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How many drugs have race-specific instructions?

#31
(2014-Dec-09, 09:51:11)Zoidberg Wrote: So what is the big genetic difference between human groups then, did they miss something? In what genetic material? One thing is little fst difference. Then what else is there? I am honestly asking, because when you have a look at the differences in say diseases its rather little. Nobody is giving me a straight answer about this issue except Chuck.


I confess that don't quite understand what you're asking. I agree with Peter Frost that Fst is often a poor measure of actual genetic differentiation. This point has been made by Lou Jost:

"If within-group variation is high, it is mathematically impossible for Fst to reach those thresholds (or any given threshold), even if the groups cannot interbreed, share no alleles, and are each on their own evolutionary course. See Hedrick 2005 or Jost 2008 for the math. Fst and its relatives can approach zero even if no alleles are shared between groups, and can equal unity even if almost all groups are fixed for the same allele."

Human populations have high e.g., microsatelite heterozygosity so they are bound show low Fst values for this loci.

Now, as I noted, I discussed this issue, and I think that my discussion wasn't bad. Let me quote:

(To the clarify, the point is something like:

(a) theoretically, fst is a poor index of true genetic differentiation, (b)
it's an even poorer index of congenital phenotype differentiation, © practically, though, it may track some differences e.g., morphological ones in some species, (d) but this doesn't help an environmental hypothesis, because the known morphological differences along with the relevant genetic ones e.g., in SNPs are large by typical social science standards, they are as about as large, large or larger than the known disease and behavioral differences.

I know it's complex -- a number of philosopher of science race anti-realists couldn't get it -- but it's how it is.)




IV-J. “Significant” Racial Differences

It is frequently argued that there can be no socially important congenital differences between the human biological races because there is “too little” genetic variation between them. For example, Brown and Armelago (2001) state: "[T]he evidence against genetically mediated differences in behavior along racial lines is overwhelming (Table 1). First of all, a host of studies, beginning with those by Lewontin in 1972 and most recently by Barbujani and colleagues in 1997, have shown that the amount of human genetic diversity that is attributable to race is only about 5% to 10%. Following this, any particular “population” includes roughly 85% or more of the total human genetic diversity." And Ossorio (2009) notes: "Finally, it is crucial to reemphasize that the amount of genetic variation between groups is very small compared to the 85 to 95 percent of variation found within human groups.... The vast majority of human genetic variation is between individuals, including individuals who can be assigned to the same racial, ethnic, or national group. Because humans have high within-group genetic variation, genes are unlikely to explain average differences in IQ test scores of different racial groups."

Since we draw the obvious distinction between the existence of biological races and the existence of socially important differences between these races, arguments like the two above would be of no interest to us were they not, for some reason, incorporated into arguments against the existence of races themselves. One relatively sophisticated version: belief in human biological races is potentially dangerous, so we should only recognize these races if there are really important genetic differences between them; no such differences could possibly exist, since the variation between human races is very small; therefore, we shouldn’t recognize the existence of race, and should instead assert that they do not exist. Though bizarre, this argument, if not in so many words, is common; Kitcher (2007), for example, elegantly states:

"The challenge for someone who intends to defend a biological approach to human races is to develop a similar account for the utility of picking out those inbred lineages that descend from populations once geographically separated, in which, as a result of the separation, there are differences in superficial phenotypic traits, characteristics which, despite their superficiality, are salient for human beings... as the researchers point out, 93 to 95 percent of human genetic variation is found within the clusters (rather than between clusters); each cluster, then, is itself genetically quite heterogeneous.... The obvious answer is that hypotheses about genes, about genetic differences and genetic similarities, play important explanatory roles in addressing questions that matter to us, so that division on a genetic basis yields categories that are more valuable than, say, dividing people up according to the curvature of their eyebrows or the length of time for which they can stand on one leg. Yet here we should tread carefully, for the emphatic disavowal of racial essences already signals the fact that the clusters demarcated on the basis of genetic similarity are not going to play a significant role in the explanation of shared phenotypic features or susceptibilities to various types of disease [.]"

More crudely, a recent editorial in Nature (2013) tells us: "For instance, in light of increasing evidence that race is biologically meaningless, research into genetic traits that underlie differences in intelligence between races, or that predispose some races to act more aggressively than others, will produce little."

....

