That was beautiful.
I had not expected a cogent discussion of the illusion of self in this thread. The parallel with race, and the analogy with neighborhoods that was brought up above are both very useful ideas. Thanks.
The first 26 posts were awesome.
C’mon; you know I’m using sickle cell as one of many hundreds–thousands–of examples where the genome is different.
It’s simply proof that genes of the “black” and “white” (or “asian”) SIRE groups do not draw from the same bag of marbles. One bag of marbles is loaded with sickle cell genes. One is not. And the self-identification correlates amazingly well with which bag of marbles mother nature let the parents choose from. It isn’t sickle cell that categorizes “race.” It’s that, since race (as we use the social construct term) has biologic underpinnings, we can point to real life examples of that. If race were purely arbitrary, all physiologic differences would be reasonably smooth. But they aren’t. For cultural and social reasons–including external appearances which are in turn driven by gene differences–we self identify with race. And that self identification assigns us to ancestral lineages with markedly different gene sets.
But you know all that.
I don’t particularly disagree. We can argue all day about an arbitrary definition of race. But the fact of genetic variation within a group has no bearing on whether or not differences between groups can be genetic.
Note that Most Recent Common Ancestor does not mean that two groups have similar proportions of gene pools. See articles by Rhodes and Chang for more on this…I need to pick up that thread when I have time.
Here’s one group: lineages that never left Africa and therefore are comprised of the group which never had the chance to incorporate any genes from out of Africa Eve on down the out of Africa lineage.
Here’s another group: lineages that descend from out of Africa Eve, including the lineage of Eurasians, who may have mated with neanderthals, injecting another few percent of completely new genes.
So, if it turns out that any of those out of Africa genes were signficantly advantageous, the African lineages never got them (or, at least, only a teeny tiny and so far unmeasured amount putatively transferred by any intercontinental admixture). On the other hand, the Eurasian group got a set of genes, and one example of such a gene is the MCPH1 haplotype D, which apparently was so advantageous that in a remarkably short period of time it reached a penetration level of 70% in Eurasians versus 0% in the African group, who aren’t descendants of out of Africa Eve.
Now, that microcephalin gene probably isn’t the “intelligence gene” so please don’t misunderstand me. But it is a very nice example (like sickle cell) that we have two distinct groups: those who got genes from out of Africa Eve, and those who didn’t. I don’t give a patoot if you want to say there are 50 races, or none. I don’t care if the San get their own category, the Mbuti another, the Ibo a third, the Mkamba a fourth…on and on as many races or categories of Africans as you want. I don’t care if you want 1 category for the out of Africans, or twenty. What I can tell you is that genetically, in the L3 line about 75,000 years ago, mutations begin appearing for the out of Africans, and the Africans don’t get those genesets. Now IF, in any of the lines anywhere, there are advantageous genes passed to descendants, you have to be a descendant to get them. And IF any particularly advantageous genes occurred post-Africa, we would see two distinct groups for whatever that advantage is.
It’s all evolutionary luck. There’s no “superiority” here. But from the standpoint of evolution, there is nothing unusual about groups having access to different gene pools as genes mutate for a particular line. That’s what evolution is all about. And the fact that we argue about what “race” is does not change a simple fundamental fact: there is a close association with SIRE group and antecedent gene pool. Those antecedent gene pools are different, and one of the major separation points is the out of Africa line as evidenced, for example, by out of Africa mitochondrial Eve, penetration of MCPH1 haplogroup D into Eurasians, and (possibly) Neanderthal and Devonision admixture of more archaic humans into anatomically modern human lines that left Africa.
Also, some good news. I am out of country and out of pocket, internet wise, for a couple of weeks. So have at it and savage me and my arguments while I’m gone. I will have forgotten everything I posted by the time of my return. 
I know that a lot of people believe all that. Some of what you posted is accurate and some of it is nonsense and a little bit of it is a straw man. (I have certainly never claimed that perceived race was “purely arbitrary.”)
I simply noted that using Sickle Cell as an example of “racial” context is rather silly and nothing you have posted has made it less so.
