? !
Where did I say or imply Tiger is black, or has most of his genes from recent sub-saharan ancestry? I am a golfer and I know what Tiger Woods’ claimed heritage is.
The point I made is that no amount of nurture does anything beyond develop a genetically-determined maximum potential. No amount of nurturing will turn my golf performance into the equivalent of Tiger Woods because I do not have the genes for it.
We are not equal blank slates. We cannot create Einsteins out of kids with Downs–we cannot even create them out of the vast majority of ordinary people. Most of us do not have the genes for it.
The point of view I’ve come around to is how stupid it is to pretend we are all genetically equivalent blank slates at birth, and how stupid it is to pretend that even though SIRE groups are obviously different for some gene prevalences (for, example, genes controlling phenotypic appearance or disease states) they can’t possibly be different for genes controlling intelligence or physical skills.
Why should only certain gene prevalences vary among SIRE groups? And where is the evidence that any given group can be nurtured to the performance potential of any other? Where’s the evidence that US caucasians can be nurtured to perform equally at basketball? When the NBA was opened up to all comers, the caucasian representation from all but a small subset of Europeans just magically went away. Did the Eurasians become lazy? Lose their previous interest in fame and fortune? Become suddenly disadvantaged for coaching or opportunity?
I don’t think so, and on this board I posted the original link to BGI.
It’s a complete confusion of the key issue to continue to throw out the fact that any given group is “genetically diverse.” That’s the straw man my opponents here cannot get past. Genetic diversity of a given group has absolutely nothing to do with whether or not a group has a greater prevalence of the geneset which codes for a particular skillset.
That’s the thing that makes a difference in outcomes for what you are measuring.
Let me give a common example: Suppose I was studying a group of very tall people versus a group of very short people. I normalize for factors like nutrition and so on, and I come to the conclusion that the tall people have a genetic predisposition to be tall while the short people have a genetic predisposition to be short. Now those two cohorts may be otherwise incredibly diverse genetically. But what makes a difference for “tallness” in the two groups is still the geneset for height.
The remainder of their genetic diversity is irrelevant with respect to the prevalence of tallness being genetically determined.
As various populations have wandered around the earth, they’ve picked up differing genesets, and exhibit different prevalences of those genesets. That’s why it’s easier to find a fine-haired blonde pale-skinned person in Europe than in sub-saharan Africa. It wouldn’t matter if, as a group, the sub-saharans were much more diverse. It’s completely irrelevant. What would matter, if we were focusing on the fair-skinned phenotype, is the geneset for that particular trait.
If we find what BGI is looking for–evidence for the geneset(s) for intelligence–then that will precipitate a “genetic crisis” for the egalitarians who continue to hope that all groups exhibit more or less the same prevalence for the genesets which confer intelligence potential. What we are going to find (I believe) is that no geneset has equal prevalence across any two populations–even groups considered by egalitarians to be “purely cultural.” They aren’t purely cultural. They may be internally diverse genetically. They may be admixed to various degrees. But–as a group–they will exhibit varying prevalences for genesets which code for maximum potential for almost any particular skillset observed to be different between the groups. And as we define which genesets we need to have to be maximally fast or maximally strong or maximally bright, we are going to find those prevalences differ among groups that are otherwise very diverse.
It’s a fairly obvious point: if you don’t study the actual genetics of a group, you can’t make useful generalizations about that group’s genetics. So, the study of IQ genetics in China is interesting, but it can’t settle the issue at hand.
More significant is the fact that you and your fellow travelers have never been able to provide a scientific definition of what a race is, and a definition of what black Americans are in particular. Socio-political definitions, which are the ones that apply to black Americans, don’t count in scientific arguments. That’s why you fail at the outset, and everything that follows is imaginary fruit from this non-existent tree.
Again, to state the obvious, it most certainly does matter that a given group is highly mixed with the group that it’s compared to, and derives its gene pool from a wide variety of sources. Any claims based in genetics have to take this into account. You can’t just say it doesn’t matter because it makes your desired conclusion too hard to achieve.
You’ve also repeatedly made the argument that the same problems are observed for “blacks” the world over.
We know for a fact that the diverse peoples you refer to as blacks have different, widely varying gene pools. We also know that many of these “blacks”, Brazilians for example, aren’t even of majority African ancestry - because phenotype has decoupled from genotype due to extensive mixing.
