Thank you. I recently started a graph to keep track of the failures and propaganda of the Eugenics movement, and I'm glad to have your article in there. This will grow, and I plan to always have the product to share as I fill it in.
Thank you for an excellent post. I dimly remember being taught not take classical heritability estimates seriously in genetics class. After reading this series, I think I understand why. And I got updated on some really cool research that I would never have read by myself, let alone be able to fully comprehend. We need more science communication like this.
Great post, extremely helpful — thank you Sasha, we needed that.
A question for you: are these newer models still mostly linear? How would you answer the objection that genome expression might be highly non-linear?
(Apart from saying that twin studies also assume linearity... I'm asking the question from the broader perspective of understanding the limitations of the state of the art.)
Yes, almost all of these models are only really interpretable under an assumption that the phenotype is fairly linear and normal-like; with some of the heritability models explicitly assuming the phenotype comes from a multivariate normal. That's on the phenotype side. On the genetics side, however, the evidence for non-linearity of genetic effects *on top* of additive genetic effects is very slim. The heritability of dominance is basically zero, for example. And a recent very large study of height found negligible gene-gene interaction when looking at top variants. Additivity on the genetic side does not mean additivity on the biological side though, it just means that the effect is additive *on average*, each individual almost certainly has extensive biological non-linearity.
There might be a deep explanation for the normal-like behavior (eg, homeostatis can't afford too much non-linearity). This might also be an aspect where social "phenotypes" differ from raw biological phenotypes: wealth can be Pareto, but height can't be. Intelligence might sit somewhere in between, as it involves a complex edifice of cultural scaffolding.
> Surprisingly, while these findings made a big splash among geneticists and were seen as essentially a coup de grâce in the heritability debate
This is a big claim and perhaps the most important claim in your post. Yet it is not substantiated with any sources. What's the evidence that the view "among geneticists" is that this paper has ended the "heritability debate"?
Thanks for writing this article, but If intelligence is not highly genetically heritable, how was it naturally selected for in our past? A trait needs to have meaningful (as in, impacts the organisms life and reproductive success) variance within a population to be selected for.
There's little to no evidence that intelligence has been under strong selection and the evidence that is there suggests stabilizing selection (which is itself very slow). For example from a study led by David Reich:
"Thus, our results provide evidence against a model in which one or a few mutations were responsible for the rapid developments in human behaviour in the last 50,000 years. Instead, changes in lifestyles due to cultural innovation or exposure to new environments are likely to have been driving forces behind the rapid transformations in human behaviour in the last 50,000 years"
So it may have been under slow selection for a very long time (100s of thousands of years), or the variants that were under selection fixed quickly prior to 50kya and were then present/absent in nearly all humans, or it is under complex stabilizing selection that is very hard to identify.
> our results provide evidence against a model in which one or a few mutations were responsible for the rapid developments in human behaviour in the last 50,000 years. Instead, changes in lifestyles due to cultural innovation or exposure to new environments are likely to have been driving forces behind the rapid transformations in human behaviour in the last 50,000 years
I already didn't believe what that quote argues against, and it doesn't actually address my question very well. I don't think your sentence is backed up by what's written.
> There's little to no evidence that intelligence has been under strong selection and the evidence that is there suggests stabilizing selection (which is itself very slow). For example from a study led by David Reich:
I don't have access to the article, and the abstract doesn't help that line of reasoning. If part of it supports your above sentence can you quote it?
Given all the factors that go into intelligence, (eg something as unrelated as immune system, uptake of any nutrient shown to impact intelligence... all of them?, etc.), it seems implausible that genes impacting intelligence could have ALL reached fixation across groups. In fact I think the abstract helps my case here:
> Our analysis reveals key features of the landscape of human genome variation, including that the rate of accumulation of mutations has accelerated by about 5% in non-Africans compared to Africans since divergence. We show that the ancestors of some pairs of present-day human populations were substantially separated by 100,000 years ago, well before the archaeologically attested onset of behavioural modernity. We also demonstrate that indigenous Australians, New Guineans and Andamanese do not derive substantial ancestry from an early dispersal of modern humans; instead, their modern human ancestry is consistent with coming from the same source as that of other non-Africans.
Hmm, I guess I don't understand your question if a section titled "No species-wide sweeps in modern humans" is not addressing it. Perhaps you can clarify what specific examples of selection on intelligence you are talking about.