We must now investigate the claim that there cannot be socially significant congenital differences between biological races. Of course, differences are possible in the sense that it was not preordained that evolution would produce human natural populations with equal genetic potential for the traits contemporaneously deemed to be valuable. Even the radical egalitarian Steven Jay Gould (1984, p. ––) agreed with this: “Equality is a contingent fact of History.” What we are investigating is the claim that there cannot be differences because there is “too little” genetic variation.

This argument is so confused and fallacious that it is difficult to know where to begin. We will briefly explain why it is unsound and why, if the argument is granted, it leads to the opposite conclusion drawn by the opponents of biological race. As for the soundness of the argument:

A1. Genetic variability as indexed by Fst and Fst analogs is not a particularly accurate index of the magnitude of the genetic influences on trait differences between populations. For example, Long and Kittles (2003) found a between-population Fst of 11% based on a sample of human populations; when they added chimpanzees to the set of human populations, the between-population Fst rose only to 18%. Mountain and Risch (2004), citing this example, noted that “a low FST estimate implies little about the degree to which genes contribute to between-group differences.”

A2. As noted prior, Fst and Fst analog values are constrained by the level of within population genetic diversity. For example, in their table 1 and 2, Xu et al. (2008), give expected heterozygosity (Hs) values for Japanese (JPT), Chinese (CHB), Uyghurs (UIG), Europeans (CEU), and Yorubi (YRI) based on 20177 SNPs. The Hs was 0.30, meaning that the maximum possible SNP Fst value -- the value that would be found if populations had no zero alleles in common -- was 0.70, not 1.0 as commonly stated (e.g., see: Fish, 2013). The upshot is that Hs dependent measures of genetic diversity (Fst, Gst, Φst, QST, etc.) can underestimate the "true" genetic diversity between populations when Hs is modest to high.

A3. What is relevant to racial formation is the variation in specific genes, not the average variation across all genetic loci. Genetic variation at a typical locus will have no functional consequence since a typical locus is selectively neutral. As such, average genetic variation tends to measure neutral mutations and so index the time of divergence between populations (Sarich and Miele, 2002). As a result, the average genetic variation across loci does not allow one to well predict the amount of differentiation in loci that were not selectively neutral -- the very ones that are relevant when it comes to discussions of socially significant genetically mediated differences. With regards to these, one must look at differentiation in specific genetic regions (e.g., Wu and Zhang, 2011).

To give a concrete example in which total genetic differentiation is unindicative of differentiation with respect to specific traits: at their extremes, northern and southern Europeans differ in height by approximately one standard deviation (Turchin, et al., 2010; supplementary data). These height differences are substantially genetically determined (Turchin, et al., 2010). Yet average European interpopulation SNP Fst values are trivial at 0.001 to 0.01 (Tian, et al. 2009).
Even if we ignore points A1 to A3 and grant the implicit premise of the "too little variance" argument --that the ratio of genetically mediated phenotypic variability in traits X, Y, and Z is roughly concordant with the ratio of average genetic variability -- we see that the argument lends itself to the opposite conclusion as that drawn by biological race antagonists. This is for the following reasons:

B1. The magnitude of genetic differentiation depends on the biological populations in question. It makes no sense to argue that differences between regional biological races (e.g., Europeans and West Africans) cannot be genetically conditioned on the account of supposedly small differences between continental races (e.g., Caucasoids and Negroids). By classic population genetic standards, the differences between many regional races are "moderate" to “great”. The magnitudes of the genetic differentiation in SNPs between some regional races are shown below:

B2. The magnitude of the measured between populations genetic differentiation varies by the class of loci analyzed (and the statistic used); for example, continental microsatelite, SNPs, and MtDNA Fst values are typically around, respectively, 0.05, 0.12, and 0.20. Part of this variation in measured genetic variation is attributable to loci variation in Hs (Jakobsson, et al. 2013). Were one to try to infer the magnitude of genetically conditioned phenetic variation from typical indexes of genetic variation (e.g., Fst values), a practice not recommended by the present authors, one should use the class of loci that most likely underpins the relevant phenetic variation. For example, since variation in single-nucleotide polymorphisms explains variation in many interesting polygenetic traits such height and intelligence (e.g., Yang et al., 2010; Davies, et al. 2011), one should attempt to infer genetic mediation of phenetic differences based on coding SNPs. For a breakdown of SNP variance by classes, readers are referred to supplementary Table 2 of Barreiro et al. (2008).

