Yes. Yes, we can. And you fucking know it.
Well said (his language; not yours) and so far the cockroaches have us by 100 million years.
I’m not betting evolution will give human species that long, since our intelligence has made us so successful as a species that we can no longer even feed ourselves without mechanisms that are utterly dependent upon highly advanced technology and therefore highly advanced brains…
Smart enough to take over the world and its ecosystem; smart enough to destroy it. Maybe erectus had it right. Maybe he’ll even show up again after we’ve crapped out.
“Nobody knows the future,
Or what skill betters the odds.
So it’s best to say we’re all born equal and leave the rest to the gods.”
–Leslie Fish
From an evolutionary survival-as-a-species standpoint, maybe we need biological races and we need to stop being so sensitive about them. 
Then we can get back to pointing out we’re all equal in value, a concept with which I heartily agree.
Happy New Year!
I agree, there is just one Race and that is the Human race, we are all running for the rights for all on earth( or in my opinion should be), when we try to measure others by the color of the skin, ethnic background, etc, It doesn’t help any one in the world. Peace is good for all of us. I would like to see the ‘race’ won for everyone.We all started as a sperm that won the race to the Ova or we wouldn’t be who we are.
Well, if there is a huge racial disparity in terms of who passes a firefighter or police entrance test, what is your reaction?
Do you think that it’s unhelpful to look at the test results in terms of race and therefore not worry about them? Or do you think that there must have been racial discrimination and that racial discrimination should be remedied?
CP perhaps you missed this part? I’m still interested in west African history… oh, I’m sorry (I forgot the scare quotes)… “Western Africa’s civilization”. You’ve clearly stated your knowledge in this field. Please, educate us.
I’d be more interested in CP’s views on East African history. Specifically, did his family leave Africa voluntarily, or were they forced out by one of the anti-Asian pogroms?
Because some people discriminate against another because of skin color, weight, ethnic back (ground etc. or we refer to them as racists, they seem to like to discriminate like Hiltler did in a way) thinking anyone who looks or acts differently than themselves are inferior in some way.No matter our bodies all share the same basic makeup, we can give transfusions if our blood type is the same etc. Now with scientific knowledge we can get transplants from some one of any color etc, To me at least it shows we are all of one race.
As an example: I have a son with a Phd in Physics, my knowledge of Physics is nothing ,compared to his,but I did not have the apptitude or education to study as he did. In his research group are people of all colors, an shapes. Genetics play a part, but not the racial qualities as we sometimes think of them.
Ummm, that’s not an answer to my question.
Let me repeat the question:
Suppose that there is a police or firefighter exam and white applicants score far better than black applicants.
Is it your reaction that nobody should worry about this since it is unhelpful to look at the test results in terms of race?
A simple yes or no will do.
You know, I was just thinking: Chief Pendant should be able to answer these questions for you. He’s presumably had the equivalent of a bachelor’s in biology and is very well read on this. I do not study (and have not studied) nor heard of MCPH1 previous to this thread, so I can only extrapolate what. Let’s give it a whirl:
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All humans have 1 active MCPH1 gene.
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Yes and No. It is the same iteration of the MCPH1 gene that encodes for a fully functioning protein performs its intrinsic functions.
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The claim would apply to all genes.
I want to expand on #2 as I think I think there’s a misconception on how genes work. I can’t find the information on MCPH1 in humans but MCPH1 data on mice are available, so we’ll use that for now. When RNA polymerase rolls over the MCPH1 gene in mice it’ll produce a primary transcript of about 208,058 base pairs. The primary transript is then cut with molecular scissors, then re-stitched to produce 6 mature primary transcripts consisting of a total of 15,054 base pairs between them. This means that the step from DNA to mRNA nearly 80% of the MCPH1 gene isn’t involved in producing a functional protein. While 4 primary transcripts 6 encode for functional proteins, 2 are non-coding which equal about 6876 base pairs or 45% of the coded message.
Now these four transcripts will code for functional proteins still must be processed by the ribosome. For example, ribosomes translate first primary transcript of MCPH1 from 4662 base pairs of RNA to protein of about 1544 amino acids. The endoplasmic reticulum and goldi apparatus cleave this 1544 amino acid protein to its final product of about 822 amino acids and the junk 722 amino acid product degraded. This means about 50% of the translated amino acids aren’t even in the final protein product.