“They look black to me” is really not enough to base a scientific argument on.
No one here is a genetic egalitarian. Everyone acknowledges that smart parents tend to have smart children.
When you try to make arguments based on race, without any solid definition of what race is, you fail.
Perhaps we have found something upon which we can agree, then: the group that is Self-Identified as “black” is a very loose-knit group, and very diverse genetically.
I’ve never argued anything differently. What I’ve argued is that it is a strawman to pretend that I consider that point to be central to the argument of whether or not group average differences–even where the groups are self-described–can have genetics as the basis of their differences. They can.
Suppose that the Math Club underperforms the Basketball Team at basketball no matter what nurturing you give them to be the best at basketball. Their underperformance is a result of the fact that their gene pool does not give them the same maximum potential for that skillset, and the same might hold true if the Basketball Team were given the same nurturing to perform maximally at quantitative academic disciplines. The individual genetic diversity is irrelevant. It would not be a counter-argument to sputter that one group or the other is “more genetically diverse.” The question is: is the geneset for the skillset more prevalent in one versus the other group? That’s the only question.
It is absolutely clear that genesets for a wide assortment of things including phenotypic appearance vary by self-identified race/ethnicity. It is absolutely clear if one looks at the evolution and dispersion of broad populations that there are good historic reasons for this, along with a generous admixture. I would wager Cecil’s salary I have fewer markers for recent sub-saharan ancestry genes than the typical black sub-saharan. There is, therefore, ample proof to say that all groups do not all have exactly equal access to exactly the same library of genes.
It doesn’t matter that there is not “a” marker for “a” race. It doesn’t even matter if race is “purely cultural” in terms of who associates with which “race.” It is a much better concept to talk about “population” and it is a much more accurate concept to look at individuals to see from which of the major population group genetic libraries they draw their own specific genes. But nevertheless, even at a self-described “race” level, the library of genes is different for blacks, whites and asians (as examples of the broadest categories) and because that base library is different, the average maximum potential for all sorts of things will be different. It doesn’t matter how much genetic diversity those groups have within or among them. What matters for any particular skillset is which of those groups has a higher prevalence of the most advantageous geneset coding for that particular skill.
This is incorrect. Suppose that genetic Group A has a 25% prevalence of a very advantageous geneset. Suppose that genetic Group B has 0% prevalence for that or any equivalent geneset. For the sake of the point, let’s make these completely separate populations.
Now we add in admixture and get genetic Group C. Genetic Group C gets about half its library of genes from each group. Group C self-identifies culturally/socially with Group A.
What would you expect the performance of Group A to be now? Well, on average it will be better (for that skillset) than the original Group A population and it will be less than Group B. And there will be a much larger subset of self-described (self-lumping) Group A’s who perform on par with Group B, since their genetic library is significantly expanded to include the advantageous genes from Group B.
“Race” is an argument about lumpers versus splitters, and I don’t like it. I don’t like it as a category and I don’t even believe it fundamentally drives culture. What drives culture is genetic similarity. I am far more culturally close with my highly-educated black colleagues who live in my world than I am from the white shrimper who had trouble finishing high school and whose world is completely different from mine. None of that has much to do with the fact that, if you decide to lump by self-described "race, then you find that the average differences are substantially determined by differences in gene prevalences. Smart parents do, indeed, have smart children (although all outliers regress to the mean of their population pool), and Erkel probably isn’t going to sire the next Kobe.
By the time the Math team is the Math team, and assuming the Math team avoids Basketball, years of Basketball nurturing has been lost. If the people who were to become the Math team were trained to be the Basketball team then they would probably be just as good as the Basketball team. Of course you say its the genes! In your world of cartoon, science-fiction-based genetics it’s always the genes despite anything anyone says, because you are so desperate for it to be true that there is a genetic basis to the differences in America between blacks and whites.
Please give an example of any trait that covaries with the appearance characteristics you are discussing.
What exactly are markers and what do they specifically do? Why might these markers change at a relatively rapid rate while other characteristics of the genome are conserved?
Actually I am going to answer that second question above because your misunderstanding of the issue seems to be the basis for your entire world view. Genetic markers, such as single nucleotide polymorphisms, restriction fragment length polymorphisms, and microsatellite markers vary quite a bit and are able to do so because, as a general rule, they are not causing significant changes in genes or their regulation.
