Ah, I see your point. I guess my ( perhaps weasley sounding ) answer is that it is a question of scale.
Ashkenazic Jews, French-Canadians, Cajuns, ( and to a much lesser extent, the Irish ) all seem to have increased prevalence of the Tay-Sachs gene. Askenazic Jews et al may have a roughly 1/27 chance of carrying the gene for Tay-Sachs vs. roughly 1/250 in all other populations, black and white. So I have no problem separating them out in that respect. But those at an increased risk for carrying that gene represent a very small proportion of the greater white population. So if you average them into that larger population you might end up with a frequency of carriers of Tay-Sachs among whites of, say, 1/249.5 vs. 1/250 for blacks ( obviously I am pulling that average out of thin air ), which to my mind is scarcely significant enough to be worth mentioning. I think it is much more informative to say that “Ashkenazic Jews et al have a significantly higher incidence of Tay-Sachs disease compared to all other groups”, as opposed to saying “whites have a very slightly higher incidence of Tay-Sachs disease compared to all other groups”.
This is a bit confusing here - I’m unsure of the true facts. Tom seemed to be saying that TS might be nonexistent among Black people - you are saying that there is some amount prevalent. This new standard that you propose is highly subjective, but I would agree that a difference of 1 in 249.5 to 1 in 250 is not significant. But a difference between 0 and 1 in 100,000 is (for purposes of categorizing, if nothing else). (I would also point out that the fact that an alternative statement might be more informative does not make a statement meaningless).
And you would presumably agree that it is a valid statement to say that “Blacks in the US have a significantly higher incidence of Sickle-Cell anemia than do Whites”. (Your colleague tomndebb took strong exception to such a statement in a previous thread.)
(In any event, I hope it is clear that this issue - what is or is not a meaningful fact or grouping - is independent of the previous issues that I’ve been discussing, i.e. whether this lack of significance can be used to imply facts.)
Izzy: Well, souces ( like this one: http://www.tay-sachs.org/whatista.htm ), cite 1/27 ( 1/30 or some variant thereof ) for certain populations like those we’ve discussed and 1/250 ( or 1/300 or some variant thereof ) for “the general population”, with no specification as to “race”. Other sources mention all the groups I listed, plus “other populations around the world” ( http://www.ncbi.nlm.nih.gov/disease/Tay_Sachs.html ).
Still others I’ve seen have made the point that the genetic weakness that causes Tay-Sachs is the result of a “common mutation”. This site would seem to bear this out ( notice the multiplicity of populations showing mutations of all different sorts on the HexA gene ): http://life2.tau.ac.il/GeneDis/Tables/Tay_Sachs/tay_sachs.html
Oh and uhh…I’m not completely qualified to explain that chart ;).
But anyway here is few reference titles from that last cite:
** A novel mutation in the invariant AG of the acceptor splice site of intron 4 of the beta-hexosaminidase alpha-subunit gene in two unrelated American black GM2-gangliosidosis (Tay-Sachs disease) patients. ** The major mutation among Japanese patients with infantile Tay-Sachs disease: a G-to-T transversion at the acceptor site of intron 5 of the beta-hexosaminidase alpha gene. Novel Tay-Sachs disease mutations from China.
So I’m assuming when they say the “general population”, they are in fact referring to everybody else, caucasian and non-caucasians alike.
I probably wouldn’t object to that particular statement, you’re correct. It may be that tomndeb and I would disagree on that point ( at least we are not completely in lockstep ). I might object if you made that phrase completely universal, since there are some Mediterranean populations with a reasonably high rate of carrying the Sickle-cell gene. But as you phrased it, I’d probably be okay with it.
Just as an aside, I’ve noticed that some of these Tay-Sachs sites have noted that Ashkenazic Jews used to be considered “non-white”. Curious factoid ( not necessarily relevant to anything, mind you, I just found it interesting ).
Completely off topic: what would account for a genetic disease being prevalent in Ashkenazic Jews, French Canadians & Cajuns, and Irish - three populations that presumably have had nothing to do with each other and have little in common?