I think we have seen this in everyday life. Einstein's family wasn't spectacular, there was a series of failed business enterprises etc. his son, Hans Albert was an esteemed professor but not really anyone famous. His other son ended up in an insane asylum.
We just don't see these "Nobel Prize clans" anywhere. James Woods, IQ 190, mother ran a preschool, father was a CIA officer. And so on. What we see is moderately intellectual parents who probably did emphasize education, but not stellar successes.
"Most of the reported IQ GWAS use data from the UK Biobank (or similar biobank cohorts) and, lucky for us, Fawns-Ritchie and Deary (2020) retested a subset of these individuals. The resulting test-retest correlation was 0.82 for the general factor of intelligence, which is typically considered high."
The resulting test-retest correlation ranged from 0.409 to 0.887, mean Pearson r = 0.55.
The 0.8 correlation you report is between PCA-extracted g factor on UK Biobank tests and PCA-extracted g factor on reference tests (i.e. standard cognitive tests paralel to UK Biobank tests), measured at the same time point.
No, I ran this analysis myself using the data from Fawns-Ritchie et al. you can see the figure here ("Retest and age stability of IQ and the general factor"):
Thanks for this. I started out disagreeing with you, but I feel like I've learned a lot from reading your posts. I have a few questions, though, if you don't mind.
First, a question about the citation to Young (2018). This study seems to be about educational attainment and height, not IQ. I understand that IQ and educational attainment are correlated, but they're not the same thing. Has Young's method been used to study cognitive ability? If so, this would help clarify whether cognitive ability is in fact less heritable than height.
Second, I'm a layman and thus can't evaluate your appeals to expert consensus. Is there any evidence that your view is closer to the expert consensus now? In other fields, there are occasionally surveys of experts that provide a sense of where the field is. Does this kind of evidence exist here?
Third, what is going on with these studies coming out in Nature that suggest that rare variants explain missing heritability? The studies that you cite seem to say otherwise. I'm at a loss to say who is right. I'm thinking of studies like:
These studies seem to suggest that rare variants can fill in much of the missing heritability. Are these studies incorrect? If Young solved the missing heritability problem, why do you think that these studies are still coming out?
Thanks for reading with an open mind! With respect to Young / RDR, while they do apply to educational attainment (and find much lower numbers than twin studies) the individual trait estimates are still very noisy, which is why I think the most definitive estimate is the average across traits. RDR has unfortunately not been applied extensively, in part because the unique IBD data is only available in small + highly genotyped populations like Iceland. A recent application looking at school grades (typically very genetically correlated with IQ) showed consistent results - 10% direct heritability vs ~20% indirect - but this was only looking at genotyped/common variation not IBD (https://x.com/krichard1212/status/1809659789439381947). Likewise, the Howe et al. 2022 paper I cited in the original post also showed a significant indirect component for IQ. So the evidence for substantial indirect effects on cognitive phenotypes is thoroughly replicated, in my opinion, but an RDR-style within-family analysis of whole genome data has not been conducted.
Regarding the other papers you cited. The Wainschtein and Jang et al. papers are estimates in the population rather than within families, so are still susceptible to all of the issues of environmental confounding and population structure, they also produced standard errors that were too wide for any definitive interpretation (see my discussion here: http://gusevlab.org/projects/hsq/#h.fdgs3vw8a1ve, and Alex Young writing about the challenges interpreting the results here: https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1008222). Hill et al. is the paper that relies on kinship models I talked about in the article (
https://theinfinitesimal.substack.com/i/148251755/what-about-kinship-studies-why-do-we-need-to-control-for-relatedness ), it is again not a within-family study and so in the presence of indirect effects it becomes hugely inflated and is uninterpretable. Part of the reason these studies are still coming out is the data and methods are available, so people will run them. The other part is that the understanding of indirect effects and within-family analyses is still fairly new, and most of these studies (Hill and Wainschtein) were conducted before these issues were even known.
There have not been any surveys of experts on this topic that I'm aware of. To be honest, even though I find the question fascinating from a meta-science perspective, it's not one that geneticists care all that much about. Even if rare variants explain very little heritability, people will still run whole-genome studies because finding *any* rare variants can point to useful mechanisms. Most likely in the next few years there will be enough sibling data to get precise within-family estimates -- reproducing the Young/RDR analysis a few more times -- and put the question to rest from the molecular genetics side. Whether that becomes the consensus more broadly we will have to see.
