance of expression would be about 1/8^2 or 1/9^2, so we will take 1/(8*9) as a reasonable average. The number of generations required is then (1/8 - 1/9) divided by 1/(8*9), which is one. In general, it will take about one generation to reduce its frequency from 1/n to 1/(n+1). Thus about 70 generations is required to reach the present level among Caucasians. That is only 2100 years, which is too small.

We can explain this as follows: A couple that has a child with CF may then have another child to make up for it. Two parents with the recessive CF gene will on the average have 1/4 of their offspring with CF. Their offspring without CF will have on the average 2/3 of a CF gene per offspring. If they have an average of 2 children then on the average 1.5 will survive, and thus one CF gene will propogate to the next generation. If for each offspring with CF, they continue having children until there are two survivors, they will propogate 4/3 of a CF gene to the next generation instead of one. This means that the loss of CF genes is reduced from 1 to 2/3, so it takes 3/2 as long to obtain a given reduction. This would increase the time to about 105 generations, or 3150 years. This is still to small, but more reasonable.

Now, we can also guess that some couples will want to have an extra child just to make sure they have enough normal ones. So parents with a CF child may actually have more children than average. If they have an average of 3 children without CF, they are passing on 2 CF genes to the next generation, so the frequency of CF in the population will hardly decrease at all. If we assume half of the parents have 3 normal children and half have 2, then each such couple passes on an average of 5/3 CF genes, which will increase the time needed by a factor of three. This gives 210 generations, or, 6300 years, possibly less with a 20 year generation time. If we assume that the stress of having a CF child leads to divorce and remarriages, then the number of children could actually be even larger. So we see that it is possible to explain just about any age one wants to. But the creationist viewpoint does explain why CF should be so high in Caucasians and low in other races, if the father or mother of the race (at the time of a severe population bottleneck) happened to have a recessive CF gene among them.

The effect of harmful mutations seems to be misunderstood frequently. Spetner (Not by Chance, page 81) states that if ten percent of the offspring suffer a harmful mutation, then the genome of most of the population will be ruined. This is based on the assumption that harmful mutations have selective advantages of about -0.1 and therefore at equilibrium will spread to the whole population. However, just because the whole population has a harmful mutation does not mean that the genome is ruined; it only means that some number of conceptions do not lead to viable individuals, so there must be an excess of births to make up for it.

Suppose, for example, that one percent of the population per generation suffers a harmful mutation whose selective advantage is between 0 and -0.001. Mutations with a selective advantage of -0.001 result in 1000 individuals having on the average only 999 descendents, assuming that a typical individual has one descendent per parent. Such mutations will eventually increase their frequency in the population a thousandfold or more, so that at equilibrium each individual will have 10 such mutations per parent. Counting both parents, there will be 20 such mutations per individual. The chance of an individual being free of such mutations is then about one in 2.718 10 , which is much less than one in a million. Now, if those individuals with harmful mutations have on the average less than one offspring per individual, this means that the one in a million individuals without harmful mutations have to have enough offspring to make up for the loss in population, which is unrealistic. In fact, it suffices for a defect-free individual to have about 101 offspring per parent to make up for the loss due to genetic defects, and so this average of 20 harmful mutations per individual is not necessarily a serious problem.

We now derive an absolute bound on rates of evolution. It is interesting that by considering rates of recombination (crossovers), one can get absolute bounds on mutations fixing per generation. This analysis applies both to beneficial and neutral mutations. There are some subtleties that I am ignoring, but I believe that the following analysis is valid. The human genome has about 3.5 * 10 9 base pairs, and crossovers occur on the average about once every 108 base pairs, for an average of 35 per generation. If a mutation spreads to the entire population, it will generally take a region of its chromosome with it, this region being larger the faster it spreads. In 1000 generations, this region would have about 105 base pairs. This region would likely have no other mutations in it that had not yet fixed. Thus we could have probably at most 35000 mutations spreading in this way at one time, in 1000 generations, for 35 per generation. If the mutations spread more slowly, more of them can spread in parallel, but the bound of 35 per generation still holds. This bound does not depend on the selective advantages of the mutations or the rate of mutation. This bound is actually reduced by the following factors:

o Smaller genomes would permit fewer mutations per generation
o If the genes are clustered on chromosomes, the rate of evolution would be less.
o There may not be enough beneficial mutations to attain this maximum rate of 35 per generation.
o Mutations tend to compete against each other and only a small fraction of them may spread to the whole population. For example, a rapidly spreading mutation can eliminate many slowly spreading ones near it on the chromosome from the population.

I am not sure what the combined effect of these factors is, but it could reduce the maximum rate to much less than 35 per generation. This might have implications for maximum speeds of evolution and the theory of punctuated equilibrium.

This maximum rate is interesting in view of the ape-human gap which is about 2 percent of the genome (I've also read one percent). This would be about 70 million base pairs. Assuming both humans and apes diverged at the same rate, this would be 35 million base pairs for each. If we can have at most 35 mutations fixing per generation, this would mean at least a million generations, which would be at least 20 million years. (ReMine gives evolutionary sources on page 208 (The Biotic Message) which say the 20 year value is the right one to use.) If the bound is much less than 35, then it would take much longer than 20 million years.

The maximum rate of neutral mutations (in the non functional DNA) cannot be very high due to error catastrophe. In functional DNA, probably 2/3 of the mutations are harmful; mutations to the first two codon positions almost always change an amino acid, and mutations to the third position sometimes do. When an amino acid is changed, the mutation is almost always harmful. Kimura (cited in ReMine, The Biotic Message, page 246) estimates that a mutation which alters an amino acid is ten times more likely to be harmful than neutral or beneficial. In fact, one can derive something close to this figure from the fact that replacement sites in DNA evolve about 10 times slower than neutral sites (fibrinogen peptide) according to evolutionists. Assuming 1/10 of the DNA is functional, we can have at most about 7 neutral mutations per generation; this would be 7/10 of a mutation per generation in the functional DNA, and about half a harmful mutation per generation. With two parents, this would be one harmful mutation per generation, and bordering on error catastrophe. Thus most of these 35 mutations per generation would have to be beneficial mutations. In a million generations we could have at most 7 million neutral mutations, which is a fifth of a percent of the genome. To get a one percent change in the non-functional DNA would require probably 5 million generations and 100 million years.

This bound of 7 neutral mutations per generation applies to any organism having one-tenth of its DNA functional. In fact, since the mutation rate is somewhat affected by chance factors, it would seem highly improbable that this mutation rate should be so close to its maximum possible value, so a much smaller value seems more likely. In addition, this rate of mutation probably fluctuates to some extent, and if it were so near to error catastrophe, when the rate increased, the species would suffer. Therefore a much smaller rate, possibly 3 or 4 neutral mutations per generation, seems more reasonable. This would put the ape-man divergence at at least 200 million years ago and might have other difficult consequences for the theory of evolution.