B3. The magnitude of SNPs genetic differentiation, as indexed by Fst, is not small, even between continental races, according to population genetic and social scientific standards. The median continental race SNP Fst value is said to be around 0.12 (Li et al., 2008; Campbell and Trishkoff, 2008; Elhaik, 2012; Bhatia et al. 2013)), with the estimated magnitudes varying somewhat due to the choice of specific loci, the method of aggregation employed, the Fst estimators used, and so on; see: Bhatia et al. (2013). With regards to population genetics standards, Sewall Wright, who helped develop the Fst index, noted that such a magnitude signified moderate genetic differentiation. By his scale, which has been frequently cited (e.g., Oliveira, et al., 2007; Zhang and Tier, 2009): 0 to 0.05 indicates little genetic differentiation; 0.05 to 0.15 indicates moderate genetic differentiation, 0.15 to 0.25 indicates great genetic differentiation, 0.25 indicate very great genetic differentiation. (Wright, S. 1978. Evolution and the genetics of populations)
As indexed by SNP Fst, then, we could infer, based on typical population genetic standards, moderate genetic differentiation between continental races. With regards to social scientific standards, if we naively translate Fst estimates into standardized differences, we see that differences are non-trivial. If one assumes normality and equal variances and directly converts a 12% between-population variation into a standardized difference, one gets a value of d ~ 0.74.
.....................
Given the law of total variance:
z= 2(sqrt((a/w)))
z=between group standardized difference; a= ratio of variance between to within populations; w= variance within populations.
........................
For reference, a Cohen’s d of 0.2 to 0.3 is typically said to be “small,” while a Cohen's d of 0.8 to infinity is said to be “large".

B4. All of these estimates are arguably low, since we are dealing with genetic variability between diploid populations (Harpending, 2002; Sarich and Miele, 2004). The 12% SNPs variance between continental races refers to the total between continental race variance and not to just the more relevant between individual, between race variance. This variance includes genetic variance of both the intra-individual and inter-individual sort; arguably, only the latter is relevant when it comes to discussions of heritable between population phenotypic differences, as between population phenetic differences represent aggregations of inter, not intra, individual differences.

To illustrate the point: Nishiyama et al. (2012) decomposed the SNP genetic variance for various Japanese populations into inter-subpopulational, inter-individual, and intra-individual variance. They found that between 96.7 and 99.6% of the variance was located within individuals. When intra-individual variance was partitioned out, roughly the same percent of genetic variance was located between individuals and between subpopulations as between individuals and within subspopulations. The decomposition is shown in the table below. Of course, most of the variance was still "inter-individual" in the sense of inter- plus intra-individual (i.e.., intrapopulational). (In the same way, of course, most diversity, in general, is "inter-racial" in the sense of inter-racial plus inter individual plus intra individual.) It just wasn't mostly inter-individual in the sense of exclusively between individuals. Does this matter? Well, it casts the oft referenced genetic variance ratios in a different light. And it is relevant if one's argument is that phenetic differences between individuals between groups couldn't be substantially congenitally conditioned because there is "too little" between group genetic variation relative to that between individuals within groups.

[link here:
http://www.plosone.org/article/info%3Ado...ne.0035000]

(From: Nishiyama, T., Kishino, H., Suzuki, S., Ando, R., Niimura, H., Uemura, H., & Tanaka, H. (2012). Detailed Analysis of Japanese Population Substructure with a Focus on the Southwest Islands of Japan. PloS one, 7(4), e35000.)

Can the "too little genetic variance" argument be salvaged? It cannot. To avoid a racial-hereditarian conclusion, it must be discarded — but how? One could, citing the points made in A1 to A3, argue that there is little correlation between average genetic variability and genetically mediated phenotypic variability. But this isn't the case at least with regard to many classes of phenetic differences. Relethford (2009), for example, notes:

Several studies have looked at estimates of FST based on the global craniometric dataset originally collected by Howells (1973, 1989, 1995, 1996), and consisting of 57 craniometric variables measured on male and female crania from 26 populations (as well as males only on four additional samples). Using an average heritability of 0.55, Relethford (1994, 2002) found that estimates of F ST based on all 57 traits ranged from 0.11 to 0.14 depending on the number of geographic regions sampled. These FST values are similar in magnitude to those estimated in a number of studies of classical genetic markers and DNA markers.

