Human Evolution Seems to Be Accelerating (Jews evolved from "financing!")

above-average intelligence in Ashkenazi Jews — those of northern European heritage — resulted from natural selection in medieval Europe, where they were pressured into jobs as financiers, traders, managers and tax collectors.

Those who were smarter succeeded, grew wealthy and had bigger families to pass on their genes, they suggested. That evolution also is linked to genetic diseases such as Tay-Sachs and Gaucher in Jews.

The new study was funded by the Department of Energy, the National Institute of Mental Health, the National Institute of Aging, the Unz Foundation, the University of Utah and the University of Wisconsin.

The Chinese word for horse is ma. I read somewhere that that may be an Indo-European loan-word (related to the English word mare).

The sign for ma was originally a drawing of a horse, and in the pre-Communist version of the character it still sort of looks like a horse. It's the first character in spelling Karl Marx's surname (which requires 3 characters--ma plus ko plus su...I don't know Chinese but I think the last two characters mean "rear end").

So your theory is that the genetic mutations that are random occur simultaneously throughout a population, and that the new species is birthed multiple times within years of each other so that breeding and replication can continue.

Despite your population theory, logic tells you that at some point a single individual representing the new species is birthed. You still have not addressed the major issue at stake.

So the results possibly can’t be duplicated?

I reckon they probably could, to a degree. However, we're talking about generations upon generations of essentially ahistorical people - whether talking of Jews in the Middle Ages or the original spreading of man into isolate populations after Babel, we don't know exactly which populations was from where, interacted with whom, and moved where. The results would not duplicate, but could perhaps explicate, such an event.

Populations evolve, no single individual will ‘break’ from his progenitors and become, inandofitself a ‘new species’.

Just as no clear line can be drawn between when Americans stopped speaking “the Kings/Queens’ English” and started speaking “American English”. Slight differences come up in the language over time until now we can barely understand the limey bastards. There was no ‘first American English’ speaker born to ‘Queen’s English’ speaking parents who suddenly could not understand their progeny. Much as the ridiculous straw man you constructed about biological evolution, how would such an individual language develop, and who would he speak it to?

No, just as at no ‘same moment’ did Americans start speaking ‘American English’ and not ‘Queens English’, at no ‘one moment’ does a population become a new species.

Language and biological evolution are similar in that they can come from an identical source but differentiate until communication / reproduction become difficult then impossible, and it doesn’t happen like a little fairy story with magic and pixie dust and happen in a flash. It happens over many generations when an interbreeding population accumulates differences until reproduction with the parent population becomes difficult or impossible.

What your describing conflicts with the common definition of a new species - one that can’t breed with it’s ancestor. When that new species emerges, with what will it breed? That new species will emerge at a singular point in time, a birth. It will be the first that can’t breed with it’s ancestors. How does it continue it’s own species?

The idea that an entire population will emerge with the traits that prevent it from breeding with it’s ancestors simultaneously is logically unsound.

Either the definition is wrong, or the theory doesn’t account for it.

The complexities of biology and language are in no way similar and do not represent appropriate comparison points. Apples and oranges. Or rather apples and porterhouse steaks.

Not at all. Can someone who speaks French communicate easily with someone who speaks Italian? Just as a Horse cannot easily reproduce with a Donkey (well they can easily, but the resulting offspring has difficulty reproducing). Once French and Italian were the same language, just as once a Horse and a Donkey were the same species.

When a new species emerges it will reproduce within its own species. It was reproducing as an independent population in the first place in order to BECOME a new species, this reproduction only within the population will continue as differences accumulate making reproduction with the parent species more and more unlikely and then finally impossible.

And the definition of species is not one that CANNOT reproduce with other species, it is a population that in the wild DOES NOT. A Lion and a Tiger can produce offspring (a Tigon) that can then reproduce with a Tiger; making a Ti-Tigon. But that doesn’t mean a Lion and a Tiger are the same species, just because it can be done in captivity. The two lineages do not and have not mated together in the wild.

So your definition of species is incorrect, the theory does account for the generation of new species, and it has been observed in numerous ‘ring species’ where given species A-B-C-D-and E in a given area where A neighbors B and B neighbors C, etc; A and B will be able to reproduce together, but not A and D or A and E. This same pattern is observed in languages where neighboring dialects of the same parent language will be able to talk easily with each other, but not dialects of the same parent language that are distant from each other.

They really messed up the science.

By most accounts, I think scientists now believe that the only reason the enzyme is lost in ADULTS of non-Northern European ancestry (though not all) is because the sources of dairy around them were not sufficient and thus they STOPPED DRINKING MILK.

If a kid is raised on milk, there is little chance he will be lactose intolerant(at least not in any serious way.)

It has to do with milk sources around those people and now millenia later, they never worked to build those sources (people develop different food and nutrition strategies) and now they believe they ‘can’t’ drink animal milk.

It’s just not true.