Spetner (Not by Chance, page 81) says that species can tolerate at most 1/10 of a mutation per generation in the functional DNA. This would increase the time required by a factor of about 5, to a billion years, assuming the mutation rate happened to be at the maximum acceptable value. Remine (The Biotic Message, page 221) states that a typical rate of lethal mutations for a species is 1.5 percent per generation. Assuming at least half of the harmful mutations are lethal, this leads to a 3.0 percent harmful mutation rate per generation. This would increase the time required for the ape-man gap by a factor of about 30 over the 100 million year estimate, to 3 billion years. To change half of the human DNA would require 7.5 billion generations at this rate.

One might attempt to get around this problem by noting that some mutations affect more than one base pair of DNA. Suppose, for example, that on the average, a mutation affects five base pairs. Then the times for the ape-human divergence could be reduced by a factor of five, from a billion to say 200 million years. However, the age estimate for the human race computed in How Non-Functional DNA Testifies Against Evolution, and Shared Errors between Humans and Apes would also be reduced by a factor of five, to 40,000 years or less. This is because of the quote "Silent sites evolved at an average rate of 4.61 nucleotide substitution per 109 years" found there. Silent sites could only change by mutations that affect a single base pair (i.e., substitutions). This indicates that the rate of base pair substitution is about one per 200 million years if evolution is true. Thus the rate of all mutations is at least this large. So if each mutation changes an average of 5 base pairs of non-functional DNA, then the rate of change of non-functional DNA would be five times as large, or, one base pair per 40 million years. This would mean that mitochondrial Eve lived 40,000 years ago or less, meaning the mitochondrial clock runs 5 times faster than assumed. Since the ape-human split is also dated in terms of the mitochondrial clock, this would reduce the ape-human split to 2 million years ago from 10 million years. We would still have a disagreement between 2 million years and 200 million years for the ape-human split. So there would still be a discrepancy in dating.

We now consider the maximum rate of evolution for asexual organisms. For these, each mutation can only spread from the descendents of one individual. After a mutation has spread to 1000 individuals, then there might be a chance of another favorable mutation. Error catastrophe prevents us from using a smaller number. The maximum selective advantage of a mutation is generally .01 or less. This would require 70 generations to double its frequency, and about 700 generations to multiply by a thousand. So we cannot expect much more than one beneficial mutation to fix in the population per 700 generations.

The subject of population genetics has been difficult for me to grasp, and, apparently, for population geneticists as well, judging from the history of the subject. I hope that this short discussion will do something to remedy this problem for users of the world-wide web.

Back to home page.
Link

This is what I can understand: Biologists study genes. They have noticed some standard patterns. But, they have also noticed certain non-standard patterns. These patterns are called 'mutations' by the biologists. They have then classified these mutations into 'beneficial' and 'harmful'. But, regardless, the non-standard patterns(or mutations) are rarer than standard patterns and are seen as a key to understanding the 'evolution'. Now, an assumption is being made that natural selection will give a selective advantage of .01 due to evolution. Why .01? I don't know. This is being called reasonable assumption. I am assuming that this is because much higher advantage would mean more dramatic changes in each generation which is unreasonable from an 'evolution' perspective. So, they assume that the selective advantage of natural selection at each generation would be around 0.01. Now, mathematically, a mutation's size would double in 70 generations because (1+0.01)^70 = 2. i.e. 1 mutation(with selective advantage of 0.01 per generation) would double(2) in 70 generations.

So, a mutation will double its size in 70 generations. But, heres the problem: what was the original size of the mutation? That is obviously unknown.

Now, they noticed that non-standard patterns(i.e. mutations) tend to be more common among certain groups. This is called haplogroup. So, each group is assigned with a non-standard pattern(i.e. mutation) which is common among that group. Then, they study if this non-standard pattern is also found in members of other groups. If it is found, then it means that the mutation is spreading. Because its assumed that the mutation started off with the group in which it is most common and is now spreading to other group. Since the mutation is now spreading, the number of generations needed for this increase in size is calculated. And this generally tends to be around 70.

Now the first thing one can notice is that this whole theory is based on 'reasonable assumptions' at each stage. These 'reasonable assumptions' are being made because there are so many unknown variables. Given the number of unknown variables, I think its simply unreasonable to think that one can come up with any real answer. Of course, one can use all sorts of assumptions and theories, but thats just hypothesis based on huge number of assumptions. That hypothesis would be right only if each of those assumptions is right. Even if a single assumption is even partly wrong, then the calculation would go haywire. And I think the real problem is that these assumptions are not falsifiable. One could easily make different assumptions and reach different conclusions. Based on these assumptions, one can reach any desired conclusion.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by member_28985 »

Some of you might be interested in this, The Cult of Mithras : https://www.youtube.com/watch?v=AQWX689T-YY
Apologies if this was already posted on this thread.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by gashish »

Not directly related to lingusitics nevertheless below validates how knowledge/ideas/stories could have propagated out of India.

How Buddhist Cultural Memes Were Appropriated By Christianity
The origin of the legend of Barlaam and Josaphat, two of the most famous Christian saints of the Middle Ages is less widely known. This legend was so hugely popular that, from time to time, the Church announced that the relics of the two had appeared miraculously and were then installed with solemn ceremony. Barlaam and Josaphat found their way into the Roman Martyrology (27 November), and into the Greek calendar (26 August).

The legend tells how an Indian king persecutes his son, Josaphat, who astrologers have foretold, will establish the Christian Church. In due course, Josaphat meets the hermit Saint Barlaam and converts to Christianity. In the end, the prince’s father accepts the son’s conversion and retires to the desert to spend his last days with the old teacher.

Church scholars now acknowledge that Barlaam and Josaphat is a play on the names Bhagavan and Bodhisattva, and it is a reworking of the story of Buddha’s enlightenment. The original story was a Mahayana text that was translated into Arabic and European languages. Indeed, this legend should not startle us for St. Ann, St. Lucy, St. Denis and St. Brigid, represent pre-Christian deities Anna, Lucia, Dionysus and Brighid were similarly assimilated.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by ramana »

Science Journal had an article on sea levels ~19,000 years ago.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Murugan »

ashbhee wrote:Some of you might be interested in this, The Cult of Mithras : https://www.youtube.com/watch?v=AQWX689T-YY
Apologies if this was already posted on this thread.
According to Antonia Tripolitis, Roman Mithraism originated in Vedic India and picked up many features of the cultures which it encountered in its westward journey.
Antonía Tripolitis (2002). Religions of the Hellenistic-Roman age. Wm. B. Eerdmans Publishing. pp. 3–. ISBN 978-0-8028-4913-7. It originated in Vedic, India, migrated to Persia by way of Babylon, and then westward through the Hellenized East, and finally across the length and breadth of the Hellenistic-Roman world. On its westward journey, it incorporated many of the features of the cultures in which it found itself.
Michael Speidel (1980). Mithras-Orion: Greek hero and Roman army god. Brill. pp. 1–. ISBN 978-90-04-06055-5. India's sacred literature refers to him since the hymns of the Rig Veda. But it was in Iran where Mithras rose to the greatest prominence: rebounding after the reforms of Zarathustra, Mithras became one of the great gods of the Achaemenian emperors and to this very day he is worshipped in India and Iran by Parsees and Zarathustrians.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by johneeG »

gashish wrote:Not directly related to lingusitics nevertheless below validates how knowledge/ideas/stories could have propagated out of India.