Thanks for the thoughtful and comprehensive reply! You've given me alot to think about. A few quick thoughts. In trying to make sense of this debate, I listened to Alexander Young talk about his own research.
At least in this interview, he had a different interpretation than you seem to have. He said that the jury is still out on whether his study or the twin studies are closer to the truth, and he suggested that the truth is probably somewhere in the middle. In any event, he apparently doesn't think that the missing heritability problem has been definitively solved. In fact, he suggests that rare variants may have an important role to play. Perhaps he's wrong about his own research, but I thought this was interesting.
My heuristic/bias is that I'm wary about relying on any individual study to arrive at a conclusion on this issue. And I find that I remain confused about this debate!
I think it is true that "the jury is still out" on this question because people are clearly still debating it. Certainly twin researchers have not abandoned their work and continue to publish twin study estimates of heritability as if they are highly precise. You should not rely on a single study, but in the post I talked about a convergence of multiple studies that are consistent with the RDR estimate: Young 2018 (RDR); Bingley 2023 (twin study with equal environment assumption relaxed), Weiner 2023 (rare burden heritability), Schoech 2019 (low frequency variant analysis), and Chen 2023 (direct rare burden scan). As far as I am aware no one has identified any fundamental flaws in these analyses or conducted independent studies that refute them. So I think the preponderance of evidence continues to be support the Young et al. RDR findings.
Great, thank you. One remaining question I have is about the studies of rare variants that you cite in your last comment. Earlier, you said that other studies of rare variants at the population level "are estimates in the population rather than within families, so are still susceptible to all of the issues of environmental confounding and population structure." Would this same concern apply to some of the studies that you cited in your above comment? I'm not sure why these studies escape these problems. I may very well be missing something, but most of these studies don't seem to use within-family data.
Good point and it is study specific. Young is within family obviously. Bingley is a twin study. Weiner accounts for population structure but not indirect effects. Schoech + Chen is susceptible to both. However, the studies that do not account for environmental confounding (Weiner, Schoech, Chen) all demonstrate that the contribution from rare variants is already low, so it would only expected to be even lower if this extra confounding was removed. In contrast, a study like Hill et al. estimates the kinship "heritability" for a phenotype could be high, but uses an estimator that can be inflated by 2x or 3x by indirect effects. Upward bias in the rare variant studies only makes the finding that rare variants explain very little heritability more striking.
I read through both articles, though in this one I skipped over some sections, and I did not see a lot of discussion on IQ test design itself and the variability it can introduce (e.g., SAT vs Raven's). You do mention how tests are normalized to a population, but I didn't see anything discussing how many "IQ" tests have strong assumptions about education/culture baked into the tests themselves.
The worst I have seen of this is people calling the SAT an "IQ test" because it is "correlated with positive life outcomes", even though it is essentially a knowledge test at best, memorization test at worst.
Has any of the types of analysis you discuss been done on a limited dataset that tries to only use tests with as little dependence on life experience as possible (like Raven's)? An ideal test seems like one you can give to a child that is old enough to see and point at things and can understand the concept of "correct answer", but otherwise has no educational/cultural history. If so, do the results come out the same?
I agree that IQ tests have very strong assumptions and it is difficult to make any definitive statements because the tests can be very different. Even though they are not intended to test "general knowledge" they are often still highly correlated with culturally-specific questions: http://gusevlab.org/projects/hsq/#h.pqhr9q81wgd5
I talk about measurement error a bit at the end here:
I've yet to see an example where GWAS heritability increased substantially because a better IQ test was used. In instances where people have looked at more "fluid" like subtests, like memory or reaction time, the heritability of those is *much* lower than that of an overall IQ test or a general factor. For example, see Supp Table 2 of https://pubmed.ncbi.nlm.nih.gov/32895543/, where the Verbal Numeric Reasoning test (which includes general knowledge / SAT-type questions) has much higher heritability than all of the more basic subtests. We do not have direct effect estimates for these subtests but in general it looks like the less cultural a test is, the less heritable it is.