Similar results have been reported in context to dental traits (e.g., Hanihara (2008)). The found correspondence between genetic Fst and estimated congenital phenotypic FST is curious given some of the points mentioned above. It seemingly suggests that genetic Fst doesn’t largely either overestimate or underestimate (between continental race) variance in (certain) genetically conditioned phenotypes. Yet, as we noted above, depending on which biological races we are discussing, the Fst measured genetic differentiation is medium to large as judged by social science (or population genetic) standards. To illustrate, the relationship between percent variance between populations and various statistics is shown below.

So if one points to the results of Relethford (2009) to argue against points A1, A2, A3, and B4, one is forced to accept, as a default position, medium to large genetically conditioned differences between such and such biological races. Of course, one could try to argue that differentiation in the genes that underlay interesting physiological and neurological functions is trivial — but the empirical evidence speaks against such an argument. As an example of such evidence, in the context of regional (European, East Asian, West African) population differences,
Wu and Zhang (2011) conclude:

"In this study, we find that genes involved in osteoblast development, hair follicles development, pigmentation, spermatid, nervous system and organ development, and some metabolic pathways have higher levels of population differentiation. Surprisingly, we find that Mendelian-disease genes appear to have a significant excessive of SNPs with high levels of population differentiation, possibly because the incidence and susceptibility of these diseases show differences among populations."

Another way to escape the reverse of the "too little variation" argument would be to maintain that the particular traits under discussion are unlike others. One might reiterate Loring Braces’ argument — which, we admit, we could never make sense of -- that there was some unique evolutionary selection against population differences in the particular traits under question. In the same way that no human populations could exist without heads, it could be argued that no human population could exist e.g., with a genetic propensity for time preference less than that of any other populations. This type of argument, of course, is ridiculous when applied to normally distributed and highly heritable polygenic traits since within every geographically defined population innumerous subpopulations manage to exist with differences in these traits.

In short, the “too little variance” argument cannot be salvaged. To the extent that it is deemed valid (despite the considerations mentioned in A1 to A3), it clearly fails to support the position which it is enlisted in defense of.
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#32
(2014-Dec-09, 19:32:48)Chuck Wrote: I confess that don't quite understand what you're asking.


Let me put it this way: (a) if you think that there are huge genetically mediated medically related differences, you are wrong, since there aren't huge medically related differences in the first place. (b) If you think that the medically related differences which are can't be genetically mediated because genetic differences are only modest, you are being silly, since the medically related differences themselves are only modest. The same, more or less, can be said for sociobiological traits. What do you disagree with? Perhaps Peter and I are not well explaining this.
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#33
I understood your post clearly Chuck thank you. So it depends on what you assume and the standards set. Ok so basically they don't know... and I will assume for now from your evidence that FST is not a good measure for within human populations.

Thats all I wanted for now.

There is this part though:
"In this study, we find that genes involved in osteoblast development, hair follicles development, pigmentation, spermatid, nervous system and organ development, and some metabolic pathways have higher levels of population differentiation. Surprisingly, we find that Mendelian-disease genes appear to have a significant excessive of SNPs with high levels of population differentiation, possibly because the incidence and susceptibility of these diseases show differences among populations."

Problem here is that most genes are involved in everything. Take Edar for example not only in hair, eyes and skin but also pretty much everywhere else, even testicles. Even then so few for associations with even the simple traits. Especially most genes are involved in the brain because its the most complex organ and uses the most energy. Also the other reason is that humans have much fewer genes than assumed(30-20k genes), less than CORN, about the same as the fruit fly.

Basically we have few diseases, few medical uses for race(all of which will be made obsolete soon), and a changing gap(some of which closed substantially) in average cognition, height and bmi, with an unknown amount attributable to genes and even a relatively low amount of genes to boot. I'll take that as support of less differences than thought before, since there are other possible explanations for the variation like epigenetics.

In relation to this argument about medicine I will look some more, but its pretty obvious that race is almost useless with regards to it. For all of them there are other more accurate and more medically ethical options available. Regardless of what the actual genetic differences between groups are there is little in the way of uses for race medicine. Also most of the medicine that exists now are pretty dangerous to humans as it is.
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#34
(2014-Dec-09, 23:23:03)Zoidberg Wrote: Basically we have few diseases, few medical uses for race (all of which will be made obsolete soon), and a changing gap(some of which closed substantially) in average cognition, height and bmi, with an unknown amount attributable to genes. ...In relation to this argument about medicine I will look some more, but its pretty obvious that race is almost useless with regards to it.