How Buddhist Cultural Memes Were Appropriated By Christianity
The origin of the legend of Barlaam and Josaphat, two of the most famous Christian saints of the Middle Ages is less widely known. This legend was so hugely popular that, from time to time, the Church announced that the relics of the two had appeared miraculously and were then installed with solemn ceremony. Barlaam and Josaphat found their way into the Roman Martyrology (27 November), and into the Greek calendar (26 August).

The legend tells how an Indian king persecutes his son, Josaphat, who astrologers have foretold, will establish the Christian Church. In due course, Josaphat meets the hermit Saint Barlaam and converts to Christianity. In the end, the prince’s father accepts the son’s conversion and retires to the desert to spend his last days with the old teacher.

Church scholars now acknowledge that Barlaam and Josaphat is a play on the names Bhagavan and Bodhisattva, and it is a reworking of the story of Buddha’s enlightenment. The original story was a Mahayana text that was translated into Arabic and European languages. Indeed, this legend should not startle us for St. Ann, St. Lucy, St. Denis and St. Brigid, represent pre-Christian deities Anna, Lucia, Dionysus and Brighid were similarly assimilated.

The connections between Ancient Rome and Bhaarath seem to be many.

- Cleopatra was ruling Egypt. Cleopatra had a fling with Ceasar of Rome. And they had a son named Ceasarion. Later, Ceasar died and Augustus became the king of Rome. Egypt was conquered by Rome. Cleopatra sends her and Ceasar's son named Ceasarion to Bhaarath for safekeeping according to ancient historian Plutarch. - 30 BCE

- There was a diplomatic(and religious) mission from Bhaarath to Rome during the rule of Augustus according to ancient historian Strabo. The mission is called Pandion mission. Most probably, it is sent by the Pandyan king. It had a Zarmarus(Shramana) who burnt himself to prove a theological point. This created a huge furor in ancient Rome. 0 CE

- A work called Nonnus Dionysiaca was written which describes a triumph of Bhaarath by greek god Dionysus. - 50 CE

- Plutarch writes about the conquest of Bhaarath by greek Alexander in his work 'Parallel lives'. - 75 CE

- Barthelowmew visits Bhaarath to take a copy of Bible to Europe. - 100 CE

- Ancient greek historian Arrain writes a work on geography called Geographica. He prominently mentions India in Indica. - 120 CE

Now, add the similarities between Roman culture and ancient Indian culture. Then, add the similarities between Buddhism and Christianity. Not to mention, the similarities between ancient Greek and ancient Indian culture.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by member_29218 »

Lalmohan wrote:
Virendra wrote:When they're showing global migrations of Pleistocene era, it would make more sense to include variations of sea level.
It is confusing for a mango reader to look at the present day map of South East Asia, and co-relate it with migrations thousands of decades ago when the landmass i.e. the canvas of migration (example-Sunda) was completely different.
the sea level piece is really crucial imho
PNAS has an interesting article on the sea levels during the last glacial maximum where the sea floor was about 130m below where it is today.
:

Key results are: (i) a rapid final fall in global sea level of ∼40 m in <2,000 y at the onset of the glacial maximum ∼30,000 y before present (30 ka BP); (ii) a slow fall to −134 m from 29 to 21 ka BP with a maximum grounded ice volume of ∼52 × 106 km3 greater than today
They also go on to say that the levels again started rising from around 16500 years ago in fits and starts and then stabilized at 2500 yrs ago after which there has been no further deglaciation until 150 yrs ago.

Here is an interesting graph that shows similar data but you get an idea of location, thus explaining how easily humanity may have reached Australia.

Image

Finally, this is quite a sensational map created by a young Slovak graphic artist Martin Vargik, who now goes by the name Jay Simons. He claims it was done in consultation with 'scientists' and may therefore well be accurate.

Image
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Re: Out-of-India - From Theory to Truth: Part 2

Post by johneeG »

Lalmohan wrote:
Virendra wrote:When they're showing global migrations of Pleistocene era, it would make more sense to include variations of sea level.
It is confusing for a mango reader to look at the present day map of South East Asia, and co-relate it with migrations thousands of decades ago when the landmass i.e. the canvas of migration (example-Sunda) was completely different.
the sea level piece is really crucial imho
Here is an article about how the sea-levels are measured for today:
How do they measure sea level?

An accurate measurement of sea level is very hard to pin down. But it is an important measurement for two main reasons:

By having an accurate sea level measurement, it is possible to measure the height of everything on land accurately. For example, calculating the height of Mt. Everest is complicated by sea-level measurement inaccuracies.
By knowing sea level, we can determine if the oceans are rising or falling over time. The concern is that global warming and other weather changes caused by man might be leading to an overall rise in sea level. If so, coastal cities are in big trouble.

The problem with measuring the sea level is that there are so many things that perturb it. If you could take planet Earth and move it out into deep space so that the sun, moons and other planets did not affect it and there were no temperature variations worldwide, then everything would settle down like a still pond. Rain and wind would stop, and so would the rivers. Then you could measure sea level accurately. If you did this, the level of the ocean's water projected across the entire planet would be called the geoid. On land, you can think of the geoid as the level that ocean water would have if you were to dig a canal from the ocean's shore to any point on land.

But the Earth is not in deep space -- it is in the middle of a chaotic solar system. There are all sorts of things changing the water level at any given point, including:

The tides, caused by the moon
Large and small waves caused by wind and the tides
High- and low-pressure areas in the atmosphere, which change the surface level of the ocean
Temperature changes in the ocean, which change the density and volume of the water
Rainfall and river water flowing into the ocean

If you were to stand on the ocean shore and try to measure sea level with a ruler, you would find it to be impossible -- the level changes by the second (waves), by the hour (tides) and by the week (planetary and solar orbit changes). To get around this, scientists try using tide gauges. A tide gauge is a large (1 foot [30 cm] or more in diameter), long pipe with a small hole below the water line. This pipe is often called a stilling well. Even though waves are changing the water level outside the gauge constantly, they have little effect inside the gauge. The sea level can be read relatively accurately inside this pipe. If read on a regular basis over a time span of years and then averaged, you can get a measurement of sea level.

