That sounds like a fascinating topic why don’t you give us a small lesson? Considering the sheer length and number of your posts I’m sure this won’t be burdensome. Please, Arab contribution to “Western Africa’s civilization”.
LOL- yes, you got me to admit something I always believed and never denied. Neither of those conclusions lead to your genetic explanation, without genetic evidence. There are many other factors that both vary by populations and may have an effect on various characteristics.
I have neither opinions nor expertise on the Asia-to-Africa topic being discussed, and hope that my comments will not be used in support of either side. However, the emerging field of reconstructing human prehistory based on Y-chromosome studies fascinates me, and there are interesting and unexplained Y-chromosome connections between Asia and Africa. The haplogroup R1b originated near Central Asia, but one branch now dominates Western Europe. The Egyptian Pharaoh Tutankhamun has R1b haplogroup (is the subgroup known?)
But most interesting is an enclave of a R1b subclade centered near Lake Chad and associated with the spread of Chadic languages. Here’s a pdf paper discussing this haplogroup. There must have been some significant Asia-to-Africa episode thousands of years ago, but AFAIK details have never even been conjectured.
<sigh> There’s no gene for lactase persistence, Chief Pedant. The gene is called lactase; the difference is the temporal expression of that gene. I’m assuming you’re talking about the paper listed on Wikipedia, the abstract says that the polymorphism does not “explain all the variation in lactase expression”. Indeed, it doesn’t because the biggest driver for lactase expression is the continued presence of lactose in the diet: ask any first or second generation Asian born and raised in the United States on a Western diet.
You have brought this up and, frankly, this one may have a kernel of truth to it. Confirming anecdotal evidence from white women for the last 200 years ago, it’s been proven that blacks tend to have bigger penises than whites and Asians. Could the fact that blacks have higher testosterone be responsible for this? Also, since testosterone is involved in rapid skeletal muscle growth, why do skinny blacks exist in the face of a high protein, Western diet? More study is needed here.
<sigh>. It’s this statement that has me doubting that you went to medical school, but whatever, this is the Internet. Every human being on this planet has the same set of genes. You know that gene MCPH1 you keep hollering about? Yep, everyone has it. If we had different sets of genes per person, our world would be akin to X-men. It would be awesome if it worked that way, though.
No.
There are about (at last count) about 30,000 genes that can be altered and changed in ways to produce about 100,000 different proteins. You’re right that gene pools can differ by population but how many have a substantive effect? Can you name 100 (less than 00.1% of the total genes in the genome) non-silent, non-lethal phenotypic genes in humans? Here, I’ll get you started: hemoglobin S, CCR5, CFTR, . . . . .
Yes, they do, but not in the way you think. Say you read a paper that blacks and whites have differences in Gene X :
Blacks
Gene X: GCCGCA****GAT **
Whites
Gene X: GCAGCCAAC**
Look different right? Well, lets look at the final protein.
Blacks
Gene X: GCCGC**AGAT **
Protein: Ala-Ala-Asx
Whites
Gene X: GCAGCC****AAC
Protein: Ala-Ala-Asx
See? No change, but maybe that was too easy. Let’s assume that we do have a change in protein sequence
Blacks
Protein Gly-Ala-Ala-Asx-Pro-Trp
Whites
Protein: Gly-Ala-Ala-Asx-Gly-Trp
Here we have a change in protein but the change (Proline <-> Glycine) are tolerable because the amino acid as a similar structure and functions. But let’s look at a more drastic change:
Blacks
Protein ** Trp**-Trp-Trp-Trp-Trp-Trp
Whites
Protein: Gly-Ala-Ala-Asx-Gly-Trp
These are now completely different proteins. This protein’s function will likely be impaired and unless there’s another protein that has a redundant role, the mutation will probably be lethal. Proteins are finely-honed tools to do a specific task, you can’t turn a screw driver into a submarine and think it’ll have the same function.
This is true. Skin color is a good one.
(bolding mine)
I think you’re misunderstood. All humans have the MCPH1 gene. In fact, didja know that all zebrafish, mice, and primates have the MCPH1 gene, too?
Let’s try this one more time.