Well, except that the AJ population has a high genetic coherence. They are a population about which some genetic observations may be made: http://www.csulb.edu/~kmacd/genetics.htm
[quote]
[ul][li]At least 1 in 30 Jews of central and eastern European descent carry the TS gene, meaning that 1 in 900 Jewish couples could have a baby with Tay-Sachs Disease. [/li][li]There is a genetic isolate of French Canadians in Eastern Quebec which also has a high TS frequency. [/li][li]Among the rest of the population, only 1 in 300 people have the TS gene.[/ul][/li][/quote]
I do not know the prevalence or absence of Tay-Sachs among blacks (hence the “(as much as 100%?)” question). The sites I have found simply refer to “general population.” However, the other population of high-incidence, the group among the French Canadians, is also identifiable as white–as well as being a recognizable “genetic isolate.”
I wonder what the context was if I said that. I certainly do recognize that the incidence of Sickle-Cell among blacks is higher than among whites in the U.S. What I do recall pointing out was that assuming Sickle-Cell if the patient was black or ignoring the possibility if the patient was white would lead to a greater number of missed diagnoses (particularly if the patient was an immigrant from regions in Africa where Sickle-Cell was not endemic or if the patient was from southern Italy or Greece). Outside of desperate triage, I prefer that doctors use tests rather than preconceptions.
Perhaps so, but subsceptibility to Tay-Sachs would not be one of them, as noted.
No need to wonder - you could revisit the Genital thread, where your initial foray into the thread and subsequent discussion concerned this issue. But - being the nice guy that I am - I shall provide you with a helpful link to the tail end of the discussion where your views were brought into sharper focus. Essentially, you regarded the above statement as a meaningless one and not worthy of being considered a “Truth” etc. etc.
Well, here is the most common hypothesis for it’s prevalence in Ashkenazic Jews:
*Scientists believe that certain disorders became more common among Ashkenazi Jews because of at least two processes: the “founder effect” and “genetic drift.”
The “founder effect” refers to the chance presence of these genes among the “founders” or ancestors who emigrated to eastern Europe at the time of the Diaspora (70 A.D.). Prior to this time we presume that these disorders were no more common among Jews than among any other people.
“Genetic drift” refers to the increase in frequency of the genes for these disorders in this group, as a result of chance. Because Jews tend to not marry outside of their faith and community, the relatively high frequency of these genes among Jews did not pass into other communities, nor were their effects diluted by the introduction of other genes from outside the Ashkenazi Jewish community.*
I imagine we can posit a similar situation for the Cajuns and French-Canadiens ( linguistic and cultural barriers, plus even more intense political barriers at times, in a sea of English-speakers ) and to a lesser extent Ireland ( isolated island, with real barriers between the Irish peasantry and the more urban and/or concentrated English plantation settlers ). Since it is apparently a common enough mutation ( in a very relative sense ), we aren’t necessarily seeing related groups, just different groups that have independently developed the mutation ( or some variant ) and propagated it mostly within a single population. As some of these groups become more and more dilute ( like the Cajuns for example ), I would expect the rates to recede. Either that has already started happening with the Irish ( and maybe that mutation was orignally confined to one isolated branch of the Irish, or the greatly reduced survivors of the potato famine that remained behind in Ireland ) or they were never as strictly inbreeding as the others.
Just an educated guess.
I’ll also note ( though I may have mentioned it before ) that the Founder Effect is also one of the leading hypotheses as to why humans are so genetically uniform compared to our nearest relatives.
To the first point I made in the preceding post I should also add that non-Ashkenazic Jews are apparently included in the group described above with the “high genetic coherence”, and they are not more subsceptable to TS than the general population.
However, your statement to Tamerlane specifically changes what I actually said.
In the initial thread, you had (in the context of race) correlated Sickle-Cell and blacks. I pointed out that this could cause diagnostic errors because Sickle-Cell did not correlate to blacks, but to specific populations within both the perceived black and perceived white populations.
Later in the discussion, I specifically noted that one could get a correlation by including other categories of definition, such as those whose ancestors were imported to the U.S. In other words, I specifically noted that blacks in the U.S. did have a higher incidence–the reverse of what you posted, above.
I’m sorry, but I did not change anything that you said. To refresh your memory here, Tamerlane was taking the position that the statement about Whites and TS was not valid because it was not terribly meaningful etc. However, he later qualified that this was because the actual difference between the two groups (i.e. Whites and non-Whites) was very small in this regard. To which I noted that this would not apply to SSA, so that such a statement would be valid, meaning - in context - more meaningful there. This was not your position in the linked thread, in which you argued long and hard that the statement about SSA was also not meaningful, similar to what is being claimed here about TS.
IOW, you would claim - or at least have claimed - you may change your mind - that the statement about SSA is meaningless, as is your position regarding the parallel statement about TS. Someone who considered the about TS statement meaningless only because of the small difference (e.g. Tamerlane) would not take this same position with regards to SSA.