You can see that getting an accurate reading (for example, down to the millimeter level) is extremely difficult. Satellites are now used as well, but they suffer from many of the same problems. Scientists do the best they can, using extremely long time spans, to try to figure out what the sea level is and whether or not it is rising. The general consensus seems to be that the oceans rise about 2 millimeters per year (although the last link below has an interesting discussion on that consensus...).

Link

So, measuring the current sea level itself is quite difficult and requires considerable time span and tedious methods. So, I think that estimating the sea level of past or future is just fancy guess-work. The best one can do is to first figure out a way to estimate sea levels of future(say x yrs from now). And if the estimation is correct, then one can use that model to estimate the sea level of past.
johneeG
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Posts: 3473
Joined: 01 Jun 2009 12:47

Re: Out-of-India - From Theory to Truth: Part 2

Post by johneeG »

The Buddhist Influence in Christian Origins
Kenneth Humphreys
11.08.15

Speculation of a link between Christianity and Buddhism first arose as a result of the translation of Buddhist texts into European languages during the British colonisation of India. Similarity in the stories of the births and lives of Jesus and Buddha were immediately apparent to scholars. It was also noted that many of their teachings had close parallels. Buddhism was unquestionably centuries older than Christianity.

Was it possible the authors of Christianity copied their ideas from Buddhism after early travel to India?



East meets West – trade and religious influence

Trade between East and West is of great antiquity. Cuneiform tablets as early as 2400 BC describe shipments of cotton cloth, spices, oil, grains, and such exotic items as peacocks from the Indus Valley region to the Middle East. We can be certain that the silk and spice routes carried more than trade goods. An Oxyrhynchus papyrus fragment from Egypt even contains a passage in a South Indian language.

Long before the word 'missionary' came to be synonymous with Christianity, Buddhist monks ('dharma-bhanakas') were traipsing across Asia. From the Buddhist heartland on the Ganges, notions of the sacred accompanied the spice and incense. Travelling the trade routes they spread their doctrines all the way from Khotan in central Asia to Antioch and Alexandria in the west.

One such visit is documented in 20 BC in Athens. A Buddhist philosopher, Zarmarus, part of an embassy from India, made a doctrinal point by setting himself alight. His tomb became a tourist attraction and is mentioned by several historians.

Clearly, the evangelists of Buddha were committed to their cause. Is it simply coincidence that the hero of the Buddhist tale is just a tad similar to the Christian superman? In both the story of the Buddha and the story of Jesus we read of a mystic or holy man, travelling from village to village. Each lives off the hospitality of the people and gets into trouble with the ruling elite by ignoring social status and taking food and refuge from prostitutes.

Is it just possible that the miracles ascribed to Jesus merely mimic the tricks practised by the 'holy men' in India?


Image
silk & spice routes


Alexander and Asoka

Alexander (336-323 BC) carried Greek civilization to the east. Cities along the trade route – Merv, Bactra, Taxila etc. – became Greek military colonies. The Indian province in the north west – Gandhara – had been a Persian satrap before the arrival of the Greeks and here, in the 2nd century BC, Greek kingdoms with a distinctive Graeco-Bactrian culture emerged.

But the flow of culture was two way – for example, the Greeks adopted the Indian war elephant and a great deal of speculative Indian thinking. Greek philosophers, like Anaxarchus and Pyrrho, had been in the train of Alexander and had mixed with the Indian gymnosophists or 'naked philosophers.' Even the more ancient Pythagoreans may have been influenced by Indian ideas – vegetarianism, communal property and the 'transmigration of souls.'

After their conquest of the Indus valley the Greeks never again returned to the simple pantheon of their Olympian gods – and founded their first school of Skepticism (see Flintoff, E. (1980), 'Pyrrho and India', Phronesis 25: 88-108.).

At the time of Alexander, the Magadha empire had dominated the middle and upper Ganges but Alexander never got that far. Yet into the vacuum created by Alexander's departure, and bringing east and west closer together, moved Chandragupta (Sandracottus to the Greeks), founder of the Mauryan empire. He conquered Magadha, and also the Greek kingdoms of the north west and much of northern India. His empire included the northern province of Kosala, where a Hindu reformer Gautama Siddhartha (aka "Shakyammuni Buddha") began advocating his 'Middle Path' between greed and asceticism.

Siddhartha's philosophising had little consequence during his own lifetime but in 270 BC, the grandson of Chandragupta, Asoka, ascended the Mauryan throne. Initially a ruthless imperialist he seems – like Marcus Aurelius – to have spent his later life in soul-searching and pondering the afterlife.

In an action that anticipated Constantine's religious revolution five hundred years later, Asoka adopted Buddhism as a unifying and pacifying ideology for his vast empire and propagated it's doctrines with all the usual zeal of a new convert.

Judging by his still extant edicts, inscribed on rocks and stone pillars to be found everywhere from Afghanistan to south India, Asoka sought further 'conquest' beyond his frontiers by dispatching Buddhist missionaries in all directions – "Conquest by Dhamma". Carved in stone is Asoka's urging of Forgiveness:

"The killing, death or deportation of a hundredth, or even a thousandth part of those who died during the conquest of Kalinga now pains Beloved-of-the-Gods. Now Beloved-of-the-Gods thinks that even those who do wrong should be forgiven where forgiveness is possible."


By this stage the Buddha's words of wisdom had been codified into a number of "sutras", propagated by a growing number of rival sects.


greek & mauryan empires

Worlds Collide

The 3rd century BC empire of Asoka included a vast area of the Greeks' eastern empire established a century earlier.



After Alexander, the Seleucides ruled the Greek empire east of the Euphrates. A century later they had taken over the kingdom of Antigonus in Syria and Asia Minor but had lost control of Parthia, Bactria and the Indus Valley.


Gandhara-Trojanhorse
Wooden horse of Troy shows up in Indian art (Gandhara)

"Conquest by Dhamma"

"Now it is conquest by Dhamma that Beloved-of-the-Gods considers to be the best conquest ...

And conquest by Dhamma has been won here, on the borders, even six hundred yojanas away, where the Greek king Antiochos rules, beyond there where the four kings named Ptolemy, Antigonos, Magas and Alexander rule ...

Here in the king’s domain among the Greeks, the Kambojas, the Nabhakas ... everywhere people are following Beloved-of-the-Gods’ instructions in Dhamma.

Even where Beloved-of-the-Gods’ envoys have not been, these people too, having heard of the practice of Dhamma and the ordinances and instructions in Dhamma given by Beloved-of-the-Gods, are following it and will continue to do so ...