There’s a protein in the brain called bone derived growth factor (BDNF), it’s basically like a shepard leading newborn neurons from the hippocampus to facilitate connections to other neurons. These newborn neurons are the cellular substrate of the acquisition of new memories. Environmental stimuli such as chronic stress or a traumatic event can trigger a molecular cascade leading to the methylation of the BDNF gene, thus silencing it. How is the gene silenced? Well, when DNA is methylated, it’s more likely to be wound around big balls called histones making the gene (and often the promoter) inaccessible to the transcriptional machinery. Antidepressants have a cool effect of reversing this.
Anyway, when patients are depressed, they have lower levels of BDNF in their cerebrospinal fluid. This depression could arise from an infinite amount of permutations from a cancer diagnosis all the way to spousal abuse and war-related PTSD. When these depressed patients commit suicide and you crack open their brains, what do you find? The gene is completely silenced. So this is an example of environmental stimuli preventing a gene from working entirely regardless of the “gene skillset”.
If you still don’t understand that or are still not convinced, I agree to disagree.
That’s because chimps, unlike humans, have a completely different genetic skillset. We don’t have the same number of chromosomes.
- Honesty
Let me recommend Oppenheimer’s Out of Eden: The Peopling of the World for a basic overview of migration patterns based on mitochondrial and Y chromosomal lines. It’s out of date now (2003) but most of the basic patterns have not been shown to be incorrect, as far as I know.
You’ll see a number of charts and maps that are nice summaries.
Northern africa is pretty interesting. Among the things that affect migratory patterns are global climate changes, and among the “gates” (putative migratory pathways) that open and close is one called the northern route, which leads to the Levant (roughly, lands around the eastern Mediterranean). It turns out we have archeological evidence that our african ancestors made it to the Levant, presumably by a northern route through a green Sahara (because of climate shifts). One theory is that the first africans made it to the Levant around 100,000 years ago (I’m giving very rough numbers for the sake of brevity) but then died off because of climate change. And their archeological record in the Levant peters out by 90,000 years ago.
There was a second exodus from africa through a southern route, and when we look at those DNA lines, it appears this second exodus (containing “out of africa mitochondrial Eve”) is the one from which the descendant lines (L3 mtDNA lines) populated the rest of the world, perhaps initially along the coasts of India and eventually up into europe and the rest of asia.
So what about northern africa? Right now it looks like most of the populations living in northern africa (meaning, not sub-saharan) reflect population lines from mtDNA line L3 populating the Levant via the second exodus using the southern out of africa route (but not the Levantines from the original northern route) who then moved south and west into northern africa.
Currently the oldest indigenous north africa line (Berber) is traced back about 30K years and appears to have descended from the west eurasian (Levant) area; not the other way around. There are a handful (perhaps an eigthth) of maternal DNA lines in northern africa that do come from more recent migrations from sub-saharan africa.
Back to your question: what about R1b? The “R” is referring to a Y chromosomal group that shows up about 30K years ago, descended from out of africa Adam’s “F” Y chromosomal group (the group letter convention for Y chromosome are arbitrary and more or less alphabetical against time). F shows up about 50,000 years ago, out of africa, and probably somewhere near the southern route out of africa (since it’s a pretty ancestral group).
OK, so R1b makes it to a lot of places, including northern africa, and apparently makes it into part of sub-saharan africa, clustered around the central Sahel (by the time it gets to the central Sahel it’s designated R1b-V88, specifically). I believe the details of that are “conjectured” in the paper you cite. The idea is that a sub population manages to make it across the sahara because of some climate changes during the Holocene Climactic Optimum around 5 or 10K years ago. See Chart a P 805 of your cite, or see this illustration from Wikipedia.
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The tone of your answer makes me think I overstated (or you overestimate) the level of my ignorance. 
IIRC, Oppenheimer associates R1b with the Cro-Magnon (Aurignacian) expansion – a guess which was popular in 2003 but is not in accord with any of the chronologies proposed by present-day experts.
Let me just summarize a response by letting you know I’m underwhelmed at your conflation of pedantry with fact.
You may think it’s productive to point out “that there’s no gene for lactase persistence” as if common communication shorthand is not a sufficent way to summarize a concept and instead communicates exactly how a process works.
“Lactase” is an enzyme. “Lactase persistence” means you keep that enzyme’s function into adulthood. Genes–the DNA blueprint–are what enables that to happen, and populations vary hugely in how prevalent is the genetic blueprint that creates lactase persistence. Your pretense that you somehow have a finer understanding of this is either complete confusion on your part, or deliberate attempt to pretend a simple concept is so complicated the next guy over can’t understand it. Knock it off.
