And the fact that biracial children do better on IQ when the mother is the white parent than when the mother is black seems strong evidence to me that genetics are not the whole story, if they play any part at all.
It is not evidence for that at all; an alternative explanation for the difference is that a child’s intelligence depends to a significant degree on the prenatal environment, which is determined by the mother’s genetics exclusively. I predict that the extra degree of correlation between a mother’s and child’s intelligence over the correlation between a father’s and child’s intelligence will be very close to equal to the degree of correlation between a genetically unrelated surrogate mother and child’s intelligence.
renatal environment, which is determined by the mother’s genetics exclusively.
Err, what? Smoking? Just to name the most obvious counter example.
Mitochondrial DNA would also be a possibility (“white” mitochondria being optimized for neurons, “black” mitochondria for muscle cells, say), but environmental factors seems by far the most obvious explanation.
I don’t know as I’d call that a possibility, insofar as African populations have the widest variety of mitochondrial haplogroups (black vs white mitochondria? That’s not biology, that’s indulging the hypothesis so much you’re willing to commit mental gymnastics on its behalf...)
African populations also have the greatest genetic variation in general. African Americans have somewhat less (but still a lot of) variation. African Americans also have considerable European ancestry, but little in the female line, and in so far as they have mtDNA of (recent) African origin they all have in common that they lack mtDNA of Euopean origin (which might have innovations that contribute to the effect observed). If you are willing to assume a genetic cause I don’t see how you can a priori exclude a mitochondrial cause. I already made clear that it’s not a hypothesis I’d ascribe much probability mass to.
I’m not ruling it out a priori, I’m ruling it out based on domain-specific knowledge. There is no reason from first principles of predicate logic to assume half the stuff that’s true and important in biology, but it’s no less critical to reasoning correctly in that domain.
Ok, using the term a priori was imprecise. I’m not sure what I should have said instead, I can’t think of anything that’s both reasonably concise and meeting your apparent standards for precision. Maybe “it seems unreasonable that your prior for the hypothesis “a statistically traceable part of racial IQ variation is caused by mitochondrial DNA variation” should be so close to zero that the posterior probability assuming above evidence still is not even worth calling a possibility.”?
-Mitochondrial DNA has 16,569 base pairs but only 13 of them code for protein (and most of those are dedicated to the electron transport chain, a pretty darn fundamental thing), so while the mutation rate of mtDNA is higher than nuclear DNA there’s a limited number of possible variations that will have an effect. There’s also a very constrained number of functional changes; most mutations of the protein-coding genes correspond to known mitochondrial diseases, which vary in their effects but do so on the basis of impaired mitochondrial activity globally. When mtDNA protein-coding regions shift, the result is usually one of the many known mitochondrial diseases, and it’s under those conditions that you see a strong variance in the expressed protein-coding mtDNA between different organs of the body. When mitochondrial genetics produces varying effects between different tissues, it’s not subtle—you’re basically talking about major, life-threatening illnesses or mosaic genetics here. Neither are common conditions; it’s difficult to imagine a functional shift in protein-coding for this producing a subtle effect that remains undetectable for a long time.
-mtDNA recombines with itself during reproduction, so mutations along the mitochondrial line are very easily tracked (indeed, it’s why we know what we do about human mitochondrial haplogroups, and why we can so readily understand which populations vary genetically by how much and when they seperated). Because one’s mtDNA is not specific to the individual, there’s a low effective population size for mtDNA changes While this does make it relatively easy for such changes to propagate upon mutation, it also makes them harder to miss when you go looking, and changes to protein-coding regions are even more obvious because there’s only a few of them and mutations to those usually affect very fundamental elements of cytochemistry.. The suggestion that IQ differences stem from a mitochondrial DNA shift implies that it would be very, very easy to spot and isolate the character responsible. We know a lot about mtDNA and the limited number of functional changes it displays. There’s nothing even vaguely like the proposed change sitting in the pool of known variations, and the pool of plausible unknown variations that just happen to look like that seems vanishingly small.
You’re right that that was too strong; I should have said it’s determined largely by the mother’s genetics (but also to lesser degrees by the father’s genetics and environmental factors.) But note that the strongest known environmental factor, alcohol consumption, is at least somewhat genetic (http://psychiatry.healthse.com/psy/more/alcoholism), and other factors like susceptibility to smoking addiction probably are as well.
Any given chemical is not equally likely to cause pleasure for human beings, so of course alcohol and nicotine consumption have a genetic basis. It seems equally obvious that the availability of alcohol and nicotine are part of the environment. Additionally, they are parts of the environment where it is easy to imagine life being substantially similar without them (unlike environmental influences such as oxygen and gravity).
As the mother is usually the more involved parent when it comes to raising the child, mother-based differences strongly suggest nurture-based differences, unless of course there is some specific and identifiable pathway by which the mother’s genetic composition could play an outsized role. I’m not aware of any evidence that the prenatal environment provided by black women is systematically different from that of white women for any genetic reason. Though, in your defense, you were decent enough to make a falsifiable prediction based on this.