This conquest has been won everywhere, and it gives great joy – the joy which only conquest by Dhamma can give. But even this joy is of little consequence. Beloved-of-the-Gods considers the great fruit to be experienced in the next world to be more important.

I have had this Dhamma edict written so that my sons and great-grandsons ... consider making conquest by Dhamma only, for that bears fruit in this world and the next."

– Asoka’s rock edict at Girnuri in Guzerat.

Buddhist monks in Egypt?

There are records from Alexandria that indicate the arrival of a steady stream of Buddhist monks and philosophers. They would surely have contributed to the philosophical speculations and syncretism for which the city was noted.

In particular, it seems the original Therapeutae were sent by Asoka on an embassy to Pharaoh Ptolemy II in 250 BC.

The word 'Therapeutae' is itself of Buddhist origin, being a Hellenization of the Pali 'Thera-putta' (literally 'son of the elder.')

Philo Judaeus, a 1st century AD contemporary of Josephus, described the Therapeutae in his tract 'De Vita Contemplativa'. It appears they were a religious brotherhood without precedent in the Jewish world. Reclusive ascetics, devoted to poverty, celibacy, good deeds and compassion, they were just like Buddhist monks in fact.

From the Therapeutae it is quite possible a Buddhist influence spread to both the Essenes (a similar monkish order in Palestine) and to the Gnostics – adepts of philosophical speculations.



Influence of Buddhism on Gnosticism
buddha-and-apostles

Buddha gives benediction to his 12 apostles


Buddhism was a religion of quite a different order to earlier 'pagan' cults. It was a scriptural religion, making a strong appeal to the emotions. It offered a moral code – and hope.



Cyril of Jerusalem

"But Terebinthus, his disciple in this wicked error, inherited his money and books and heresy, and came to Palestine, and becoming known and condemned in Judæa he resolved to pass into Persia: but lest he should be recognised there also by his name he changed it and called himself Buddas."

—Cyril of Jerusalem, Catechetical lecture 6.23.

Image
Queen Maya With Infant Buddha.
Gandhara, 2nd Century (British Museum)


The doctrine of Incarnation

The Gnostic idea of liberating the soul from entrapment in matter is not dissimilar to the teachings embodied in the "4 Noble Truths" of the Buddha.

In Buddhism, Mankind is seen as trapped in suffering (dukkha) by desire (tanha). Its cessation (nirodha) is to be realised by an eight-fold path of 'right thought, right deed, right attitude' etc. (magga). Rather than Salvation an equally whimsical Nirvana is postulated.


Nirvana Lite

The path of self-liberation (by meditation, asceticism etc.) is demanding and fails to deliver the immediate consolation ordinary people hope for. An easier option ('outer mystery') soon developed, within both Gnosticism and Buddhism by which 'devotion to the god' (prayer, chanting, ringing of bells, waving incense sticks about, etc.) bestowed liberation (salvation/nirvana) to the god's devotees.

From Gnosticism emerged the Literalists of Christianity, for whom the Saviour was given a real historic presence.

From Buddhism, Mahayana ("greater vehicle") Buddhism emerged, in which the real historical Buddha was gradually raised to the status of a divine incarnation (one in a series of enlightened beings). The Lotus Sûtra (Saddharmapundarîka-sûtram) emphasizes mere faith in the Buddha as sufficient for salvation, and advises Buddhist missionaries to convert humanity, where necessary, through symbolic language, codes, parables, etc.

And interestingly, both developments occurred towards the end of the 1st century AD.



Where Did They Get Their Ideas From?

More than two dozen story elements borrowed from the Buddha

1. Pre-existence. 2. Royal origin and genealogy. 3. Virginal Conception by mother/Virgin Birth. 4. Dream Vision. 5. White Elephant / White Dove parallel. 6. Annunciation to the Husband. 7. Annunciation of Birth by a Woman 8. Righteous foster father. 9. Marvellous Light/Star. 10. Angels and others at birth. 11. The Magi's´ visit 12. Giving of Gifts. 13. Presentation in the Temple. 14. Infant prodigy / precocious youth. 15. Nature Miracle. 16. The Naming Ceremony. 17. The Taming of Wild Animals. 18. The Miracles of the Bending Tree and Gushing Water. 19. The Fall of Idols. 20. Healing Miracles. 21. Sage recognition - Asita / Simeon parallel 22. Anna and Shabari/Old Women parallel. 23. The Appellation of King. 24. Mary / Mahâprajâpati parallel 25. Fast in wilderness / temptation by the devil. 26. Preparing the Way. 27. Reference to Signs 28. Offer of universal Salvation.
BIRTH of the Saviour

The conception and birth of Christ in the Gospel of Luke has an uncanny resemblance to the birth stories of Buddha.

In both cases the mother was a paragon of virtue, had a vision and, without sex, became pregnant with an extraordinary child. Each was delivered while the mother was on a journey and their births were both announced by angels.

After the birth of Buddha a hermit sage, who had heard the celebrations of angels, was told by them that the infant would sit on the throne of enlightenment.

In the Christian story, the angels appeared and told shepherds that a child was born who is Christ the Lord.

Both narratives stress that holy people came to pay homage to the world's saviour.
LOST and FOUND
The homespun 'wisdom' of Buddha & Christ

Sinner returns to the Father!!

Younger son leaves home and squanders his inheritance on wild living; bankrupt and reduced to feeding pigs he returns home; delighted father kills the fattened calf for him. Sensible elder brother indignant and angry but father explains celebration is justified because his brother had been 'lost and is found'. (Luke 15:11-32)

Sufferer attains Nirvana!!

Young son leaves home for distant lands. Father distraught. Years later, looking for work, son doesn't recognize his now rich father (who does recognize him). He flees. Father secretly hires him as a scavenger. Years later, dying, he tells son of his inheritance. (Lotus Sutra)


TRIAL

After a meal, an innocent man Charudatta is accused of murdering the courtesan Vasantasena, and is brought to trial. The judge, admitting his incompetence to condemn a Brahmin, sends the case over to the king who condemns the man to be executed and impaled with an inscription on him.

Charudatta is then ordered to carry his cross (Sanskrit sulam) to the place of execution. Meantime, the king’s brother-in-law, who actually murdered the courtesan, buries her body under a pile of leaves. But she is found by a Buddhist monk who raises her from her 'deadly swoon.' Vasantasena then saves Charudatta from death.

Charudatta forgives his accuser, Samsthanaka, and appoints the Buddhist monk as the head of all the Buddhist monasteries in the realm. There is a marriage in the end as well: Charudatta accepts Vasantasena as his second wife.
2nd BC Sanskrit play Mrchchakatika (Little Clay Cart)


PASSION

In this story of 'Gautama, a holy man' our hero is wrongfully condemned to die on the cross for murdering the courtesan Bhadra. Gautama is impaled on a cross, and his mentor Krishna Dvapayana visits him and enters into a long dialogue, at the end of which Gautama dies at the place of skulls after engendering two offspring – the progenitors of the Ikshavaku Dynasty.