I am not attacking your beliefs about SIRE; I just pointed out that you used one poor example to demonstrate those beliefs.
Would you consider taking a college-level molecular biology class to further your knowledge in this subject? I think you’ll find the subject enlightening. Here’s a bit of foreshadowing. Read carefully, I get paid to teach this stuff, there’ll be a test at the end: Human haplogroups consist of mostly silent mutations which means there’s a change in a nucleotide but due to the degeneracy (e.g. or, in layman’s terms: redundancy) of the genetic code, there’s no change in the resultant protein (the physical expression of the gene, or the phenotype).
Now, using your example, this means while Europeans and Blacks have a change in nucleotide sequence, there is no change in the final protein. I’ll repeat: there’s no change in the final protein. There are evolutionary examples in which groups carry real, phenotypic changes that are passed down (e.g. Southern Europeans & CCR5 and Sub-saharan Africans & Hemoglobin S) but these were due to infection-induced bottlenecks, and these should be considered the exceptions not the rule.
What you and the peanut gallery fail to see (because your knowledge of genes does not extend past year 1999) is that a phenotype does not emerge due to a genes alone; indeed, traits are an intricate interplay between genes and epigenetics (environment). If you need any proof of this unassailable fact, just look here where the fur coloration of a cat is different from its clone. Further, why do you think that nearly all suicide victims show epigenetic silencing of BDNF? It’s because the genes are responsive to the environment.
The OP is correct. Race does not exist in biology nor in reality. What we perceive as differences in characteristics (e.g. curly hair, narrow noses, full lips, brown skin, etc) are referred to as a specific cline not a race.
- Honesty
Short question: that being the case, how much more stupid is it to discriminate according to color? I’m assuming there is such a thing as color.
And I suppose dog breeds don’t exist while we’re at it. I see very little difference between acknowledging the differences between a Bantu African and an Australian Aborigine; and a German Shepherd and a Welsh Corgi. Both are the same species, but it’s lunacy to pretend that no genetic drift and other mild speciating effects have occurred to differentiate between them.
Humans have not been intensively bred.
Of course we can.
Dogs – or any domesticated animals or plants – are the products of centuries of artificially-selective breeding by humans; there is no meaningful comparison between their genetic diversity and that of any species not so bred, including humans.
Just because I took a bus and you walked doesn’t change the fact that we arrived at the same destination. In this case, single species with multiple variant “breeds.” In our case, the process was by a mixture of many evolutionary factors such as geographic isolation, sexual selection, and the founder effect among the earliest human colonists from Africa.
No. Not the same destination.
The genetic distance between different breeds of dogs can be much greater than any found in humans.
In this type of discussion, reaching for the dog breed analogy is ill advised.
@ Samsaric Helicoid,
This topic has been discussed quite extensively previously. You may wish to check out the “Meaningful Biological Definition of Race” thread. I’m sure there are a few others too.
The problem is that there isn’t a meaningful biological definition of race. Our genetic blueprint can be influenced by all sorts of factors including environmental pollutants and psychological stress all the way to random X-inactivation and caloric restriction. Despite identical twins having the same genome, expression patterns of those genes diverge as twins get older which suggest that the environment’s influence on genes is not only pervasive but also inexorably persistant.
The theory of racial differences rests upon the idea that genes are immutable fixtures that environment has little effect. This is not true. Here’s a real example: Chronically depressed patients begin to silence a gene that’s involved in neural growth and proliferation; this silencing is reversed by antidepressants. Nearly all suicide victims show epigenetic silencing of that gene (BDNF). See the pattern? Environment effects genes which equals the phenotypic trait expressed.
In sum, your science is outdated because it fails to take into account the advances in the 2000’s.
As an aside, props to OP for this thread. Seems every month we get another “blcs r da dum!111oneone” thread. This is certainly a refreshing and more insightful change of pace.