The parts of the genome that are most important for regulating gene expression and the parts that actually are the code for a protein are very well conserved. It makes sense that they are conserved because it would be to the detriment of the organism if too many changes occur in the protein coding regions of the genome. Even when there are changes to the coding region or regulatory region of genes the sequence differences do not lead to changes to the amino acid sequence of the gene in the former case nor alterations to the transcription factor binding sites in the latter case.
The markers that you are talking about are indicators of populations because they vary without causing major changes in genes or their regulation and the people who hump together tend to share them. Historically, our mating behavior was isolated to those near us. The best demonstration of this is the study where markers could be used to predict what village people come from in parts of Europe.
On the other hand the genes (I am going to stop saying ‘and their regulatory regions’) themselves do not change nearly as rapidly or at all. One great demonstration of this is in comparing across species. You would expect genes might vary far more between species than within species so what I am about to say is an exaggeration of what we would see within the human species. What I have seen from practice is that although the places outside of genes are incomparable among species, the coding regions are almost identical. I used to use clustalw and the NCBI sequences of genes for many species to find regulatory regions of genes. The idea is that regulatory regions would be conserved because they are just as important for the integrity of the organism as the coding region themselves and as long as the function of the gene is the same across species (for example a neurotransmitter receptor important in regulating reward would perform the same job in the brain of a rat, human, kitten, etc.) all these genetic elements would be conserved. Importantly, when these sequences are lined up based on syntenic regions of varying species genomes the output shows near identity in the exons of genes and in the regulatory sequences. Other regions, especially the non-regulatory parts of introns varied tremendously. It is in these relatively unimportant regions where the markers tend to come from.
(Look, go download clustalw and get familiar with the NCBI sequences of genes and do this yourself. I figured it out and since, from what I gather in your other posts, you are or were a MD and are richer than me you must be genetically superior to me.)
The reason why we see so many differences in phenotypes related to outward appearance is because of the sexually and naturally selective advantages of these traits. Darker and lighter skin has appeared all over in the human species because the advantages of these traits in dealing with the immediate environment. My guess is that most of these changes occur in the regulatory regions of these genes that control skin color because the genes’ functions are too important to alter.
Let me just cut through the chase of your various strawman arguments regarding how one genetically defines race and ask you if you think there are gene prevalence differences within Self-Identified Race/Ethnicity groups.
As an example, suppose I took SIRE whites and SIRE blacks in the US. Would I observe a gene prevalence difference for the gene coding for Hemoglobin S?
If so, then I argue all of your insistence that there need be a purity of category is a strawman. If there is a difference for that gene prevalence, there is obviously some sort of difference in the genetic pool from which those two SIRE groups are drawing their genes.
If such a difference exists for that particular gene, there is no basis to argue that there cannot be differences for other genes. Your snide remarks relating to my training and wealth are the sort of distracting trivia that do not add to the discussion and make me think you simply think slinging around unrelated items will somehow confuse a very basic question enough to make some sort of real point.
I ask you the same question I asked Orcenio:
Do we have good evidence that gene prevalences vary by SIRE groups? Focus, please.
Of course there are “gene prevalence differences” between blacks and whites. Of course when you limit the discussion to blacks and whites in the US you get a difference in the prevalence oh Hemoglobin S. Hemoglobin S, like skin color, can be shown to have a selective advantage under particular environments. Of course these patterns do not hold true for subpopulations in Africa and these subpopulations can best be demarcated by malaria and no other characteristic. This pattern does not necessarily hold up when comparing various worldwide populations of people we would say are white to people we would say are black. Once again these patterns can best be described by the prevalence of malaria.
It is interesting how you go from talking about a disease and then ignoring disease dependent upon whether it seems to benefit your argument. You ignore the results of studies on the genetics (and environment) of common mental disorders but suddenly run to it for your single-gene-trait-with-a-well-known-selective-advantage-under-particular-conditions because you think it proves your point. Cystic fibrosis is an example of disease associated more with whites than blacks in the US. It does not have a selective advantage that is know or that I am aware of. It is also a single gene disorder. See? Now you can bring that up whenever you like.