1. The death episode begins for Buddha crossing the Ganges at Magadha, from whence he goes on to Kusinagari for a last meal.
The fable of Matthew (15:39) similarly has JC aboard ship, to the (unknown) "coasts of Magdala", from whence he goes on to Jerusalem for a last meal.
2. Both Buddha and JC forecast their own death 3 times.
3. Buddha arrives at Ku-kut-tha, JC at 'Gol ga tha'.
4. Both Buddha and JC twice refuse a drink.
5. Buddha dies between 2 trees, JC between 2 criminals.
6. Both promise their last convert that "today you will be in paradise."
7. Death occurs during 'darkness'.
8. A disciple of Buddha – Kas ya pas – travelling with 500 monks – encounters an unknown personage from whom he learns of the death of Buddha. Another unnamed disciple disparages the dead Buddha.

The fable of Luke has the disciple Kle o pas encounter an unknown personage on the road to Emmaus. This 'unrecognised' Jesus disparages the evident lack of faith.

In a variation of the story, the 500 Buddhist monks become Paul's 500 brethren (1 Cor. 15.6) – though Paul renders Kas ya pas as 'Cephas' (Simon Peter has his own origin in Sâri Putra, also in the Buddhist 'gospel').

9. The dead Buddha is burned and it is the smoke of his corpse which rises– the true "resurrection."
– From a 2nd/1st century BC play 'Samghabhedavastu' (Mahâparinirvâna sûtra)



Essenes – esoteric Buddhists?

The Essenes were a monastic order having much in common with contemporary Buddhists.

Most lived an austere existence in the desert where they eschewed the animal sacrifice of the Jerusalem temple priesthood (they were vegetarians).

Renouncing all normal enjoyments, they lived without personal property, money or women (they recruited from newcomers.) The Essenes extolled the merits of asceticism, penance, and self-torture.

They were, however, interested in the magical arts and the occult sciences.They believed in the pre-existence of the soul and in angels as divine intermediaries or messengers from God.



Influence of Buddhism on the Christians – Q?

Close, striking parallels exist between early Buddhist texts and what Bible scholars postulate as the 'Q' material – ('Q' is shorthand for Quelle, the German for 'source'). The earliest translations of Buddhist texts into Greek date back to the time of king Asoka (3rd century BC).

It seems highly probable that the core of the body of Q material was made up of aphorisms, sayings originally ascribed to the Buddha but later attributed to Jesus. To these sayings were added mini-stories and micro-scenes to produce what became the Gospels of Matthew and Luke.


Aphorisms

From the Dhammapada, Buddha's observation:

"The faults of others are more easily seen than one's own, but seeing one's own failings is difficult."

Compare to Gospel of Thomas 26

"You see the mote which is in your brother's eye; but you do not see the beam which is in your own eye."

This subsequently was given a more theatrical flourish when it became Matthew 7:3

"And why beholdest thou the mote that is in thy brother’s eye, but considerest not the beam that is in thine own eye? "


From the Dhammapada:

"When a mendicant, though still young, yokes himself to the Buddha's teachings, the world is illuminated like the moon freed of clouds."

Jesus's statement:

"He who wishes to follow me must know himself and bear my yoke."



The Mûlasarvâstivâdavinaya begins with a long list of kings. This is combined with a list of the last seven Buddhas, to give three periods of “fourteen generations” and a total of 42 – an identical format to the Gospel of Matthew!

Love?

The whole idea that man should care about his brother, that he should accept responsibility for society as a whole or for needy human beings in particular, clearly precedes Christianity – in Greek thought and in Buddhism.

The Buddha's philosophy of compassion, his vision of Dhamma, the eternal law that sustains the cosmos, manifests itself among humanity as the moral law.

The Buddha's most celebrated dictum is:

"Hostility is never conquered by hostility in this world; hostility is conquered by love. That is the eternal law."


500 Witnesses

"After that, he was seen of above five hundred brethren at once; of whom the greater part remain unto this present, but some are fallen asleep."
1 Corinthians 15:6


Buddhist tradition states that shortly after the passing away of the Buddha five hundred of his Arhats and disciples met in council at Rajagaha for the purpose of recalling to mind the truths they had heard directly from their hero during the forty-five years of his teachings.

The Coptic biblical text actually identifies the 500 as 'Indian Brahmans'!
In short, we find opportunity, motive, method, location and scriptural evidence, for a profound and detailed Buddhist influence in Christianity's origins. That it was so cannot be doubted.



Sources:
Symposium on “ The Sanskrit and Buddhist Sources of the New Testament" Klavreström, Sweden 9/11 2003
Z. P. Thundy, Buddha and Christ: Nativity Stories and Indian Traditions (Leiden, 1993)
L. Adelskogh, Jesus in Comparative Light
E. R. Gruber, H. Kersten,The Original Jesus (Element Books, 1995)
Elaine Pagels, The Gnostic Gospels (Vintage, 1979)
J. Duncan M. Derrett, The Bible and the Buddhists (Sardini 2000)
N. S. Chandramoul, Did Buddhism influence early Christianity? (The Times of India May 1, 1997)
Christian Lindtner, Wer war Kleophas Radikalkritik

-----

Indian figure – excavated from Pompeii (79 AD, Naples Museum)

Image
Buddhist Teacher?

There is mention of a teacher called Ammonius Sakka teaching in Alexandria in the 1st century AD. This philosopher-teacher who believed in reincarnation, has been called a Neo-Platonist.

He was the teacher of Plotinus – and Church Father Origen!

buddhist-trinity
The Sanskrit TRi-RaTNaS becomes the Latin TRi-NiTaS ... even the name is copied!


Diamond Geezer

Another Buddhist variant Vajrayana ("Diamond Vehicle") introduced Tantric or Esoteric Buddhism. It may have influenced the notorious Carpocratians ... Tantra with a Christian varnish!

"Sermon on the Mount ... Buddhist verses from the Dhammapada"?
So said Barnett Hillman Streeter in the 1930s

Omm

"The contemplative ideal – since it led to pure mathematics – was the source of a useful activity. This increased it's prestige and gave it a success in theology, in ethics, and in philosophy."

–Bertrand Russell on Pythagoras

"Saint Buddha" !

The most amusing Buddhist story that made its way into Christian lore is the tale of 'Barlaam and Josephat' – nothing less than the story of the Buddha himself, disguised as a Christian Saint!

In the story, Josephat, an Indian prince (!) has a father who persecutes Christians. At Josephat's birth his future greatness is predicted, not as a king, but as a convert to Christianity. Eventually allowed to leave the palace, the young prince for the first time saw a crippled man, a blind man and a senile man, and so learned of life's darker side (that life is suffering?).