It is not evidence for that at all; an alternative explanation for the difference is that a child’s intelligence depends to a significant degree on the prenatal environment, which is determined by the mother’s genetics exclusively. I predict that the extra degree of correlation between a mother’s and child’s intelligence over the correlation between a father’s and child’s intelligence will be very close to equal to the degree of correlation between a genetically unrelated surrogate mother and child’s intelligence.
It may not be proof, but it’s certainly evidence.
Err, what? Smoking? Just to name the most obvious counter example.
Mitochondrial DNA would also be a possibility (“white” mitochondria being optimized for neurons, “black” mitochondria for muscle cells, say), but environmental factors seems by far the most obvious explanation.
I don’t know as I’d call that a possibility, insofar as African populations have the widest variety of mitochondrial haplogroups (black vs white mitochondria? That’s not biology, that’s indulging the hypothesis so much you’re willing to commit mental gymnastics on its behalf...)
African populations also have the greatest genetic variation in general. African Americans have somewhat less (but still a lot of) variation. African Americans also have considerable European ancestry, but little in the female line, and in so far as they have mtDNA of (recent) African origin they all have in common that they lack mtDNA of Euopean origin (which might have innovations that contribute to the effect observed). If you are willing to assume a genetic cause I don’t see how you can a priori exclude a mitochondrial cause. I already made clear that it’s not a hypothesis I’d ascribe much probability mass to.
I’m not ruling it out a priori, I’m ruling it out based on domain-specific knowledge. There is no reason from first principles of predicate logic to assume half the stuff that’s true and important in biology, but it’s no less critical to reasoning correctly in that domain.
Ok, using the term a priori was imprecise. I’m not sure what I should have said instead, I can’t think of anything that’s both reasonably concise and meeting your apparent standards for precision. Maybe “it seems unreasonable that your prior for the hypothesis “a statistically traceable part of racial IQ variation is caused by mitochondrial DNA variation” should be so close to zero that the posterior probability assuming above evidence still is not even worth calling a possibility.”?
My prior is based on the following:
-Mitochondrial DNA has 16,569 base pairs but only 13 of them code for protein (and most of those are dedicated to the electron transport chain, a pretty darn fundamental thing), so while the mutation rate of mtDNA is higher than nuclear DNA there’s a limited number of possible variations that will have an effect. There’s also a very constrained number of functional changes; most mutations of the protein-coding genes correspond to known mitochondrial diseases, which vary in their effects but do so on the basis of impaired mitochondrial activity globally. When mtDNA protein-coding regions shift, the result is usually one of the many known mitochondrial diseases, and it’s under those conditions that you see a strong variance in the expressed protein-coding mtDNA between different organs of the body. When mitochondrial genetics produces varying effects between different tissues, it’s not subtle—you’re basically talking about major, life-threatening illnesses or mosaic genetics here. Neither are common conditions; it’s difficult to imagine a functional shift in protein-coding for this producing a subtle effect that remains undetectable for a long time.
-mtDNA recombines with itself during reproduction, so mutations along the mitochondrial line are very easily tracked (indeed, it’s why we know what we do about human mitochondrial haplogroups, and why we can so readily understand which populations vary genetically by how much and when they seperated). Because one’s mtDNA is not specific to the individual, there’s a low effective population size for mtDNA changes While this does make it relatively easy for such changes to propagate upon mutation, it also makes them harder to miss when you go looking, and changes to protein-coding regions are even more obvious because there’s only a few of them and mutations to those usually affect very fundamental elements of cytochemistry.. The suggestion that IQ differences stem from a mitochondrial DNA shift implies that it would be very, very easy to spot and isolate the character responsible. We know a lot about mtDNA and the limited number of functional changes it displays. There’s nothing even vaguely like the proposed change sitting in the pool of known variations, and the pool of plausible unknown variations that just happen to look like that seems vanishingly small.
I don’t know about exclusively.
You’re right that that was too strong; I should have said it’s determined largely by the mother’s genetics (but also to lesser degrees by the father’s genetics and environmental factors.) But note that the strongest known environmental factor, alcohol consumption, is at least somewhat genetic (http://psychiatry.healthse.com/psy/more/alcoholism), and other factors like susceptibility to smoking addiction probably are as well.
Maternal Stress affects offspring.
So does malnutrition.
Any given chemical is not equally likely to cause pleasure for human beings, so of course alcohol and nicotine consumption have a genetic basis. It seems equally obvious that the availability of alcohol and nicotine are part of the environment. Additionally, they are parts of the environment where it is easy to imagine life being substantially similar without them (unlike environmental influences such as oxygen and gravity).
As the mother is usually the more involved parent when it comes to raising the child, mother-based differences strongly suggest nurture-based differences, unless of course there is some specific and identifiable pathway by which the mother’s genetic composition could play an outsized role. I’m not aware of any evidence that the prenatal environment provided by black women is systematically different from that of white women for any genetic reason. Though, in your defense, you were decent enough to make a falsifiable prediction based on this.