These examples have key features which are not at all useful in understanding whether the group differences in your favorite tests have a genetic basis. First, intelligence itself is not a disease and the differences in IQ is not a sign of mental illness. Second, no genetic analysis on the inheritance of intelligence in man or animal supports the notion that differences in cognitive abilities are determined by single-genes of major effect. Despite the paranoia that genetic analysis of intelligence is forbidden among PC-liberal-ivory-tower-right-wing-stereotypes, there are plenty of studies on the subject. Third, if your theory on the origin of IQ differences between blacks and whites and it isn’t a sign of rampant disease among blacks, then what was the selective advantage that only affected everyone who left Africa? Fourth, few environmental modifiers affect the outcomes of these diseases. These aren’t PKU where diet will prevent the symptoms. CF can only be treated by medicines in the environment and they are not of permanent benefit. Performance on tests of intelligence on the other hand is demonstrably affected by nutrition, parenting, environmental toxins, intrinsic motivators, language, and on and on. Your examples are not analogous; they suck.
I was not arguing a strawman earlier. I was remarking on a bit of ignorance you and Chen019 like to spread. It disgusts me that you try to conflate the results of population genetic studies using genetic markers with your rampant speculations on arbitrary group differences between this or that trait. This data has only one specific meaning: people hump those who are closest. The wild speculations that are used beyond this are akin to the worst sci-fi I see involving genetics.
As I said before, I am not above convincing on this subject. The evidence is supportive, or its not, or it does not exist. But I am really bored of discussing your group differences without any context or understanding of how they are related to each other. If you really want to further your cause then why don’t you find the research and educate us on it? Right now, the best you and Chen019 can come up with are variance partitioning studies and you alone can’t even do that. There must be studies on the genetics of sprinting for example. It is far too important a trait for a major segment of society and the social costs of its investigation are far too weak for this work to have been avoided. At this point, your continued abuse of the data is getting boring.
I think you are missing the point about gene prevalences.
One approach to arguing that there are no genetically-based differences between populations (including SIRE groups) is to take a position that populations are so mixed that it makes no sense to separate them other than purely culturally. That is the only point I wish to dissuade you of when talking about gene prevalence differences. Cystic fibrosis, for example, is proof that the US white and black populations draw from different libraries of genes. They are separate gene pools (with a generous admixture for the black SIRE group). They are not purely cultural groups, as is so often argued here. Gene prevalence vary by group because those groups, over time, have genetically separated and not been fully mixed again.
I am frequently surprised that the same folks who can admit that intelligence or athletic ability is inherited, and that gene prevalence varies by SIRE groups, turn right around and argue that races are purely cultural and that therefore there is no basis for thinking performance differences might be genetic in nature. The controversy will probably rage for some time regarding the reason for group performance differences and the persistence of those differences despite efforts to erase nurturing differences. But I see no reason to dismiss a genetic explanation out of hand when it is obvious that different groups draw from different gene libraries.
Didn’t you say I was the one arguing the strawman? Genetically speaking, races do not make sense on a global scale. It will look like races make sense if you take a population from one place and a population from a completely separate place and throw them into a new place - genotypically and phenotypically. Also I wouldn’t be shocked to find that genetically speaking those who claim to be white, despite where they’ve been sampled from historically, are more homogeneous today because of interbreeding and the same would be true among those who identify as black. It further would be totally unsurprising if, due to a lack of interbreeding, there were allele frequency differences between blacks and whites for markers and genes. This is not a point of contention.
You don’t understand what is meant by “intelligence is inherited”. You focus on the genes. We aren’t inbred Mm domesticus in a laboratory. We aren’t strains of bacteria or an agriculturally important plant. We do not simply inherit a proportion of the alleles of genes our parents carry (Also to think that these examples are truly controlling for everything but genes is naive but it’s the best there is for genetic analysis). Here is what we inherit, to the best of my knowledge, beyond our genetic variation (warning: this mixes together nonhuman and human results but is restricted to mammals):
(1) Imprinting of genes - To take the extreme case - our grandparents’ behavior (particularly diet) can alter the imprinting of our genes, which alters their expression levels regardless of your particular version of the gene (this would be restricted to those genes that are imprinted obviously).
(2) Gestation -all manner of our mothers’ behaviors, especially during early development of each of the organs, can permanently alter the development of our brain.
(3) Postnatal development - Despite what Chen019 would have us believe, our mothers, our fathers and the environment they provide can have effects on our personality (some permanent, others probably not - e.g. Attachment Theory) right from birth.
(4) Family development - once again mothers and fathers - the real trick here is that our mothers and fathers often provide environments that correlate well with our genes. So we may have the ‘smart genes’ but also the smart environment.