Josephat soon met a monk named Barlaam, who converted him to Christianity and the two lived as hermits.

They were canonized by the Catholic Church in the 16th century.

Check for yourself –
Comparative Sayings of the Buddha and Jesus
Link
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Re: Out-of-India - From Theory to Truth: Part 2

Post by member_29218 »

johneeG wrote:
Here is an article about how the sea-levels are measured for today:
How do they measure sea level?

An accurate measurement of sea level is very hard to pin down. But it is an important measurement for two main reasons:

By having an accurate sea level measurement, it is possible to measure the height of everything on land accurately. For example, calculating the height of Mt. Everest is complicated by sea-level measurement inaccuracies.
By knowing sea level, we can determine if the oceans are rising or falling over time. The concern is that global warming and other weather changes caused by man might be leading to an overall rise in sea level. If so, coastal cities are in big trouble.

The problem with measuring the sea level is that there are so many things that perturb it. If you could take planet Earth and move it out into deep space so that the sun, moons and other planets did not affect it and there were no temperature variations worldwide, then everything would settle down like a still pond. Rain and wind would stop, and so would the rivers. Then you could measure sea level accurately. If you did this, the level of the ocean's water projected across the entire planet would be called the geoid. On land, you can think of the geoid as the level that ocean water would have if you were to dig a canal from the ocean's shore to any point on land.

But the Earth is not in deep space -- it is in the middle of a chaotic solar system. There are all sorts of things changing the water level at any given point, including:

The tides, caused by the moon
Large and small waves caused by wind and the tides
High- and low-pressure areas in the atmosphere, which change the surface level of the ocean
Temperature changes in the ocean, which change the density and volume of the water
Rainfall and river water flowing into the ocean

If you were to stand on the ocean shore and try to measure sea level with a ruler, you would find it to be impossible -- the level changes by the second (waves), by the hour (tides) and by the week (planetary and solar orbit changes). To get around this, scientists try using tide gauges. A tide gauge is a large (1 foot [30 cm] or more in diameter), long pipe with a small hole below the water line. This pipe is often called a stilling well. Even though waves are changing the water level outside the gauge constantly, they have little effect inside the gauge. The sea level can be read relatively accurately inside this pipe. If read on a regular basis over a time span of years and then averaged, you can get a measurement of sea level.

You can see that getting an accurate reading (for example, down to the millimeter level) is extremely difficult. Satellites are now used as well, but they suffer from many of the same problems. Scientists do the best they can, using extremely long time spans, to try to figure out what the sea level is and whether or not it is rising. The general consensus seems to be that the oceans rise about 2 millimeters per year (although the last link below has an interesting discussion on that consensus...).

Link

So, measuring the current sea level itself is quite difficult and requires considerable time span and tedious methods. So, I think that estimating the sea level of past or future is just fancy guess-work. The best one can do is to first figure out a way to estimate sea levels of future(say x yrs from now). And if the estimation is correct, then one can use that model to estimate the sea level of past.

I think there is sufficient information available to estimate past sea levels. It is not guess-work although several assumptions are made, just like in genetics.

For present sea levels (ocean depth) measured on a day to day basis obviously different methods are used and tidal gauges are quite adequate.

Thus:
Estimates of variations in global sea level come from direct observational evidence of past sea levels relative to present and less directly from temporal variations in the oxygen isotopic signal of ocean sediments
The other sources of data are geographical features of shorelines, core samples from the Greenland and other ice sheets, coral samples and other cores from offshore areas etc. Then you have the evidence of submerged habitats like 'Doggerland'.

Some links:

A 17,000 year sea level record :
Coral reefs drilled offshore of Barbados provide the first continuous and detailed record of sea level change during the last deglaciation. The sea level was 121 plus-minus 5 metres below present level during the last glacial maximum. The deglacial sea level rise was not monotonic; rather, it was marked by two intervals of rapid rise. Varying rates of melt-water discharge to the North Atlantic surface ocean dramatically affected North Atlantic deep-water production and oceanic oxygen isotope chemistry. A global oxygen isotope record for ocean water has been calculated from the Barbados sea level curve, allowing separation of the ice volume component common to all oxygen isotope records measured in deep-sea cores
USGS article - simplified considerably. Also suggests that in the previous interglacials, sea levels were up to 20 meters higher than they are today.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by member_29218 »

johneeG wrote:
The Buddhist Influence in Christian Origins
Kenneth Humphreys
11.08.15

Speculation of a link between Christianity and Buddhism first arose as a result of the translation of Buddhist texts into European languages during the British colonisation of India. Similarity in the stories of the births and lives of Jesus and Buddha were immediately apparent to scholars. It was also noted that many of their teachings had close parallels. Buddhism was unquestionably centuries older than Christianity.

Was it possible the authors of Christianity copied their ideas from Buddhism after early travel to India?



Check for yourself –
Comparative Sayings of the Buddha and Jesus
Link
I've believed this for a long time.

Here is a superb documentary by an ex fundamentalist Christian, Brian Flemming. It explores the Jesus myth and basically argues that he is just one in a long line of mythical heroes sprinkled through the folklore and sagas of all cultures. Not much different from our Marvel Comics heroes if you think about it.

The follow up interview with Sam Harris, the well known atheist is also compelling. Highly recommended.

Prem
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Prem »

http://www.newsgram.com/we-romas-would- ... -diaspora/
We (Roma) would like to be treated as Indian diaspora’
New Delhi: An International Conference on Roma culture held in the city concluded on Sunday with a call to recognize them as India’s diaspora. This appeal from the Roma community came after External Affairs Minister Sushma Swaraj described the Roma community spread across the world as ‘children of India’“Roma people are an Indian nation, the autochthonous territory of southeastern and western Europe, but also in other parts of the world, with all attributes that make them a special national entity,” Jovan Damjanovic, president of the World Roma Organization, said at the three-day International Roma Conference and Cultural Festival 2016 here.“We would like to be treated as the Indian diaspora and can make a contribution to our country of origin’s growth,” he said at the conference organized by the Indian Council for Cultural Relations (ICCR) and the Antar Rashtriya Sahayog Parishad (ARSP) – Bharat.Inaugurating the conference on Friday, Sushma Swaraj said: “You are the children of India, who migrated and lived in challenging circumstances in foreign lands for centuries. Yet you maintained your Indian identity.A strong 20 million population of your community spread over 30 countries, encompassing West Asia, Europe, America, and Australia speaks of your unique ability of adapting to foreign cultures. We in India are proud of you… Welcome you with an open heart.”Said to be descendants of nomadic groups in northwest India like Dom, Banjara, Gujjar, Sansi, Sikligar, Dhangar and others, Romas are known as “Zigeuner” in Germany,”Tsyiganes/Manus” in France, “Tatara” in Sweden, “Gitano” in Spain, “Tshingan” in Turkey and Greece, “Tsigan” in Russia, Bulgaria and Romania and “Gypsies” in Britain.A resolution adopted at the conclusion of the conference on Sunday called for people-to-people contacts between Indians and Romani people to be encouraged.“The cultural recognition of Romani people is of utmost importance for strengthening bonds with Roma,” it stated.
Virendra
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Virendra »