Hmm.

Well, that’s not what I had read.

Why the hell did I make such a rigid assertion?! LOL Even when I was typing it, I felt like I should have couched my assertion a bit better.

In any case, while there is apparently some interesting reactions to alcohol in some Asians, as far as I know, the enzyme is produced so long as you steadily supply milk to the growing child.

But maybe I’m wrong. I did read an older book, Food in History, and then some stuff on the net.

You are incorrect. All the milk drinking in the world (past infancy) is not going to help the 98% of Southeast Asians who are lactose intolerant. Someone who is lactose tolerant can become slightly lactose intolerant after a long bout of not drinking milk (it is a gene under inductive control after all, and any gene not used tends to get buried in chromatin, making it harder to activate).

Here is the source and data....

http://arstechnica.com/journals/science.ars/2006/12/11/6246

Prior to the domestication of cattle about 8,000 years ago, humans had access to lactose only when they were young and nursing. As a result, the gene that allows us to digest lactose (called lactase) typically gets shut off during childhood, and stays off for the rest of human life. With the domestication of cattle, that equation changes; anybody that keeps the gene on has access to a whole new source of calories in the cow’s milk. A mutation that prevents the gene from shutting down occurred shortly after domestication of cattle; since it was so advantageous to the herders, it spread with the cows throughout many European populations, being present at frequencies of over 90 percent in Scandinavians.

And from another source....

Lactose intolerance rates as given on the above site:

Southeast Asians/98%
Asian Americans/90%
Alaskan Eskimo/80%
African Americans Adults/79%
Mexicans from rural communities/73.8%
North American Jews/68.8%
Creek Cypriots/66%
Cretans/56%
Mexican American Males/55%
Indian Adults/50%
African American Children/45%
Indian Children/20%
Caucasians of N. European and Scandinavian decent/5%

So if anyone out there adopts an Asian or African infant, please only feed them milk when they are a baby. As they age when they start to show signs of distress from drinking milk, please do not think that they are ‘faking it’ and just need to drink even more milk to raise their tolerance for it. It doesn’t work, and the reason is molecular. They don’t have a mutation in the gene that will shut down the lactase gene after nursing as an infant. This gene shuts down the lactase gene in almost all mammals when they stop nursing. European populations have a mutation of this gene and are able to produce lactase, a molecular machine that breaks down lactose, throughout their life and not just as a nursing infant.

So it isn’t just our milk drinking culture, it is one of the rare circumstances where there is an actual underlying biological difference; which is actually rare among humans as we are a very young and very homogeneous species. Most differences between peoples are cultural, lactose tolerance is NOT one of them.

Not that wikipedia should be trusted fully but here’s the link and then a link to a study in Japan of the decline in lactose intolerance. let me also state that it’s not that NO ONE is congenitally lactose intolerant, just that much of what we attribute it to genetically, is overstated. I don’t want to quite say ‘we’re both right’ because it’s a cop-out but I think I made a simplistic assertion but I think there’s some credibility to it, scientifically.

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

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=1234085&dopt=AbstractPlus

The above is the link to the Japanese study.
Primary cause listed: # Primary lactose intolerance. Environmentally induced by weaning in non dairy consuming societies[3]. In many Asian and African cultures, where industrialized and commercial dairy is uncommon, milk consumption beyond infancy is not commonplace. After children become weaned, they no longer consume milk, which is the same normal weaning process for all mammals (domesticated and wild). However, cultures such as that of Japan, where dairy consumption has been on the increase, demonstrate a lower prevalence of lactose intolerance in spite of a genetic predisposition[4]. For any given individual the degree of weaning is probably genetically influenced.

I wonder what the % of milk intolerance is by ‘western standards’? The prevalence of lactose intolerance in Asian Americans is still 90% by our standards, 19% in Japanese by theirs. My source said there was a specific mutation of a gene that inactivates lactase that is prevalent in European populations, and this is what I have heard before. I will hunt down the data...

abstract of paper.....

“1. The incidence of milk intolerance is approximately 19% in Japanese adults when 200 ml of milk is given. However, a much greater incidence was assumed when considered under the criteria of Western standard. 2. The lactase activity was significantly greater in milk drinkers than non-drinkers. And, internationally, the active is higher in those nationalities whose milk consumption is greater. 3. Lactase is an adaptive enzyme and rather easily induced by lactose load feeding in animals. From the data of our own and of the literature, it was further confirmed that environmental factors play a more important role than genetic factors in the etio-pathogenesis of milk intolerance.

PMID: 1234085 [PubMed - indexed for MEDLINE]

Neato....New info is that not only is there a specific SNP (single nucleotide polymorphism, i.e. an allele of a gene that differs only at a single location) associated with lactose persistence in European population, there is a different mutation that gives African populations that domesticated cattle lactose tolerance in adulthood.