In sum: you seem to be assuming (for whatever reason) that I have claimed that your position is that Blacks in the US are not more likely to have SSA than Whites in the US. I have made no such claim - rather, I’ve said that you consider this fact to be a meaningless factoid, which are your words in the linked thread.
While on the topic, how would you answer the question above about the comparison between an AJ who does not have the TS gene and a non-AJ?
Sorry, it now occurs to me that you actually have adressed this issue, and that I’ve made two counterpoints. (Strange mental block - to have forgotten all that). As we left off, it seems that your position is that AJ’s are a coherent genetic group, and my position is that they are not coherent with regards to TS, and probably not at all (as other Jewish groups are among the population you linked to). While on the subject, are Cajuns and French Canadians a coherent genetic group? Irish?
In the thread in question, I never challenged the notion that “Blacks in the US have a significantly higher incidence of Sickle-Cell anemia than do Whites.” Following your initial example of a doctor in the U.S. using perceived race to indicate a direction for examination (11-26-2001 07:54 PM), I pointed out (11-27-2001 07:56 PM) that using a perception that blacks corresponded to Sickle-Cell could lead to bad diagnoses and indicated that using blood work was a better test. In your post of 11-28-2001 10:55 AM you appeared (to me as I read it at the time) to broaden the categories to race, again, irrespective of the association of the specific population of the U.S. On11-28-2001 11:59 AM I posted what is, in hindsight, an opening round in this discussion, distinguishing between saying that “blacks” or “whites” are susceptible to a disease from noting that specific populations within the generally vague categories of “black” and “white” may be so susceptible. On 11-28-2001 12:39 PM I explicitly noted that by qualifying the terms to limit the discussion to blacks in the U.S. one could arrive at a correlation. Your comment to Tamerlane that I took exception to the statement regarding “blacks in the U.S.” is a reversal of my specific position–although it looks more as though we are talking across each other, again, than that we are misquoting each other.
AJs are a recognizably coherent group:
A signature significantly different from the surrounding peoples in NorthEast Europe with an apparent founder effect in Rome indicates a fair pattern of coherence. That Tay-Sachs is not part of what identifies that group does not change the fact that the group is coherent.
The French-Canadians that are subject to Tay-Sachs are (as indicated by the link and quote I provided) “a genetic isolate of French Canadians in Eastern Quebec”. I do not yet have any information of the Cajuns. As for the Irish, I had never heard that there was any prevalence before Tamerlane’s post.
Are you now taking the position that while we can define “blacks” irrespective of genetic coherence, we have to limit ourselves to “carriers” in order to identify groups among whom there is a higher incidence of susceptibility?
I do feel that you are way understating my contribution to these debates. grienspace’s later arguments applied the possibility of greater genetic diversity of Africans(unless someone before I joined the SDMB brought it up) to explain the phenomenon of both East African dominance in long distance running andWest African dominance in short distance running and associated sports like soccer and basketball. Once again we are talking about a very limited number of elite athletes, and Edwino while not endorsing my position has articulated it in better fashion with statistical jargon. E.g. “outliers”
The challenge to the East African/Kenyan/Eldoret genetic hypothesis has been environmental and cultural. Of course this dominance does not occur in other highland regions of the globe. No evidence here, merely circumstantial suppositionIt appears that some of the “esteemed” race debaters here however are keeping an open mind.
The West African genetic hypothesis was challenged on several fronts. It was said that West Africans haven’y shown superiority in sports. Well what about little Senegal ( population approx 8 million. They, and Camaroon (population approx 11 million) as well as Nigeria have quickly become soccer powerhouses on the world stage providing star talent for the European leagues. It was said that there is a lot of Amerindian genes in American blacks, so why couldn’t the superior geneitic contribution come from there instead of WEst Africa. Only if you could point to me one non-black Amerindian running under 10 seconds or starring in the NBA, then you might have a point. It was said that a number of American blacks were brought over from south and east of the Cameroon highlands and not from West Africa. Exactly what that percentage is, no one knows, but it is not that significant, and if it was, we would just have to expand the genetic pool in Africa that provides for elite athletes. Furthermore, it was also challenged that admixture of “races” should dilute any genetic advantage amonst African Americans, ignoring the fact that we are only talking about several hundered athletes maybe from a pool of African Americans say 40 million or so.
So what is this real evidence arguing against my position?