(5) Culture - humans love separating themselves into groups and thinking less well of the outgroup and feeling better about the ingroup. All the while creating stereotypes on limited information. These are behaviors that are easy to form - the simplest statistically significant manipulation of this kind of behavior is to literally tell a subject “You are in group A and so are these people.”; these behaviors are also difficult to erase. It’s really hard for me to believe that this mechanism alone isn’t the major stakeholder in separating your SIRE groups on a vast number of behaviors.
(6) Environment - as much as you like to pretend we do live in a socially stratified society with a key factor in this stratification being your SIRE groups, it is the case and few argue it. Along with this stratification are huge disparities in the quality of the ecological environment in which we are raised from exposure to toxic chemicals to the food we have available to us.
(7) Imprinting X Gestation X Postnatal Care X Family Environment X Cultural Environment X Ecological Environment interactions. These interactions have barely been touched. We are primitive cave men thinking that a hot Neanderthal chick is “not great, but good enough” in terms of our understanding of these types of interactions and just how much they can alter the trajectory of an individual’s development.
(8) Stuff I haven’t thought of: How about use of steroids among Olympic athletes from one training venue versus another?
Of course there are the genes themselves and how the sequence variation can alter the protein structure or rate of expression of a protein. These are obviously important as demonstrated by Hemoglobin in Sickle Cell Anemia, Cystic Fibrosis Transmembrane Conductance Regulator in Cystic Fibrosis, Methyl CpG Binding Protein 2 in Rett Syndrome, and the list goes on.
Yet as I argued before, these are not great examples except in the sense that two of them show allele frequency differences between SIRE groups. They are single gene disorders meaning that almost the entire phenotypic variation in these traits is due to variation in alleles for one specific gene. The variation in intelligence is not due to alleles of a single gene, it is due to alleles of multiple genes, or that is what the best models tell us. Although I hesitate to compare disorders to normal variation in behavior such as intelligence, the most instructive data that we have comes from understanding the genes involved in the development of complex behavioral disorders such as Schizophrenia and most forms of Autism. No evidence supports a single gene of major effect and there are no genes with universal or near-universal support among all the different laboratories performing similar studies. This points toward genes of relatively minor effect - yet these diseases show huge phenotypic differences between cases and controls! The huge phenotypic differences, in the absence of reliably repeatable genetic association, are probably due to the environment or more importantly due to interactions between developmental susceptibility and the environment. This is known as Diathesis-Stress and along with its cousin Gene X Environment interaction, can do a very good job of explaining differences between cases and controls.
Still this is disease so far and not normal human variation such as what you see in intelligence testing. So considering the weight of what we know about human development and intelligence on the one hand, and what we know about the genetics of complex characteristics on the other, I do find myself “turning right around” and arguing against your point-of-view because I find it to be cartoonish. It represents the kind of cartoonish explanation for group differences that marked the abuse of real scientific data used to justify Racism and Class Differences during the 19th and 20th centuries and I would like it to disappear so that the public can discuss important issues.
Genetic explanations for group differences are not panning out the way sci-fi has predicted for us. That is the only looming genetic crisis.
Where is the looming genetic crisis? For all the flimflammery this thread turned into, the OP asked a question, the Economist made a promise, and I see no crisis. If it doesn’t show up before midnight, it was a lie.
Where did I say these things have no effect? I said that those things can’t explain the inability of anyone from Asia or Europe to run the 100 metres in under 10 seconds. That would appear to be due to differences in ability that stems from divergent evolution.
That’s simply a question of lumpers versus splitters, and I’m uninterested in arguing it.
Here’s the question that that strawman masks:
If I take the SIRE groups in the US and I find significant large and persistent performance differences given reasonably similar nurturing, then the residual average differences are a result of different gene pools.
There are two counter-arguments to this.
The first says there is no such thing as similar nurturing. However there is a great deal of evidence that equal money, equal educational opportunity and equal parental educational levels do not eliminate the average gap among sire groups. This does not create much confidence for a position that persistent differences are a result of nurturing, since those are the key variables “nurturing” proponents have historically hidden behind when presented with data showing average performance differences among SIRE groups for educational performance.