Convergent adaptation of human lactase persistence in Africa and Europe. 2007 Department of Biology, University of Maryland, College Park, Maryland 20742, USA. Tishkoff@umd.edu

A SNP in the gene encoding lactase (LCT) (C/T-13910) is associated with the ability to digest milk as adults (lactase persistence) in Europeans, but the genetic basis of lactase persistence in Africans was previously unknown. We conducted a genotype-phenotype association study in 470 Tanzanians, Kenyans and Sudanese and identified three SNPs (G/C-14010, T/G-13915 and C/G-13907) that are associated with lactase persistence and that have derived alleles that significantly enhance transcription from the LCT promoter in vitro. These SNPs originated on different haplotype backgrounds from the European C/T-13910 SNP and from each other. Genotyping across a 3-Mb region demonstrated haplotype homozygosity extending >2.0 Mb on chromosomes carrying C-14010, consistent with a selective sweep over the past approximately 7,000 years. These data provide a marked example of convergent evolution due to strong selective pressure resulting from shared cultural traits-animal domestication and adult milk consumption.

PMID: 17159977 [PubMed - indexed for MEDLINE

1: Am J Hum Genet. 2001 Jan;68(1):160-172. Epub 2000 Nov 28. Links
Lactase haplotype diversity in the Old World.Hollox EJ, Poulter M, Zvarik M, Ferak V, Krause A, Jenkins T, Saha N, Kozlov AI, Swallow DM.
MRC Human Biochemical Genetics Unit, Galton Laboratory, Department of Biology, University College London, London NW1 2HE, United Kingdom.

Lactase persistence, the genetic trait in which intestinal lactase activity persists at childhood levels into adulthood, varies in frequency in different human populations, being most frequent in northern Europeans and certain African and Arabian nomadic tribes, who have a history of drinking fresh milk. Selection is likely to have played an important role in establishing these different frequencies since the development of agricultural pastoralism approximately 9,000 years ago. We have previously shown that the element responsible for the lactase persistence/nonpersistence polymorphism in humans is cis-acting to the lactase gene and that lactase persistence is associated, in Europeans, with the most common 70-kb lactase haplotype, A. We report here a study of the 11-site haplotype in 1,338 chromosomes from 11 populations that differ in lactase persistence frequency. Our data show that haplotype diversity was generated both by point mutations and recombinations. The four globally common haplotypes (A, B, C, and U) are not closely related and have different distributions; the A haplotype is at high frequencies only in northern Europeans, where lactase persistence is common; and the U haplotype is virtually absent from Indo-European populations. Much more diversity is seen in sub-Saharan Africans than in non-Africans, consistent with an “Out of Africa” model for peopling of the Old World. Analysis of recent recombinant haplotypes by allele-specific PCR, along with deduction of the root haplotype from chimpanzee sequence, allowed construction of a haplotype network that assisted in evaluation of the relative roles of drift and selection in establishing the haplotype frequencies in the different populations. We suggest that genetic drift was important in shaping the general pattern of non-African haplotype diversity, with recent directional selection in northern Europeans for the haplotype associated with lactase persistence.

PMID: 11095994 [PubMed - indexed for MEDLINE]

Last one I promise! ;) Here is the original paper that studied the phenomenon. The ‘cis acting’ element they are talking about is probably responsible for recruiting a protein that will help deactivate the lactase gene upon weaning (by burying the gene in chromatin where it cannot be turned on), it is mutated in European populations leading to lactase persistence.

: Hum Mol Genet. 1995 Apr;4(4):657-62. Links
The lactase persistence/non-persistence polymorphism is controlled by a cis-acting element.Wang Y, Harvey CB, Pratt WS, Sams VR, Sarner M, Rossi M, Auricchio S, Swallow DM.
MRC Human Biochemical Genetics Unit, Galton Laboratory (UCL), London, UK.

Lactase activity is present at high levels in the small intestine of some human adults and not others. This is due to a genetically determined polymorphism which affects the developmental regulation of the expression of the lactase gene. This polymorphism is of considerable interest in relation to cultural differences in nutrition but despite exhaustive studies, the molecular basis has not yet been found. It has not even been shown whether the sequence differences reside within or adjacent to the lactase gene itself or in a trans-acting factor. We have therefore exploited known DNA ‘marker’ polymorphisms within the exons of the lactase gene to examine the expression of the individual lactase mRNA transcripts from persistent and non-persistent individuals in order to determine whether the regulation is in cis or trans. Our results show that in certain lactase persistent individuals one allele of the lactase gene is expressed at much lower levels than the other and these individuals tend to have intermediate lactase activities. It is proposed that these people are heterozygous for the lactase persistence and non-persistence alleles and that this means that the nucleotide substitutions responsible for the lactase persistence/non-persistence polymorphism are cis-acting. This narrows down considerably the area of the genome that needs to be searched for the relevant sequence differences.

PMID: 7543318 [PubMed - indexed for MEDLINE]

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