Right, one cold hard truth is that we currently do not have any methods or data to outperform the prediction accuracy set by the GWAS heritability + the rare burden heritability. Even for people who believe there is missing heritability still out there, we would not currently have any way to leverage it for prediction. I do think the broader biological questions of how much rare variant heritability there is in truth and how much Gene-Environment interaction are interesting, of course.
Thank you. I recently started a graph to keep track of the failures and propaganda of the Eugenics movement, and I'm glad to have your article in there. This will grow, and I plan to always have the product to share as I fill it in.
https://embed.kumu.io/8ef99af0bd6e6efa398aef8698828a5a
"Robert Plomin tends to make shit up"
Sometimes the truth hurts.
Thank you for an excellent post. I dimly remember being taught not take classical heritability estimates seriously in genetics class. After reading this series, I think I understand why. And I got updated on some really cool research that I would never have read by myself, let alone be able to fully comprehend. We need more science communication like this.
Great post, extremely helpful — thank you Sasha, we needed that.
A question for you: are these newer models still mostly linear? How would you answer the objection that genome expression might be highly non-linear?
(Apart from saying that twin studies also assume linearity... I'm asking the question from the broader perspective of understanding the limitations of the state of the art.)
Yes, almost all of these models are only really interpretable under an assumption that the phenotype is fairly linear and normal-like; with some of the heritability models explicitly assuming the phenotype comes from a multivariate normal. That's on the phenotype side. On the genetics side, however, the evidence for non-linearity of genetic effects *on top* of additive genetic effects is very slim. The heritability of dominance is basically zero, for example. And a recent very large study of height found negligible gene-gene interaction when looking at top variants. Additivity on the genetic side does not mean additivity on the biological side though, it just means that the effect is additive *on average*, each individual almost certainly has extensive biological non-linearity.
Thank you Sasha, very clear and informative.
There might be a deep explanation for the normal-like behavior (eg, homeostatis can't afford too much non-linearity). This might also be an aspect where social "phenotypes" differ from raw biological phenotypes: wealth can be Pareto, but height can't be. Intelligence might sit somewhere in between, as it involves a complex edifice of cultural scaffolding.
> Surprisingly, while these findings made a big splash among geneticists and were seen as essentially a coup de grâce in the heritability debate
This is a big claim and perhaps the most important claim in your post. Yet it is not substantiated with any sources. What's the evidence that the view "among geneticists" is that this paper has ended the "heritability debate"?
Thanks for writing this article, but If intelligence is not highly genetically heritable, how was it naturally selected for in our past? A trait needs to have meaningful (as in, impacts the organisms life and reproductive success) variance within a population to be selected for.
There's little to no evidence that intelligence has been under strong selection and the evidence that is there suggests stabilizing selection (which is itself very slow). For example from a study led by David Reich:
"Thus, our results provide evidence against a model in which one or a few mutations were responsible for the rapid developments in human behaviour in the last 50,000 years. Instead, changes in lifestyles due to cultural innovation or exposure to new environments are likely to have been driving forces behind the rapid transformations in human behaviour in the last 50,000 years"
https://www.nature.com/articles/nature18964#Sec7
So it may have been under slow selection for a very long time (100s of thousands of years), or the variants that were under selection fixed quickly prior to 50kya and were then present/absent in nearly all humans, or it is under complex stabilizing selection that is very hard to identify.
> our results provide evidence against a model in which one or a few mutations were responsible for the rapid developments in human behaviour in the last 50,000 years. Instead, changes in lifestyles due to cultural innovation or exposure to new environments are likely to have been driving forces behind the rapid transformations in human behaviour in the last 50,000 years
I already didn't believe what that quote argues against, and it doesn't actually address my question very well. I don't think your sentence is backed up by what's written.
> There's little to no evidence that intelligence has been under strong selection and the evidence that is there suggests stabilizing selection (which is itself very slow). For example from a study led by David Reich:
I don't have access to the article, and the abstract doesn't help that line of reasoning. If part of it supports your above sentence can you quote it?