I say all this to stress the insignificance of polymorphisms in defining race. Only a very small portion of mutations in genes will actually lead to changes in proteins. Proteins are what matter, it’s the color of your eyes, your skin, your fingernails, your mouth, your teeth, etc. A more fruitful exercise, although undoubtedly more expensive, would be to look at whether different races have different proteins and whether they perform better at their job than proteins isolated from other races. I suspect you’d find very few changes because genes encode for finely-honed, narrowly focused tools to perform a very specific function. If a gene encoded for a screwdriver, polymorphisms would be the equilavent of a different colored handle. You can’t turn a screwdriver into a submarine and think that this submarine will be beneficial to the organism - what’s gonna happen when the cell needs a screwdriver? You’d have a completely non-functional protein.
Sorry, buddy, I was playing nice, but now it’s time for the coup de grâce. I know that MCPH1 causes microcephaly, in fact, most mutations (and autosomal microcephaly is caused by a missense mutation) that change the translated amino acid in the final, functional protein can have an effect on the activity, localization, and/or shape on the protein. The fact that a missense, loss-of-function mutations in MCPH1 causes autosomal recessive microcephaly should show you that changes in the translated protein is what matters, not changes genes which may or may not affect final protein product, but I suspect bad habits die hard.
A cursory search on Pubmed shows that scientist have studied polymorphisms in humans have not found a correlation between MCPH1 polymorphisms and head circumference, grey matter, intelligence, cortical volume, and brain size. I’ve bolded the relevant parts.
And, finally, the coup de grâce:
Will this knowledge of there being no correlation with MCPH1 and these variables keep you from going on and on about MCPH1 as a centerpiece to your ridiculous argument in every thread; or, maybe, hopefully, will you find another gene to run to? Now, if you’ll excuse me, I need to find a purple suit, a horse, and a slice of white cake.
- Honesty
I already know what his answers would be. I’m trying to nail down your position – not his.
That’s not an answer to my question. I asked if you felt that all humans have the same pair of alleles for the MCPH1 gene.
You are stating something which is true but unresponsive to my question.
If you don’t know, please just admit your ignorance. Otherwise, please just answer the question.
Again you are evading the question.
According to you, every human has an active allele for the MCPH1 gene and an inactive allele for MCPH1 gene. I am simply asking you if that active allele is the same for all humans.
Either it’s the same for all humans or it’s not the same. Yes or no. Please answer the question.
Well in that case, why are all humans not the same like identical twins are the same?
Are you able to even grasp what I am saying? I have used MCPH1 to point out the following:
- It is an example of a nickname (MCPH1) for a gene that has many different variants, and therefore is an example of how your contention that “every human being has exactly the same genes” reflects complete ignorance or deliberate obfuscation. We don’t all have the same genes, nor do the various populations of humans have access to the same gene pools.
- MCPH1 is an example of how different populations of humans, descended from different lineages, have access to different gene pools. Eurasians have about 70% penetration of the haplogroup D variant for MCPH1; africans a negligible percent penetration. This is because the mutation for the haplogroup D variant occurred after humans migrated out of africa perhaps 60+ thousand years ago, and there has been very little geneflow of these descendant lines back into african populations.
- The marked penetrance of the haplogroup D variant of MCPH1 is suggestive, but not absolute proof, that it is an advantageous mutation because as a rule of thumb advantageous mutations achieve relative rapid, relatively high penetration. But the study for genes and intelligence is still very nascent.
You might be interested in furthering your knowledge with some reading on HMGA2. Paul Thompson’s research analyzing DNA associated with 20,000 MRIs of Europeans suggests that a single mutation–cytosine for thymine–on a single section of this gene correlates with slightly larger brain sizes and IQs 2.6 points higher for groups with two such C-for-T mutations than the population with two thymines at these positions. This IQ difference correlated with brain size difference; the groups with two cytosines had brains about 1.2% larger than the groups with thymine at both positions.
This (preliminary, but remarkable) data is the kind of study coming along that shows your grasp of genetics and mutation changes is rudimentary. Here in this example, a single mutattion causing substitution of a single amino acid causes a measurable positive effect; get the right gene from both parents and it doubles the effect.
Evolution produces thousands and thousands of these sorts of tiny changes, and sooner or later it gets some of them right. In populations lucky enough to be descendants from parents with advantageous mutations, the advantage is propagated. Populations not descended from those lucky mutations will not get the advantage (or will have to hope they get a similar mutation or some other advantageous mutation). This is how evolution works, and the pattern of human migration over the ages has conspired to separate human populations, with different gene pools, from one another.