I find your position to be absurd, but I agree that this depends on priors: What would constitute an important difference? Genes can explain, at least statistically, a substantial fraction of social outcome differences, medical and otherwise. If you consider the phenotypic differences themselves be important and significant then you should logically consider between groups genetic differences to be also. If not, then not -- it's that simple.

As for the actual, genetic data, it's abundant.

"In the fall of 2005, the first two genome-wide admixture studies were reported in Nature Genetics for hypertension and for multiple sclerosis in European Americans (56, 84). Five years later, admixture scans have been conducted for a range of traits and diseases that have different rates in Europeans, Latinos, and African Americans (Table 5). Admixture mapping has been successfully applied to discrete disease phenotypes [prostate cancer (9, 26) and nondiabetic kidney disease (33, 34)] and quantitative traits [e.g., interleukin 6 and IL6 soluble receptor levels (57), lipid levels (5, 6), obesity (14, 15), and white blood cell counts (46, 55)], as well as hypertension (83, 84), type 2 diabetes (21, 33), breast cancer (23), and peripheral arterial disease (67). Because of the extensive length of ALD, it was widely predicted that the admixture scan, like family linkage studies, would coarsely map a region of interest, and extensive fine mapping would be needed to identify a disease gene and its causal variation."
http://lesacreduprintemps19.files.wordpr...141523.pdf

We are not then dealing with a scientific issue but a philosophical or social one -- are the magnitudes of the know differences "significant"?
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#35
(2014-Dec-09, 23:48:37)Chuck Wrote: We are not then dealing with a scientific issue but a philosophical or social one -- are the magnitudes of the know differences "significant"?


Another issue is that I seem to have a much broader conception of "race" than you. A race, to my mind is just a genealogically defined intra-specific division. So many ethnic groups are these. Now, between these there are important genetic differences, for example in terms of high altitude adaptions. This has practical significance for some. For example, when I was traveling in Western Sichuan a few years back, I came down with a severe case of Mountain sickness, demanding medical attention. The hospital staff was quick to recognize that I was not Tibetan and probabilistically diagnosed the condition. Race medicine!
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#36
(2014-Dec-09, 23:48:37)Chuck Wrote: [quote='Zoidberg' pid='2485' dateline='1418160183']
As for the actual, genetic data, it's abundant.

"In the fall of 2005, the first two genome-wide admixture studies were reported in Nature Genetics for hypertension and for multiple sclerosis in European Americans (56, 84). Five years later, admixture scans have been conducted for a range of traits and diseases that have different rates in Europeans, Latinos, and African Americans (Table 5). Admixture mapping has been successfully applied to discrete disease phenotypes [prostate cancer (9, 26) and nondiabetic kidney disease (33, 34)] and quantitative traits [e.g., interleukin 6 and IL6 soluble receptor levels (57), lipid levels (5, 6), obesity (14, 15), and white blood cell counts (46, 55)], as well as hypertension (83, 84), type 2 diabetes (21, 33), breast cancer (23), and peripheral arterial disease (67). Because of the extensive length of ALD, it was widely predicted that the admixture scan, like family linkage studies, would coarsely map a region of interest, and extensive fine mapping would be needed to identify a disease gene and its causal variation."
http://lesacreduprintemps19.files.wordpr...141523.pdf

We are not then dealing with a scientific issue but a philosophical or social one -- are the magnitudes of the know differences "significant"?


Its not abundant, you telling me what you posted now is abundant? How long will the rate difference last? You see how fast they change? They are just associations and are obsolete anyway with regards to medicine now or soon to be. Pretty much every disease and trait that you just mentioned is pretty easily diagnosed and its heavily effected by environment, you can just see from the trends. Most of the traits can be detected by simple, xrays, urine and blood tests. No need for correlation on rates(that constantly change). Its literally unethical to make medicine based off an average and then put that out into the market. Especially when humans can vary so much individually and the average change so quickly.

Most of the the traits and rate differences can be due to things like this.
http://www.nature.com/nm/journal/v17/n5/....2337.html
http://www.epibeat.com/aging-environment...ension/48/
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#37
(2014-Dec-10, 00:11:26)Chuck Wrote:
(2014-Dec-09, 23:48:37)Chuck Wrote: We are not then dealing with a scientific issue but a philosophical or social one -- are the magnitudes of the know differences "significant"?


