The same study I linked also seems to find:

"LOW CROSS-VALIDITY OF GWAS BETAS AND POLYGENIC SCORES FOR EDUCATIONAL ATTAINMENT IN AAS(African Americans:my parenthesis) "

(title of section 6)

What does it matter? Firstly, biometric modeling can incorporate epigenetics as a variance component. So pointing out that epigenetics is a possible factor does not decrease the utility of the method. In fact, it increases it. If researchers want to show the epigenetic factors account for a substantial portion of the variance in a given trait they should employ a biometric model instead of pointing to local associations.

Second, present methodologies can partition variance in a way that can exclude possible epigenetic effects. For example GCTA can not be so confounded, nor can kinship estimates of AM and dominance. Nor can estimates of share environment based on unrelated sibs reared together. Nor can estimates of measurement error. Epigenetic effects could explain some portion of unshared environment -- it would just count as another form of intrauterine effect. But so what? And it could explain some residual H^2 as H^2 - (h^2SNP + H^2D + H^2AM) but for traits like g, there is not much here. For other traits e.g., personality, that's another issue. But Hereditarians don't usually focus on these -- because there aren't large differences between the groups of interest! Indeed, given this, epigenetics could salvage some hereditarian positions, by offering an explanation for the lacks of apparent differences i.e., a masking effect.

Third, whole genome comparisons will substantially narrow the uncertainty since they will capture rare variants, which are thought by many to account for the "missing H^2kinship".

IMO, you're being silly.

(Also, as I have noted numerous times, epigenetic differences are perfectly consistent with a racialist model since, for one, early such models prior to Darwin (who adopted a Lamarckian frame) were mostly epigenetic, at least when races were conceptualized as intraspecfic divisions.)

The findings related to the relatively poor, but non-zero cross-validity of GWAS betas between European and African samples throw some doubt on the SNP evidence found by Piffer in his studies of the population/country IQ and cognitive ability SNP factors (29). If the betas for the SNPs identified in European sample GWAS do not work well as predictors for Africans, they would be equally unsuitable for estimating mean genotypic cognitive ability from SNP frequencies. Thus, further research is needed to more precisely estimate the cross-racial validity of GWAS betas, especially with regards to African vs. Eurasian samples."

There results are not very informative since the studies looked at different trait associated alleles. Thus, there was an apples to oranges comparison. The African-European comparisons concerned primarily Asthma related alleles, which show low replicability across all populations. You would want to compare the effect of alleles associated with the same traits, for example height, to get a sense if associations that replicated between Asians and Europeans also did between European and Africans. (I pointed this out to Emil, but he neglected to comment on the issue.)

Regarding the alleles for cognitive ability, the association -- at least with regards to cognitive scores -- has been replicated in an East Asian sample and in a nationally representative African American one.

Do the MZ pairs with more mutations between them (in their brain tissue) differ more in cognitive ability? (Controlling for age.)

This has been done, with negative results. "CNV concordance rates were compared between the different sources of DNA, and gene-enrichment association analyses were conducted for thought problems (TP) and attention problems (AP) using CNVs concordant within MZ pairs. he gene-enrichment analyses on concordant CNVs showed no significant associations between CNVs overlapping with genes involved in neuronal processes and TP or AP after accounting for the source of DNA."

This is another blow to the mutation-load theory of intelligence, especially after the finding that paternal age isn't related to offspring IQ.
Twin Research and Human Genetics: http://dx.doi.org/10.1017/thg.2014.86

The same study I linked also seems to find:

"LOW CROSS-VALIDITY OF GWAS BETAS AND POLYGENIC SCORES FOR EDUCATIONAL ATTAINMENT IN AAS(African Americans:my parenthesis) "

(title of section 6)

You realize that you are quoting my paper, right? :)

Yes.

It's unfortunate that such a statement is becoming so popular among anti-hbd folks, because in my opinion it is wrong. Differences in LD should simply reduce the observed allele frequencies differences between populations. There is no reason why these should be smaller than they appear. Correction for attenuation due to different LD should actually make the results observed by Piffer even stronger.
Edit: by observed I mean "at the sampled SNPs"..by real I meant "at the real CAUSAL variants". So correction for attenuation will increase race differences at causal variants compared to differences at the observed variants (which are in LD with the causal variants)".

Yes, and I had already thought about this ( I would not have criticized your thought if the GWAS hits had frequencies above 50%): it depends on how it deviates from the background frequency of SNPs. As a matter of fact, the average frequency of the IQ increasing alleles is lower than that of the other alleles, which has to be 50% for obvious mathematical reasons.So the systematic error works the opposite direction from what you predicted. You should edit your paper or people will keep citing that wrong argument. Look at table 1 and table 5 (the top hits actually have a much lower than 50% freq): (https://docs.google.com/document/d/1BUmH0WHAfjpmTrChX-yUB9jnh8p7kG2x8V4KSEyy5PU/edit?usp=sharing). The frequency is about 50%, slightly less so (49%). Same with top hits (table 5).

You could have changed it if you had not archived it already. Normally one waits to get some feedback before archiving on Winnower. Now critics will keep citing that paper, I am not sure how much it would help to have a reply paper.

The study appears to claim that the alleles for those traits correlated well between Asians and Europeans but less so for Africans.

Again, it depends on the trait. And on what one means by "replicate". In Ntzani et al. table 2 (attached) ~19/24 = 80% SNPs go in same direction for Eu and Afr and ~80/97= 82% for Eu and Asians. I would have to examine in detail why Marigorta et al., seem to find different results. For them, though, "replicate" means "go in the same direction" and "meet a p-value".

Which is the African American study. Do you have a link?

The r(SNP-IQ) was ~ the same for AfrAm and EuAm. The r(SNP-edu) was lower for AfrAm but in the same direction, which is what matters. SNPg is not necessarily a good predictor of African American edu for a number of reasons so I wouldn't make much of the discrepancy.