I hope this helps your understanding, and I hope you’ll stop wasting your time researching MCPH1 and brain size in mice. I don’t care, and it has nothing to do with the arguments at hand except to show you don’t understand them.
I’m not how clear I can be: The base pair sequence of MCPH1 gene varies among and between individuals, however, the resultant protein likely does not. My analogy of the gene/screwdriver in my previous post was to illustrate that genes encode for proteins that act as molecular tools to perform a specific function. What matters is the MCPH1 protein and if you need proof of this, look at individuals who inherited the missense mutation in MCPH1 that leads to a non-functional protein product; while their heterozygote parents live a productive and healthy life. Moreover, the degenerancy of genetic code coupled with the extraordinarily long human MCPH1 gene (2.5 million nucleotides long) and alternatively spliced varients suggest that the MCPH1 gene can handle a higher-normal rate of nucleotide substitutions without deleteriously affecting protein function.
Here’s some questions I have of you, if you’d be so kind.
- If there was a polymorphism in MCPH1 (or any gene for that matter) that found to be concentrated in Europe but translates into the same protein as all the other known MCPH1 gene variants from other ethnicities, how do you parse those results under the framework that one is superior than the other?
- What kind of genetic mutations do you think exist between races? Does one race have a gene that works better? Works worse? How pervasive do you think either of these would be in the genome?
- In your opinion, what role does the environment play on the genome?
- There is evidence that blacks have bigger penises than white men. What could be the biological determinants for this? Moreoever, how do we explain white men whose penis length is over 8 inches? Could it be that most black men have a penis gene and a lesser, unknown percentage of white men have variants of this gene? Could a bigger penis increase reproductive success by increasing vaginal coital contractions and uterine thrusting onto the orgasmic platform? Why might smaller penises be unsuitable for this role?
- In relation to #4, if Ethnic group X and Y both had polymorphisms in the gene needed to synthesize testosterone, yet the enzyme (protein) was functionally the same BUT found Ethnic group X and Y had different standard deviations of penis length, how might you explain this phenomena?
- Honesty
While I am piling on, have you figured out yet that no-one disagrees that gene variants might have no, or even deleterious, effects?
What you’ve done is promote that notion to imply that there isn’t any such thing as an advantageous mutation. But there is, of course, and I’d like to hear specifically cough up that admission so that we can stop chasing a strawman. Stop wasting time pretending I don’t realize that many variants are not advantageous. Of course they aren’t. As I said before, what has that to do with anything?
I just need one of my ancestors to hit the jackpot. They don’t need to all hit. (figuratively speaking)
Ok, so in your view all of the alleles for the MCPH1 are essentially the same in the sense that they have the same effect.
You also believe that this is the case for all human genes.
It is trivial to show that your view is wrong. For example, there are evidently one or more genes which control the texture of hair. Blacks are clearly more likely than whites to have alleles which result in kinky hair.
Similarly, there are one or more genes which control blood type. Blacks are more likely than whites to have the allele which gives you type U.
Indeed, the fact that all human beings are not the same like identical twins are the same shows that your views are completely wrong and ridiculous.
I hope that you are not teaching your wrong views to anyone.
I would conclude that there is some other genetic difference which was resulting in observed racial differences which are clearly the result of genetics.
Besides the obvious genetic differences which affect things like skin color, hair texture, and facial features, there are probably a lot of other genetic differences. Probably most things about the body that (1) can be measured; and (2) varies genetically from person to person also varies genetically from race to race. Of course the most infamous difference is in the potential for intelligence.
I believe that environment and genetics both have an important role in determining the final result. Of course, as more effort is made to equalize the environments between different people, the greater the role is played by genetics.
I don’t know.
They have some combination of genes and environment which resulted in having a big penis. Duh.
Yes it could be. I would guess that women too can have a big penis gene which can be passed on to and expressed in their sons.
I don’t know.
I don’t know.
I would hypothesize that either (1) there was some difference in the average environment between ethnic groups x and y which affected penis growth; (2) there was some other difference in their genetics; or (3) some combination of (1) and (2)
Anyway, what you really need to learn is that
(1) different people often have different alleles for the same gene and these different alleles can result in measurable phenotypical differences between the people; and
(2) the same thing can apply to races, ethnic groups, and any other grouping of people you choose.