Not that I hate Roma people, the timing looks a bit opportunistic.
There are a plenty of examples in history, where people try to board your party as soon as they deduce that you're headed for greener pastures.
Never heard the Roma shout 'we are Indian' so loudly anytime before.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Pulikeshi »

^^^Funny comment if you are of Indian origin onlee no?
The Roma have been blamed historically by even non-racist, but pernicious Europeens for being too opportunistic :P :mrgreen:

Look at the list of folks in the 20 odd million that are proved diaspora to the West of India:
List of Romani People

If you peer down the list - there is one Anjezë Gonxhe Bojaxhiu (Mother Theresa) who is a Roma. :eek:
There is political win-win for India and Roma - irrespective of how one feels about it!
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Virendra »

I was scanning academia.edu for papers and stumbled on this. Nothing out of the ordinary so far in cursory reading. Thought to share anyway.
https://www.academia.edu/7893126/Geneti ... n_Theories

Regards,
Virendra
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Re: Out-of-India - From Theory to Truth: Part 2

Post by RajeshA »

If

- somebody feels as belonging to India
- somebody has a convincing case of Indian ethnicity
- somebody does not adhere to ideologies inimical to Bharatiyata

Then that person, regardless of where he is in the world, regardless of when he or his ancestors left India, should be treated as Indian.

In the case of Roma, it is true.

JMHO
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Re: Out-of-India - From Theory to Truth: Part 2

Post by gashish »

Hear Stories Read in Proto Indo-European, a 6000-Year-Old Language
“In 1868, German linguist August Schleicher used reconstructed Proto-Indo-European vocabulary to create a fable in order to hear some approximation of PIE,”
Listen to these PIE sounds "fabricated" by German linguist! Surprise surprise, it sounds like German!
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Lalmohan »

in 1868 the germans were busy proving what a great nation and people they were to take on the brits and french
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Re: Out-of-India - From Theory to Truth: Part 2

Post by Prem Kumar »

2 good points made in this Rajiv Malhotra lecture + Q&A in JNU for his Sanskrit book:

1) RM makes the point that, while the real destructive politics is played by the Dravidian parties (i.e. there is no Aryan party), the academics are busy focusing on Aryan Theory. Instead he suggests a focus shift to understand better South Indian culture, literature, commonality between South & North languages/culture/religious-beliefs etc. I think this is a great point. There is plenty of evidence to suggest that say, Sangam literature has a lot in common with the Vedic culture. The ancient Tamils didn't view themselves as "different" from the North Indians and in fact, revered Vedic knowlege. There is the Agasthya story etc. But all these need to be studied in detail, papers published, propagated in media etc. That's how the "Indian Grand Narrative" can be established and fake Aryan-Dravidian split be countered

2) Prof Girish Jha (JNU Computational Linguist) talked about how, when his team tried to create a common language framework for India (based on Sanskrit), he was surprised by the commonalities between the "supposedly different" North & South language families. This shouldn't be surprising at all, considering India was continuously populated from at least 65K years ago. If all Indians are genetically indistinguishable due to inter-mingling, then languages must have also inter-mingled! So, Prof Jha suggests that we should look at a Proto-Indic common ancestor from which the Indian languages like Sanskrit, Tamil etc must have emerged. This is a great idea, one that I haven't seen anyone articulate before! Obviously the West isn't interested in this, because it doesn't do anything for their origins & if anything, will be politically disastrous for their Indological-interventions. But this should be of great interests to Indian linguists. Rather than rehashing Western-imported PIE model (which has its strengths but also lots of weaknesses), we should also look at Proto-Indic language tree, which predates & subsumes the PIE separation. This tree will have relationships with the PIE tree & can fit in with a model of how some PIE branches of the Proto-Indic tree would've separated and left India


The full video is here .

Volunteers have also broken it up into short, 5 minute chunks. Just Google it. Results here:

https://www.google.com/search?q=rajiv+m ... u+sanskrit
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Re: Out-of-India - From Theory to Truth: Part 2

Post by RoyG »

Prem,

If you look at the linguistic presentation by Talageri, you'll see why PIE makes sense. The origins of PIE however are somewhere between Afghanistan and Punjab (Indian subcontinent) rather than the Central Asia. He constructs his theory very logically.

Once Sanskrit made further inroads into the subcontinent it interacted quite a bit with the South Indian language family. However, the sort of oppression inherent in Sanskrit that some Western Indologists claim is refuted by the simple fact that Tamil classics don't make any mention of it.
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Re: Out-of-India - From Theory to Truth: Part 2

Post by shiv »

The so called North South divide; the description of south Indians as Dravidians and North Indians as Aryans; the archetypal "madrasi" as opposed to a northie are all the fallout of the Aryan invasion theory. Hindi "imposition" and anti-Hindi riots are also a result of a divide that did not exist prior to 1700 AD

The British (and Europeans) heard the word Arya in the Rig veda and felt that they were "Aryans" - the noble people. Initially they gave India some credit for the Rig Veda but gradually found that Indians, even "upper castes" who they saw as brothers were too different and too black for their taste. That is how Dravidians got invented as the inferior black race that corrupted the Indian Aryans. To some extent Northern Indian colonized minds saw themselves as Aryans and deep South colonized minds said "fuk off we are Dravidians and we don't give a damn for you Aryans"

When you look at genetics and find that this is all bullshit you realise how much damage has been done to India by the AIT

South Indians speaking South Indian languages find it easy to see how much Sanskrit they use in their languages. Carnatic music and temple rituals are full of Sanskrit anyway like all Hindus. North Indians or even east Indians who do not know any South Indian language fail to see the amount of Sanskrit in South Indian languages and hear only gibberish.

Two points here:

Modern Kannada, Malayalam and Telugu are full of Sanskrit words. Tamil too but a little less so
Modern Tamil is a language that emerged from the ancestor language of Kannada - called "Halegannada" (Pronounced "Halay-gun-ada"-Old Kannada).

Many Halegannada inscriptions exist. And if I am not mistaken the Aihole inscription from a Karnataka king that mentions the date of the Mahabharat war is in Halegannada script but Sanskrit language

Our nation owes a debt of gratitude to Rajiv Malhotra. Thanks due to Shiva/Vishnu/Brahma for producing him
Last edited by shiv on 26 Feb 2016 07:08, edited 1 time in total.
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