- Honesty
Why in the world would you arbitrarily designate a hemoglobin prevalence change as “an infection-induced bottleneck” and therefore an “exception”? Do you not understand that the whole driver behind evolution is adaptation with successful reproduction? Your implication seems to be that some sort of genetic Rule keeps all human populations the same unless there’s some minor difference for infection or the like. That’s not what happens. What happens is that any and all differences resulting in more successful reproduction get passed along, whether they code for disease resistance or anything else.
Many many European/Black nucleotide sequence changes do result in the expression of completely different phenotypic outcomes. The reason Europeans and Blacks look different in the first place is the easiest proof to give you of that…
This doesn’t not mean “race” is a sharp division biologically, but it is a simple example that there are real genetic differences in the gene pools for SIRE groups, and that those gene pool differences drive real (average) phenotypic differences not based on environment.
Since “race” is definitional, I don’t care how you choose to define–or not define–it.
What I would like to teach you is that non-africans and sub-saharan africans (for example) have different gene pools that result in different phenotypic expressions unrelated to environment. These genesets reflect the fact that about 75,000 years ago a small (probably single) african population left Africa to populate the rest of the world. As a consequence, those two population lines have been separated ever since, with minimal admixture among some populations (say, the San and the Swedes, to give you an example). There are any number of other division points among populations that have peopled the world; if you are interested in a readable history of reasonably current thinking, try Oppenheimer’s Out of Eden and look at the charts for the duration of separation of mitochondrial lines.
I am concerned if you are “getting paid to teach this stuff” and what you are teaching is that phenotypes are not largely due to genes (versus epigenetics), or that changes in nucleotide sequences don’t result in shifts of phenotype expression.
You are using exceptions to try and prove a general rule. The general rule you want to promote is that as a species, human beings are more or less the same genetically (i.e., they all pull from the same gene pools in terms of what those gene pools can phenotypically express) and that the actual outcome differences we see among human populations should be ascribed to epigenetics/environment/nurturing/etc.
This is patently ridiculous pap. Evolution is all about driving phenotypic differences using nucleotide changes as the molecular engine. Sure; a given substitution may make no difference. It may make a degenerative difference. But it may also make an advantageous difference. Which differences are phenotypically significant is evolution. The fact that environment–including epigenetics–is superimposed upon the fundamental geneset does not mean that the fundamental geneset is not the major driver for many, many traits. If an advantageous trait does appear during evolution, only populations descended from that individual will exhibit the advantageous gene and its consequent phenotypic expression. If MCPH1 appears only after we’ve left Africa, it will be found only in descendant populations from out of africa eve, and not anywhere else. If it’s an advantageous gene, only non-African populations will have access to the advantage derived from it. If only out-of-africans mated with Neanderthals, only the non-african groups would have access to any advantageous Neanderthal genes.
It’s absurd to pretend that, because there is such a thing as an environmental influence on the way genes express themselves, the entire human population has fundamentally the same potential. Of course most of the human geneset is “silent.” Of course most genes are turned off. What has that to do with anything? Are you really trying to say there are not measurable differences among populations? That cystic fibrosis is not really commoner among whites? That’s just silly.
I understand arguing about how to segment populations. But you are completely confused about how genes evolve and work. And I wonder if you are not also confused about humans came to populate the world, how various groups are separated by tens of thousands of years, and how much research has gone into showing that those groups have substantially different genesets coding for all sorts of phenotypic expressions that are not a result of environment or nurture.
True or false?
- Different ethnic groups are at higher risk for certain diseases or disorders.
- Some medicines affect different ethnic groups differently.
- One can determine ethnic group from skeletal analysis.
- True
- True
- False
Now we have a 66% confirmation of the existence of ethnic groups. How is that germane to the issue of race?
I agree. A lot of people have trouble understanding the difference between the following two claims
(1) race is difficult or impossible to define in terms of genetics; and
(2) none of the observed differences among races (with the exception of defining characteristics) are the result of genetics.
Well for one thing one, can take the arguments which are made to deny the existence of race and apply those same arguments to ethnic groups. If the conclusion is that ethnic groups don’t exist, it shows that there was something wrong with the argument.