Another issue is that I seem to have a much broader conception of "race" than you. A race, to my mind is just a genealogically defined intra-specific division. So many ethnic groups are these. Now, between these there are important genetic differences, for example in terms of high altitude adaptions. This has practical significance for some. For example, when I was traveling in Western Sichuan a few years back, I came down with a severe case of Mountain sickness, demanding medical attention. The hospital staff was quick to recognize that I was not Tibetan and probabilistically diagnosed the condition. Race medicine!


But they gave you the same medicine that they give the Tibetans who get mountain sickness didn't they? There are more symptoms for it than there are races.
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#38
"Most of them {dog breeds} (if not all) can be very accurately identified using much fewer loci than when determining within humans.

If you use several genetic markers simultaneously, you can increase the probability of assigning an individual dog to its breed. But the same logic applies to humans. If you use several genetic markers simultaneously, the amount of genetic overlap between human races decreases considerably.

"You are nitpicking extremes"

Far from it. This is a common finding when we compare sibling species, especially those that have diverged within less than 1,000 generations.

"Stop giving me nonsense arguments. You have a measurable amount of genetic difference when you consider everything and its there between dogs, ants whatever and also between human populations"

I'm not giving you nonsense. I'm giving you basic evolutionary theory. A population boundary is a boundary between different sets of selection pressures. So genetic variation across a population boundary is not the same thing as genetic variation within a population. Fst is not a reliable measure of adaptive, functional differences.

"You also seem to think that because a species can be different between groups within its species that the differences are automatically mostly(all?) hardwired fixed genetic differences that come via natural selection."

No, that is not what I think. Here's what I think: between-group differences are more likely to be functionally significant than within-group differences. It's a matter of likelihood. The words "automatically", "mostly" and "all" don't come from me. They come from the caricature of me in your mind.

I read your links. They have no bearing on my argument.
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#39
(2014-Dec-10, 00:39:39)Zoidberg Wrote: They are just associations and are obsolete anyway with regards to medicine now or soon to be. Pretty much every disease and trait that you just mentioned is pretty easily diagnosed and its heavily effected by environment.... Its literally unethical to make medicine based off an average and then put that out into the market. Especially when humans can vary so much individually and the average change so quickly.


Let's diagnose the disagreement. Race medicine can mean the following:

(a) Taking genes into account when it comes to assessing the etiology of ethnic disparities.
(b) Taking population structure into account then it comes to evaluating clinical efficacy and recruiting participants.
© Taking into account ethnic background when it comes to diagnosing conditions.

(a) isn't going anyways, because interest in the origin of ethnic/racial outcome differences isn't.
(b) isn't going anywhere because "personalized medicine" in the sense of "personalized drugs" is still largely science fiction. Medicines are evaluated based on the average efficacy.
© is soon to be obsolete in wealthy countries.

Where do we disagree?
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#40
(2014-Dec-10, 02:32:45)Peter Frost Wrote: "Most of them {dog breeds} (if not all) can be very accurately identified using much fewer loci than when determining within humans.

I'm not giving you nonsense. I'm giving you basic evolutionary theory. A population boundary is a boundary between different sets of selection pressures. So genetic variation across a population boundary is not the same thing as genetic variation within a population. Fst is not a reliable measure of adaptive, functional differences.

"You also seem to think that because a species can be different between groups within its species that the differences are automatically mostly(all?) hardwired fixed genetic differences that come via natural selection."

No, that is not what I think. Here's what I think: between-group differences are more likely to be functionally significant than within-group differences. It's a matter of likelihood. The words "automatically", "mostly" and "all" don't come from me. They come from the caricature of me in your mind.

I read your links. They have no bearing on my argument.


I agreed that FST is not a good measure, but your are still giving me nonsense about we cant compare genetic differences within a human population with the same genes to people outside. There is no special difference.

There is already incredible FUNCTIONAL within group differences per individual far greater than most if not all the averages between groups especially for complex traits. You can even bring out the bell curve to prove it. What other functionality are you talking about? Non functional variation will be there along with functional variation because non functional variation tags along with whatever is being selected for. Non functional and functional variation increases simply by population growth. Things like being in warmer climates can increase mutation rates too. There is already great variation within Africa, physiologically... bigger than between European groups. EG: Pygmies and Masai. Thats all functional, so your argument about the likely hood of functionality is bs. There is no special difference in the genes that vary within to ones that vary between. Its the same genes.

If you read those links and you think it has no bearing then my caricature of you is true.
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