I’m really surprised you were never taught this and never figured it out on your own.
You haven’t got a clue about whether or not variant genes coding for variant MCPH1 proteins vary in structure or function (with the exception that at least one variant codes deleteriously), do you? As far as I know, it isn’t known for humans. But you are just pulling the “likely does not” phrase out of your behind.
The argument for or against race as a biological construct does not hinge on advantageous mutations of MCPH1. But there is an interesting tidbit (besides the marked prevalence of the haplogroup D variant among only the non-african human descendant lines). Among the researchers uncovering MCPH1 prevalence details is Bruce Lahn. He tackled evolutionary genetics with great enthusiasm, and after presenting his findings suggesting that evolution might have created positive selection pressure for genes related to intelligence and brain size in some populations but not others, was subjected to quite a hostile reaction from the egalitarian crowd. Lahn caved, and decided stem cell research and epigenetics were safer pursuits for a young scientist hoping for tenure.
Currently, many genetic researchers consider that there are “ethical considerations” for using genetic research to show that genes vary among human populations. If those genes vary, their functions vary (no else I’ve ever heard of buys into your notion that all genes code for about the same, or else deleterious, functions) and this represents an ethical dilemma because one’s research might end up “proving” the notion that human populations vary for ability as a result of their disparate gene pools.
Let me recommend this article on Neurobiology and Intelligence for your perusal. It’s a thoughtful approach to the problem of researching genetic underpinnings for intelligence, especially if that research leads us to uncomfortable (“incendiary” is one word the authors use) conclusions about genetic underpinnings for intelligence that vary by population.
After concluding that “the data unambiguously indicate a neurobiological basis for intelligence,” the authors raise a cautionary question. “Is it ever ethical to assess population-group (racial or ethnic) differences in intelligence?”
They go on to say, “It is easier to set aside such difficult and distasteful questions…In light of such unresolved ethical issues, many neuroscientists have been reluctant to investigate individual or group differences in intelligence. Few scientists investigate race differences in intelligence; those who do are overwhelmingly white. Under the status quo, target groups will continue to feel alienated and attacked, unimpressed by the need for freedom of inquiry when other important freedoms are lacking…” They go on to emphasize the need not to come to premature conclusions about biology driving differences among races, and to always include ethical considerations such as full consent from individuals being tested for their DNA.
Now, I agree with all of that, but I want you to consider why this “ethics” topic receives such consideration and such careful guidelines. The answer is that, at a gut level, scientists in this field consider it a likelihood that there are genetically-based differences among groups driving phenotypic outcomes that include intelligence.
If that were not the case, genetic researchers would be stumbling all over themselves to prove that every human has identical genes and those genes code for identical outcomes among identical populations. The push would be to hurry up and do that research, prove all our populations are equal genetically, and move on to fixing what would then become purely socially-driven unequal outcomes.
Instead, anyone with the courage to do research in the area of population genetics and genetic underpinnings of intelligence does so with the greatest sensitivity and disclaimers every other sentence about how their findings should not be interpreted too hastily.
Yes, with the exception of the missense mutation, of course. I had wrote out a great deal more but I think we’re at an impasse and I agree to disagree (to both of you). I’m not going to go on wild goose chases over the Internet to prove to some laymen how some obscure gene works that, by the way, has been empirically proven to not have an effect on intelligence, cranial volume, grey matter, and cortical density. Moreoever, I can’t even convince you both of the central dogma of biology. So this discussion and subsequent moving of the goal-post to another gene (new goal post: HMGA2) is like banging my head against the wall: fruitless and pointless. So I’m done.
You see, once I prove that HMGA2 isn’t involved in intelligence, Chief Pendant will undoubtedly then find another gene, then another, and another, just like he did with MCPH1. Although I’m sure you both knowledgeable in your respective fields/specialties, I don’t believe you nor him are as smart as you think are in science. Frankly, if Chief Pendant went to med school as he claims and, god-forbid, is a practicing doctor, it means the AMA has dropped the ball in setting forth a medical school curriculum that ensures M.D’s are trained - or at least exposed to - graduate-level genetics and molecular biology. This isn’t slight, it’s down right scary.
- Honesty
Suit yourself, but there is no need to look at that particular gene to see that your position is 100% ridiculous and wrong.
If your position were correct, one would expect all humans to have pretty much the same blood type just like identical twins normally have the same blood type.
Of course it’s well known that blood types vary from person to person and that blood type frequencies vary from group to group.
