← Autodidact Archive · Original Dissent · Ed Toner
Thread ID: 4124 | Posts: 3 | Started: 2002-12-20
2002-12-20 20:54 | User Profile
Asperger's Syndrome, a variety of Autism that has to do with, among other things, physical coordination, language development, social interaction and genius. Frequently, those afflicted with AS teach themselves to read at an early age often at 2 or 3 years, and are compulsive readers for life.
Among the symptoms of AS are clumsiness, a disputatious conversational style, difficulty in socializing, pedantic language, an un-willingness to take advice and/or criticism, an increased ability to concentrate on an abstract subject, and an obsession with the underclasses.
The syndrome was first described by Dr. Hans Asperger, a psychiatrist in Hungary during WWII, but it was first included in DIAGNOSIS AND STATISTICAL MANUAL OF MENTAL DISORDERS to which American mental health practitioners refer in the 1994 issue.
Recent research in the Human Genome project has found that an abnormality in gene WNT2 of Chromosome 7 causes the condition which is incurable.
AS is inherited. Many Jews have it. Many prominent Jews have had it: Einstein, Leonard Bernstein, Oppenheimer and other mathemeticians, scientists and musicians.
AS first occured maybe thousands of years ago as a genetic accident in an individual member of the Russian/Turkish tribe, the Khazars, that in the 8th century converted to Judaism It was probably a factor in the tribe's converting to Judaism, their disputatious conversational style providing a natural sales resistance to Christian and Islam proselytizing.
That disputatious, confrontational conversational style has served them in business. If you have ever seen a Jewish scrap dealer buy or sell a load of scrap, you know what I mean.
I can't help but wonder if this is what all the (sob) Holocaust is all about. Jews with this syndrome are the likely propagandists of the Holocaust, or so it would seem to me.
Do a search of Asperger's Syndrome, and notice the interesting hits you come up with.
2002-12-20 21:42 | User Profile
[url=http://www.jerrypournelle.com/reports/cochran/overclocking.html]This article[/url] by science writer Gregory Cochrane suggests certain neurological disorders found among Ashkenazi Jews are a result of selection for high intelligence. This supports Kevin MacDonald's theory, found in Culture of Critique and other books.
Overclocking
Gregory Cochran
There is a good chance that an odd cluster of hereditary neurological diseases among the Ashkenazi Jews is a side-effect of strong selection for increased intelligence. The idea is not really new, but the evidence has gotten stronger with time, and I have recently found some intriguing supporting data.. Four of these syndromes - Tay-Sachs, Niemann-Pick, Gaucher's, and mucolipidosis type IV - are recessive lysosomal storage diseases. The first three of these are caused by deficient variants of enzymes that break down sphingolipids, which play a role in neuron membrane structure and also as signaling molecules. Homozygotes, who have no working copy of the breakdown enzymes, become ill. Tay-Sachs and Niemann-Pick cause retardation and death in childhood, but Gaucher's disease is milder and more variable. The form common in Ashkenazi Jews does not cause brain damage, although there can be other problems with the spleen and bones. . Mucolipidosis type IV probably involves a defect in endocytosis. It causes retardation and death in early life.
Canavan disease is caused by mutations in the aspartoacylase gene. It is the only known genetic disorder caused by a defect in the metabolism of a small metabolite, N-acetyl-L-aspartic acid, synthesized exclusively in the brain in a cell-specific manner. It too is fatal in early life.
Familial dysautonomia is a recessive disease that results in abnormalities of the sensory and autonomic nervous systems. It does not cause retardation, but greatly shortens life.
Torsion dystonia is caused by a dominant gene with low penetrance.. The symptoms involve inappropriate contractions of muscles. In a mild case, that might mean a tendency to writer's cramp: in a severe case, it means uncontrollable contractions that leave your limbs twisted and useless. About 30% of the individuals with this gene have some noticeable symptoms, about 10% have very serious symptoms that can leave them in a wheel chair. The problem is not in the muscles, but in areas of the brain that control muscles. Torsion dystonia does not cause retardation... not hardly.
Each of these hereditary neurological diseases is more common among the Ashkenazi than in any other group, and in several of these syndromes, the great majority of all cases are found among the Ashkenazi, who make up less than 0.2% of the human race. ~4% of the Ashkenazi are carriers for Tay-Sachs, about 1% are carriers for Niemann-Pick, ~5% carry a Gaucher mutation, ~1% carry a mutation for mucolipidosis type IV, ~2% carry a Canavan mutation, ~3% carry the familial dysautonomia gene, and about 0.03% have the dominant torsion dystonia mutation. Altogether about 16% of Ashkenazi Jews carry one of these mutations.