Apologies grienspace, I brought up your ( or Entine’s if you prefer ) argument to illustrate a minor point, but I’d rather not reargue this particular case again. Based on the evidence you think a genetic correlation/component is strongly indicated. Based on the evidence I am undecided but leaning against, partly for the reasons cited above by you ( as well as others, like the multiplicity of environments in that huge chunk of territory we call West Africa, which presumably wouldn’t select for across the board genetic similarities ). IMO it justs seem to be less likely it is the case. Some day in the future when better physiological and genetic data comes in, I may change my tune.
But I’d rather not go another ten rounds on the why I believe that. I cede the floor to your greater endurance ( genetic or otherwise ).
It’s not dishonest, since you yourself would presumably agree that the answer is “technically” yes. In any event, “no” is a much more misleading answer, since it implies that the disparity is caused by non-genetic factors.
Further, I notice that you didn’t respond to my last point in the paragraph, that “if you claimed that the question is meaningless, it obscures the reality of the situation.”
Nor did you respond to my first point, that even if we accept that a genetic advantage is “meaningless,” this does not give rise to an inference that cultural/sociological explanations account for the observed disparity in elite short-distance running.
Why won’t you concede this obvious point?
**
I’ll be happy to oblige, AFTER you have stated your position on the subject.
So is it your position that any generalization which applies to less than 0.01% of the group in question is “utterly meaningless”?
And you still haven’t defended this statement:
Why won’t you admit that I never said anything like this?
I’m not sure why you keep changing the terms I used to ask you the question. But I’ll assume that by “average genetic difference,” you mean the same thing as the “genetic advantage” I had referenced earlier.
So you are saying that G.A. does not imply E.R. That’s fine.
The consequences of this statement are simple. If somebody asks whether G.A. exists, then, as far as you’re concerned that fact (?) that race does not exist is irrelevant.
Apologies. I was thinking of something else, but hopefully my comments below will clarify.
Depends how you phrase it.
The only statement I would categorily object to is some variant of “Blacks perform better at elite athletic levels because of a genetic advantage.” What’s my objection ( aside from the fact that it is so far unproven )?
1.) It implies universality - i.e. All blacks have a inborn potential superiority in this regard compared to all other groups. Modern population genetics suggest that this is extremely unlikely.
2.) It implies the existence of the classical biological race category based on observed skin color, a concept that has been shown to scientifically bankrupt in most respects.
These implications I consider misleading. Now you may disagree that such a statement implies any such thing, but that’s just my own take on it.
That’s it. I don’t object to the possibility of some population, somewhere, having your GA, especially in the very limited terms that it has been cast in this thread ( i.e. elite performance by a tiny percentage of athletes ). I’m a little sceptical that such can be demonstrated and the larger the group the less likely I am to think it is possible, but I’m not completely closed to the idea.
Race only enters it ( for me ) when broad, unqualified statements like the one I quotated above get thrown around.
Now, wouldn’t we all rather move on to the question of whether the sublimated sexual tension between Yasser Arafat and Ariel Sharon is behind some of the current unpleasantness in the Middle East? No :)? Ah, well.
Sorry to have made you do all that coding - I don’t see anything in your summation of your views that I dispute - or have ever disputed. Again, you have never denied that US Blacks, as a group, have a higher incidence of SSA than US Whites. However, you consider this to be a “meaningless factoid”. Others (apparently including Tamerlane - hence my comments in this thread) may consider it to be a more significant fact.
It would appear that you are correct that the Ashkenazi population is genetically distinct from the other Jewish populations. But I’m still not convinced of the significance of this. If, as Tamerlane suggests, the prevalence of TS in this population is due to a founder effect and genetic drift, it would seem to be completely unconnected to any genetic coherence that they might have. (IOW, even if the group shares some genetic signature, this has nothing to do with the prevalence of TS, which is purely random). But I can understand your position here, and I don’t anticipate arguing this further.
Of course not - that would be quite a contradiction. Personally I think you can ascribe characteristics to any group that is defined in any way at all. My point about carriers was directed at those who would deny this.
Well, I believe I referred to “A small average genetic advantage in short-distance running, whether possessed by blacks in general, or by a sub-group of blacks”
I take it you agree that your “no race” position doesn’t rule this out.
). I might object if you made that phrase completely universal, since there are some Mediterranean populations with a reasonably high rate of carrying the Sickle-cell gene. But as you phrased it, I’d probably be okay with it.
).