Similarly, if your position were correct, one would expect all people to have pretty much the same eye color just like identical twins normally have the same eye color.
That may very well be so, but it doesn’t matter. There are a number of genes which affect intelligence and for some of those genes, the frequency of particular alleles varies between blacks and whites. It’s not necessary to identify the particular genes and alleles in play to know that this is so.
Lol, nice attempt at strawmanning. There is nothing in the central dogma of molecular biology which contradicts the basic point you refuse to accept, which is that many genes have different alleles which have a measurable phenotypical effect and those alleles sometimes vary from person to person and group to group.
It’s not necessary to identify the particular genes in play. Besides which, you are claiming that all people have essentially the same alleles for all genes. Your claim is not limited to any one gene. You have assumed a heavy burden of proof, but that’s your problem – not mine.
One doesn’t have to be that smart to see that your position is ridiculous and totally wrong. I learned in 9th grade biology that there are different alleles floating around for the same gene. That’s why there are different blood types. That’s why people are not all the same like identical twins are the same.
Earlier I asked you the following question:
For all your self-proclaimed training and intelligence, you seem to be completely unable to answer that question. I can answer it. Chief Pedant can answer it. And yet you are (apparently) unable to.
Wonderful- so not only do you know for a fact what scientists in this field believe (can you read all scientists’ minds, or just neurobiologists?), they just happen to agree with you (though they have no actual genetic evidence) but don’t speak up for political concerns or whatever. How convenient for you.
It can’t be answered with a straight yes or no; any one with the qualifications should e able to get the job. Is it discrimination to use color, ethnic back ground or etc, wrong…Yes!
The wild goose chase you’ve gone on is looking for specifics of how haplogroup D MCPH1 improves intelligence when I never claimed it did. I simply claimed it was an example of a gene variant whose prevalence was markedly different from one population to the next, suggesting a positive selection pressure for a presumably advantageous gene. The enthusiasm for finding out the relationship between haplogroup D MCPH1 and intelligence waned after Bruce Lahn’s fiasco when he made the mistake of thinking such associations would be looked at as pure science, and not “sensitive” research. A key point you’ve missed with haplogroup D MCPH1 is your naked assertion that, “with the exception of missense mutation,” all genes nicknamed MCPH1 code for the same phenotypic expression. That is a ridiculous assumption, unsupported by millions of years of evolution for every other gene.
I missed where you proved that HMGA2 isn’t “involved in intelligence”; I gave you the only reference I know citing a very large study that HMGA2 cytosine for thymine substitution changes IQ measurements and brain sizes. Not only does that suggest this particular gene is involved in intelligence, it’s a pretty good example that I buy into the “central dogma of molecular biology” that DNA drives proteins which in turn drive genetically-determined phenotypic outcomes.
What is wrong with you, Honesty? Surely you are bright enough to figure out that you have not won a single argument here about genes. Here are some of the areas you might want to clear up in your own mind:
- Humans do not all have exactly the same genes.
- Changing DNA–even at the level of a single substitution–can have either a deleterious, neutral or beneficial effect on how an organism functions.
- Genes change with evolution, and descendant pools are recipients of those changes, with prevalences for the new variants driven by things such as environmental pressures. and the relative advantageousness of the new mutation for driving reproductive success.
- There are genes “involved in intelligence,” and that’s why we are smarter than cockroaches. No one I know thinks all the genes are worked out; no one I know thinks genes are unrelated to an organisms intelligence (or any other skillset).
- Gene pools for both genes and gene variants vary by population, and some of those populations have been separated by tens of thousands of years for any significant gene variant admixing.
- The functional effect of gene variants can be markedly different.
Feel free to post any cites or arguments disagreeing with the above. That’s a debate.
Mocking the AMA for “dropping the medical curriculum ball” on genetics, and setting yourself up as some sort of expert whose understanding shouldn’t be questioned by laymen, is risible. Sighing, misrepresenting the opposing position, and reiterating your own schooling without backing up your points, is a pretty lame way of supporting a position.
Since you are “done” here (and I heartily agree: you are pretty much hoist on your own petard), let me suggest something on your way out the door: No one cares about your schooling. No one cares about a claimed authority on an anonymous message board. Even in real life, no one cares about those things. Stop trying to plead your own authority and the diminished comprehension of others. Instead, focus on making a supportable point, even if you are a patent office clerk and the academics with whom you are arguing take a different position.