Of course it’s true that many mutations are silent (they end up coding for the same protein) or deadly (they end up screwing up how we are supposed to work). But some of them end up being highly advantageous and end up getting reproduced successfully. The word you are looking for is “evolution” and if your basic premise is that human populations have stopped evolving, you need some more education. You are wasting your time pretending that, with humans, all evolutionary changes are trivial or else exceptions such as disease resistance related to local ecology.
A word about MCPH1, and how genes are nicknamed, and one more expression of my irritation at your apparent determination to pretend shorthand statements embrace my full understanding. MCPH1 is the nickname for a gene, but MCPH1 has many variants. One of these variants (haplogroup D), appeared about 35 or 40,000 years ago, is widely distributed among non-africans (i.e. out of africa descendant lines, but not intra-african lines). The breadth of distribution for this particular variant of MCPH1 is and example of how populations show markedly different gene prevalences. In this case, the two populations would be out-of-africa, and left-in-africa. Moreover, the marked penetration for this particular variant suggests positive selection pressure; this in turns suggests (but does not prove) an advantageous variation.
Of course environment and genes interact. But it is genes which create the blueprint for that interaction.
Keep sighing, but your notion that every human being on the planet has the same set of genes is beyond ludicrous, unless you are talking about the genetic nicknames. If so, you are attempting to make an end-run for your egalitarianism by using nomenclature to obfuscate fact. That’s pitiful. Every nicknamed gene has any number of variants, and those variants have differing degrees of functionality. (Evolution again.) Get the wrong MCPH1 variant and you don’t have a functional brain. Get the right variant of gene(s) coding for sprinting ability and you have a shot at beating out Usain Bolt. Get the wrong variant and you might not be able to walk.
That such a gene might carry the same nickname for its parent group or function does not mean “Every human being on this planet has the same set of genes” and if that’s what you are teaching, well…I guess we’re not supposed to insult people in GD so maybe I should just <sigh>. The fact that all cars on the planet have something we nickname an “engine” does not mean that every car on the planet has an engine creating an identical outcome to every other car.
Are you saying that all humans have the same allele for the MCPH1 gene?
Or are you saying that all humans have some allele for the MCPH1 but those alleles are not necessarily the same for all humans?
Well does this happen all the time? Or just some of the time? If it’s just some of the time, then so what?
You seem to be saying that any genetic difference between blacks and whites will either (1) have no effect at all; (2) have a negligible effect; or (3) have a lethal effect on people unfortunate enough to be on the wrong end of the difference.
You seem to be saying that it’s impossible for there to be a genetic difference which results in a measurable but non-lethal effect.
Do I understand you correctly?
No insult intended; it’s impossible to assess anyone’s grasp from a single post, usually.
Oppenheimer’s book is certainly not the only authority, but you’ll see on the Y Chromosome charts on page 375 that all the R1b groups he lists derive from (Y-chromosome) R173 lines, in turn derived (ultimately) from out of africa Adam (M168) lines. These are all anatomically modern human lines. On page 132 he shows the Aurignacians making it to northern africa, but of course most of the migratory charts in that book are sketches…it’s not clear to me exactly what you are asking (or teaching me).
Can you clarify?
That R1b derives from M173 is tautologous; that these derive from M168 is hardly in doubt. 
The coarse structure clading charts of the Y-chromosome tree were already well known in 2003. Since then much has been learned about the finer structure and views on the chronology have changed. While the chronological calibration is still controversial, it is agreed that R1b did not yet exist at the time of the Aurignacians! The European branch of R1b (somewhere between M269 and M412) probably migrated from the Fertile Crescent to Greece early in the Neolithic, but how it eventually overwhelmed Western Europe is rather mysterious. (DNA testing of ancient corpses would be useful, but Y-chromosome is harder to test than mtDNA. Among the handful of corpses tested, the earliest R1b, AFAIK, is from early 3rd millenium Germany and associated with Bell Beaker.)
Sibling to European R1b are clades found among the Bashkir (near the Urals) and Hazara of Pakistan! But, AFAIK, historical or archaeological knowledge of those groups is nowhere nearly deep enough to shed light on the Y-chromosome data.
My mention of R1b-V88 in Africa wasn’t really intended to ask or teach, but just to reflect the existence of Asia-to-Africa migrations. Assuming, as many do, that modern man underwent favorable adaptation in Asia, the R1b-V88 migration could be used by either side of this debate: as evidence of “Asian superiority,” or to suggest that favorable mutations had a route to impart them back into Africa.