The second (your persistent strawman) argues that race is a sloppy grouping–so sloppy that it renders baseless any genetic underpinning for SIRE groups. This is wrong. If it were that sloppy, then we would not find gene prevalence difference by SIRE groups. We are not homogeneous enough to warrant any pretense that SIRE groups are purely cultural.
It’s a position of faith that gene prevalence differences among SIRE groups cannot extend to genes determining performance outcome differences for skillsets such as quantitative reasoning or athletic abilities. There is no evidence for it. It’s plain old hope.
All of the evidence to date is that we are a product of our genes more than our nurture. Within any given family, children subject to nearly identical nurturing will have markedly different performance outcomes, generally within a bell curve range determined by the pool of genes from which they draw their individual genes.
I don’t think we’ll ever have a “genetic crisis” in the sense of a sudden and public gasp of despair when we find out we are our genes and our gene pools vary by population. We will simply quietly come to grips with the cold fact that nature has given various populations different gene pools from which to draw, and that the human race is not yet homogeneous enough to give every population the identical library of genes. Therefore, since we are our genes, for the foreseeable future we’ll see blacks winning the sprinting competition at the Olympics (and wherever else sprinting competitions are held across the world and across every sociopolitical system regardless of history) and asians excelling in quantitative disciplines–again, across the world and across every sociopolitical system.
Flail away with all the obfuscating strawmen you want to promote. Have at it with the tactic that we’ll never be able to identify all those tricky nurturing variables (see Belowjob2.0’s list above), or never be able to define “race.” What you will see is the persistent average successes based on the gene pools involved despite every effort to ameliorate nurturing differences among SIRE groups.
No, there’s no “crisis” here. Just gene libraries that differ among populations and drive persistent and immutable performance differences.
Actually forgive the sentence you quoted for your response - it and the entire list had many examples of bad grammar and unclear writing that I thought of cleaning up but decided against it because it is 2011. Crisis averted!
If I had written it better it would have been clear that I was referring to your Navajo and Chinese baby story but I ended up combining two different thoughts to make an unclear statement. So I was commenting on your assumption that parents, especially mammalian parents, have no effect on their offspring’s brain and behavior within the 1st 36 hours after birth.
There has been no time in US history when there has been “reasonably similar nurturing”. Go check out the most recent racism thread to see only one of several reasons why this is the case.
I know you have tried to post links to studies that support your argument but these studies can never hope to fully control for environmental variables. They are essentially correlative studies and the only interpretation that can be made is that one variable is or is not associated with another. The fact that studies have still found an association between SIRE and test scores despite controlling for a few variables does not say anything about other potentially important variables. As I claimed above, I think group prejudice is possibly the most important variable and this simply cannot be controlled for. I can also waste my time finding study after study on the role of group prejudice in shaping human behavior but I doubt anything will convince you and anyone curious can just go look it up.
I do not ever make this claim and would never argue that there are not gene prevalence differences among SIRE groups as defined by American culture. I do argue that your examples support only the notions that people hump those nearest and that disorders determined primarily by alleles of single genes can be shown to vary in prevalence with SIRE groups.
I have also argued at length on why using examples of marker alleles and single-gene disorders as ways to understand more complex traits are really very poor examples. To summarize: (1) marker alleles are generally not under selective pressure (unlike the genes for traits like running and intelligence); (2) the very best modern data on quantitative traits like intelligence shows demonstration after demonstration of many genes with alleles of very tiny effect. Alleles of such tiny effect that they cannot by themselves explain the kind of variability seen in intelligence. Linked with this, it is unreasonable to assume that there is some kind of genetic loading in black people for all the lower-IQ alleles of these genes. Further, there is not a single piece of evidence supporting your notions about the origin of white and black differences in test scores. You know this.
So it is not “plain old hope” and there are plenty of models we can use to get an idea about how the genetics of intelligence may contribute to our understanding of human variation in test scores. You are contorting what little you know on the subject to your race-based ideologies without taking in the whole field or thinking critically about the data that you actually have in hand.
This is simply untrue, but given that you think this I see no point in arguing the obvious to you.
I predict that people will continue to stereotype, to uphold these stereotypes, and to pick and choose their science in order to willfully promote scientific racism.
That was my list actually. And since you are ascribing an argument to me that I do not make I can only conclude from these two data points that you are not really reading my posts.
So racists and nonracists alike can agree! There is no crisis! 2011 is going to be great! Continue to enjoy your God of the Gaps faith Chief Pedant!