Rare genetic diseases can become common in a group by chance, especially if that group does not mix much with others and if it has recently expanded from a small founding population.. Both of those conditions existed among the Ashkenazi, but that explanation probably does not work in this case, because for most of these diseases, more than one mutation of the same gene has become common in this population. That is the case for Tay-Sachs, Niemann-Pick, Gaucher's disease, mucolipidosis type IV, and Canavan disease. Only torsion dystonia and familial dysautonomia are caused by lone mutations. It would be incredibly unlikely for chance to greatly elevate the frequency of two or more mutations of the same gene. It would be even less likely to do this repeatedly in genes involved in closely related metabolic pathways. So somehow, natural selection, rather than chance, must have favored these mutations. If mutations that affect a particular organ or function give a reproductive edge in some environment, they can become common, even if they cause disease in double dose. The most famous example of this is the sickle cell mutation, which gives heterozygotes good protection against falciparum malaria and causes very serious problems in homozygotes. We know of a number of other malaria-protective mutations besides sickle-cell affecting red cells; Hemoglobin C, Hemoglobin E, G6PD deficiency, alpha- and beta- thalassemia, and Melanesian ovalocytosis. The malaria resistance mutations involve multiple common mutations of the same gene, and multiple mutations of closely related genes that affect the same physiological system - in this case the red cell. Among the Ashkenazi we find the same pattern, only the system affected is the central nervous system. Jared Diamond and others have suggested that these Ashkenazi hereditary neurological diseases might have given protection against tuberculosis, but this seems unlikely. These mutations are not common in other adjacent ethnic groups, and they modify molecules whose primary function is in the central nervous system. In some cases, such as Canavan disease, they are only found in the brain.
So a change in brain function, as the source of the fitness advantage in heterozygotes carrying these mutations, is the way to bet. That notion is not just based on this genetic and biochemical evidence: we start out already knowing that Ashkenazi Jews have a higher average IQ than any other group, something like 110-115. What, other than natural selection, could cause this? We also know that for a long time they lived under very unusual conditions, conditions very favorable to this kind of evolutionary change. They had a very different job mix from their neighbors: none of them were farmers ('Scribe, banker, jeweler, shopkeeper'), and they almost never intermarried.
Some new evidence - new to me, anyhow - strengthens the case. It turns out that GM2-ganglioside, which accumulates in Tay-Sachs and Niemann-Pick patients, is a signal for dendrite growth. In homozygotes it causes inappropriate dendrite growth neurons. In heterozygotes, GM2-ganglioside levels would only be slightly elevated and might favor moderately increased dendrite growth - which might increase IQ. The build-up product in Gaucher's disease seems to caused increased axonal growth.
The story in torsion dystonia is more obvious Unlike most genetic diseases, it is dominant. You only need one copy of the mutant gene to have problems. That also means that any benefit must be large. When a recessive mutation is rare, there are many more carriers than homozygotes, and even a small advantage among heterozygotes can balance serious bad effects in the rare homozygtes. A dominant has to give a hefty advantage, even more so if it has any costs, which the torsion dystonia gene surely does. So if torsion dystonia is part of this Ashkenazi pattern of hereditary neurological disease and pays off in IQ, it must make a big difference, and that difference will probably show up in patients. ( Note that in diseases like Tay-Sachs, nobody even studies carriers. Doctors are not geneticists.) Apparently it does. I found several reports of materially increased IQ among Ashkenazi torsion dystonia patients. . The difference is apparently so striking that it is mentioned in the very first scientific article on the disease, by Flatau back in 1911. Many other physicians made the same observation. And if you think that plenty that being crippled makes you smarter, think again: nobody every said that about polio victims. Roswell Eldridge, in a small group of patients, found that the average IQ was 122, 10 points higher than their controls matched for age, sex, ethnic background, and school. . The same mutation has been seen elsewhere, but is very rare. In this group the payoff outweighed the trouble, while in every other human group it did not. We have found the gene (in 1997), which codes for an ATP-binding protein, but as yet I don't believe that we know exactly how it causes trouble or what it does normally. But I'll hazard a guess: the change accelerates some brain system tied to cognitive functioning - nearly redlines it, leaves it vulnerable to common insults in a way that can cause spectacular trouble. You might compare to overclocking a chip. Sometimes you get away with it, sometimes you don't.
More generally, if this is what I think it is, all these Ashkenazi neurological diseases are hints of ways in which one could supercharge intelligence. One, by increasing dendrite growth: two, by fooling with myelin: three, something else, whatever is happening in torsion dystonia. In some cases the difference is probably an aspect of development, not something you can turn on and off. In other cases, the effect might exist when the chemical influence is acting and disappear when the influence does. In either case, it seems likely that we could - if we wanted to - developed pharmaceutical agents that had similar effects. The first kind, those affecting development, would be something that might have to be administered early in life, maybe before birth. while the second kind would be 'smart pills' that one could pop as desired or as needed. Of course, we have to hope that we can find ways of improving safety. Would you take a pill that increased your IQ by 10 or 15 points that also had a 10% chance of putting you in a wheel chair?
Gregory Cochran
2002-12-20 22:50 | User Profile
Good stuff.
This also raises another issue: "Brainwork" has occupational disorders just like any other kind of work. Shovel enough coal and your back goes out; breathe it in and you get black lung. If you cogitate for a living, your head will give you problems too.
Since the shift from largely physical work to largely intellectual work the number of mental and neurological ailments have increased exponentially. This surprises people. Why?