No. Humans are born with two alleles for the MCPH1 gene. One from moms, the other from pops. The nucleus of a cell tends to have only one copy of a gene active and/or available at one time; the gene that is usually active is the dominant gene while the silenced homolog is the recessive one.
And this conveniently brings us to your next question.
Yes to the first part, No to the second part. All humans have a pair of MCPH1 genes which of which one is active and the other is silenced. While there may be changes in the iteration of the MCPH1 gene, it still performs its normal function. Polymorphisms are the molecular equivalent of a different colored screwdriver - the color provides no other function other than to tell you where your ancestors are from. Nothing more, nothing less. Mutations are more likely to have no effect or have a deleterious effect than to produce a gain of function. Why? Because there are very few biological systems that are redundant where a loss-of-function from one gene can be rescued from other genes with no harm to the organism.
Ok, back to this MCPH1 stuff.
According tothis, the MCPH1 gene (introns and exons) is nearly 2.5 million base pairs long. Then, when you splice it, put it back together, and put a few ribosomes on it, you get a huge protein that’s over 8000 base pairs long. So, hey, I’m not too good at statistics, but I don’t think finding 20 or 30 changes at the nucleotide level is going statistically effect the function of the resultant protein.
- Honesty
In this very specific example of looking at Gene X from blacks and whites, yes, you understand me correctly. The effect of a mutation can be non-lethal (CCR5 mutation) all the way to lethal which can be chronic (Hemoglobin S) and/or acute (Zellweger’s syndrome).
- Honesty
Ok, and in your view, not all humans have the same pair of alleles for the MCPH1 gene. Agreed?
I’m not sure I understand your answer. Let me try to rephrase the question:
You seem to be saying that all humans have 1 active MCPH1 gene. Do all humans have the same active allele for that gene or not?
So the claim does not apply to all genes then, only some subset? Or does it apply to all genes?
What does your point that some mutations are lethal and some are non-lethal have to do with the central idea of evolution that a subset of mutations are beneficia,l and drive evolution?
Just to help you out a little: The effects of mutations can be all the way from advantageous to lethal. The CCR5-Δ32 variant in the CCR5 gene is an example of such an advantageous mutation for HIV resistance; Zelweger’s and microcephaly are examples of lethal mutations.
Have you retracted your position that “all humans have exactly the same genes”?
That, to me, is the most ignorant statement you’ve made to date, because it is so far off base (no pun intended 
) that it would substantially mislead a naive audience since it conflates a gene nickname (“MCPH1,” for example) with the notion that every human has the same MCPH1 variant. And since the variants of genes are what underlie the actual phenotypic expression, the statement “all humans have exactly the same genes” is patently false.
In your response below, you’ve arbitrarily–without a shred of scientific support–stated the following:
This seems to leave an impression that you’ve doped out on your own that MCPH1 codes for exactly the same phenotypic result no matter what variant it is, and that all humans have exactly the same gene, coding for exactly the same outcome.
Are you even aware that one of those variants causes microcephaly? (!) That the haplogroup D variant of MCPH1 is distributed in an estimated 70% of non-african populations, and that the marked penetration of that variant is taken as evidence of substantial selection pressure? That selection pressure does not occur unless a gene variant has a different effect from the baseline gene? That Bruce Lahn decided other, less controversial, topics would be a better choice of careers after the announcement of the prevalence of haplogroupD MCPH1 variant started speculation around the specific genetic underpinnings of intelligence?
Your grasp of how genes work and evolve is either rudimentary in the first place, completely confused, or so distorted within a paradigm that evolution does not occur, that your statements have become absurd.
<sigh>, indeed
As often, RationalWiki is a good source here:
It seems to me there are two possibilities here:
(1) He’s claiming that all humans are genetically the same, like identical twins and that any deviation from this sameness will either have a negligible impact or will almost certainly kill the unfortunate soul who happens to be different; or
(2) He’s claiming that with respect to some genes, all humans are genetically the same, like identical twins and that any deviation from this sameness will either have a negligible impact or will almost certainly kill the unfortunate soul who happens to be different.
The first claim is patently absurd. The second claim may very well be true but is pretty much irrelevant since nobody disputes that all humans are the same in many respects.
I’m trying to figure out whether his position is (1) or (2) but I have a feeling that it will be like nailing Jello to the wall.
Thanks for the clarification; let me just comment on your last paragraph, quoted here.
I think the paper you cite makes a pretty irrefutable case that R1b arises post-africa, and then (the V88 variant) jumps the Sahara over to the central Saheel for that population. It’s more than a stretch, though, to generalize that fairly well-defined migration into a broader implication that Eurasian genes flowed back to the vast majority of sub-saharan africa. In fact, the genetic evidence is the opposite: a clear migration into the central Saheel, and not much genetic admixture beyond that point.
I think it’s actually a good example of how populations tend to stay relatively isolated. That is, just because a population hikes over to a new area doesn’t mean they all become a common, genetically admixed family with the locals. R1bV88 is a good example of that, with distributions (if I’m reading it right) that still follow linguistic divisions even with the putative migratory inflow happening 7K years ago.
As the paper you cite points out at the beginning, even migrated populations stay remarkably distinct. For example, “The emerging picture indicates a clear differentiation between central/western sub-Saharan and northern African populations.” V88 isn’t found in Western, Eastern, or Southern Africa, and once you get south of the central Saheel, V88 prevalence drops dramatically.
Perhaps we’ll find other entry points into the rest of africa–surely the eastern coast would be candidate for this, especially in the last few thousand years. I think as our story unfolds, it will be along the lines of “almost all of us have small pieces that come from all over the world,” and I don’t think anyone who looks at populations and gene flow would try to deny that. None of us are purebred no matter how much of a splitter you are; very few are completely homogenized mutts no matter how much of a lumper you are.
Whether or not “race is non-existent” is a matter of definition, and populations vary markedly for gene prevalences from one population to the next.
If you define “race” this way, it’s easy to show it’s “debatable” as a biological construct. And of course, adding modifiers like “clear” and “well-define” make it particularly easy to discard “race.”
But I think the question in most people’s minds–even if they don’t know how to ask it precisely enough–is this: “Are the differences among our human groups driven by biological differences, or are they purely environmental? When I look at the NBA, is there an over-representation of blacks because good NBA genes are commoner among blacks? When I look at academic success for STEM fields, is the over-representation of asians because genes for the skillset are more common in the asian group than in other groups? Or are these differences all due to culture, political history, racism, and so on?”
What is wrong is the pretense that discarding “race” as a useful biological term diminishes the argument that the history of human evolution and migrations lays down a reasonably clear mechanism by which some populations might contain a high prevalence for advantageous genes while other populations might have a nearly zero chance that an individual within that population would receive that (advantageously mutated) gene.
What is also wrong is the pretense that self-assignments to the “purely social” construct of race do not correlate well enough biologically to divide those SIRE groups into groups which have differing prevalences for mutated genes based (again) on historical migration patterns and consequent descendant lineages separated by tens of thousands of years. The haplogroup D variant of MCPH1 mutated after humans left africa, so individuals in the self assigned groups of “white” and “asian” have a 70% probability of carrying it; a sub saharan black has a much lesser chance of carrying it; a US black (all self-assignments here) might have an intermediate chance of carrying. But overall, as an average chance, the “black” group has a much different chance for the haplogroupD MCPH1 gene than the “white” or “asian” group even if “race” is based on a “haphazard variety of characteristics” typically centered around phenotypical appearance.
There is a practical consequence of getting it wrong. If “race is non-existent” ends up meaning “there are no biological differences among races,” and there actually are biological differences driving average outcome differences, then social policies predicated upon the presumption there are no biological differences will fail.
The test for admission to university will be an absolute standard, adjusted for opportunity. Where opportunity is normalized, no allowance will be given for racial group (see the Fisher v U Texas case). If group differences are, in fact, biological, at every opportunity level we will see the asians on top, the whites in the middle and the blacks at the bottom, and at every opportunity level asians and whites will beat out blacks for entry.
We don’t do this in analagous situations. We don’t say, “Men and women are biologically the same, so we’re only going to take the top performers on the physical tests as potential firefighters.” As a society we want to accommodate everyone, and we want to find ways to make all groups and all heritages as equal a participant in the stuff of life as possible.
Where mother nature has failed us in driving her gene pools to an egalitarian conclusion, we can find ways to build a better society than one where the accident of one’s birth is the only determinant of the potential for success.
Well, as to that, the fucking anarchist bitch Leslie Fish said it best, as often so.