Given all the factors that go into intelligence, (eg something as unrelated as immune system, uptake of any nutrient shown to impact intelligence... all of them?, etc.), it seems implausible that genes impacting intelligence could have ALL reached fixation across groups. In fact I think the abstract helps my case here:
> Our analysis reveals key features of the landscape of human genome variation, including that the rate of accumulation of mutations has accelerated by about 5% in non-Africans compared to Africans since divergence. We show that the ancestors of some pairs of present-day human populations were substantially separated by 100,000 years ago, well before the archaeologically attested onset of behavioural modernity. We also demonstrate that indigenous Australians, New Guineans and Andamanese do not derive substantial ancestry from an early dispersal of modern humans; instead, their modern human ancestry is consistent with coming from the same source as that of other non-Africans.
Hmm, I guess I don't understand your question if a section titled "No species-wide sweeps in modern humans" is not addressing it. Perhaps you can clarify what specific examples of selection on intelligence you are talking about.
I think we have seen this in everyday life. Einstein's family wasn't spectacular, there was a series of failed business enterprises etc. his son, Hans Albert was an esteemed professor but not really anyone famous. His other son ended up in an insane asylum.
We just don't see these "Nobel Prize clans" anywhere. James Woods, IQ 190, mother ran a preschool, father was a CIA officer. And so on. What we see is moderately intellectual parents who probably did emphasize education, but not stellar successes.
"Most of the reported IQ GWAS use data from the UK Biobank (or similar biobank cohorts) and, lucky for us, Fawns-Ritchie and Deary (2020) retested a subset of these individuals. The resulting test-retest correlation was 0.82 for the general factor of intelligence, which is typically considered high."
The resulting test-retest correlation ranged from 0.409 to 0.887, mean Pearson r = 0.55.
The 0.8 correlation you report is between PCA-extracted g factor on UK Biobank tests and PCA-extracted g factor on reference tests (i.e. standard cognitive tests paralel to UK Biobank tests), measured at the same time point.
https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0231627&type=printable
No, I ran this analysis myself using the data from Fawns-Ritchie et al. you can see the figure here ("Retest and age stability of IQ and the general factor"):
http://gusevlab.org/projects/hsq/#h.pqhr9q81wgd5
and the code is here:
https://github.com/gusevlab/hsq_ancestry_examples/blob/main/iq/visualizations.R#L24
Thanks for this. I started out disagreeing with you, but I feel like I've learned a lot from reading your posts. I have a few questions, though, if you don't mind.
First, a question about the citation to Young (2018). This study seems to be about educational attainment and height, not IQ. I understand that IQ and educational attainment are correlated, but they're not the same thing. Has Young's method been used to study cognitive ability? If so, this would help clarify whether cognitive ability is in fact less heritable than height.
Second, I'm a layman and thus can't evaluate your appeals to expert consensus. Is there any evidence that your view is closer to the expert consensus now? In other fields, there are occasionally surveys of experts that provide a sense of where the field is. Does this kind of evidence exist here?
Third, what is going on with these studies coming out in Nature that suggest that rare variants explain missing heritability? The studies that you cite seem to say otherwise. I'm at a loss to say who is right. I'm thinking of studies like:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9119698/
https://pubmed.ncbi.nlm.nih.gov/29321673/
https://www.nature.com/articles/s41562-022-01408-5
These studies seem to suggest that rare variants can fill in much of the missing heritability. Are these studies incorrect? If Young solved the missing heritability problem, why do you think that these studies are still coming out?
Thanks for reading with an open mind! With respect to Young / RDR, while they do apply to educational attainment (and find much lower numbers than twin studies) the individual trait estimates are still very noisy, which is why I think the most definitive estimate is the average across traits. RDR has unfortunately not been applied extensively, in part because the unique IBD data is only available in small + highly genotyped populations like Iceland. A recent application looking at school grades (typically very genetically correlated with IQ) showed consistent results - 10% direct heritability vs ~20% indirect - but this was only looking at genotyped/common variation not IBD (https://x.com/krichard1212/status/1809659789439381947). Likewise, the Howe et al. 2022 paper I cited in the original post also showed a significant indirect component for IQ. So the evidence for substantial indirect effects on cognitive phenotypes is thoroughly replicated, in my opinion, but an RDR-style within-family analysis of whole genome data has not been conducted.
Regarding the other papers you cited. The Wainschtein and Jang et al. papers are estimates in the population rather than within families, so are still susceptible to all of the issues of environmental confounding and population structure, they also produced standard errors that were too wide for any definitive interpretation (see my discussion here: http://gusevlab.org/projects/hsq/#h.fdgs3vw8a1ve, and Alex Young writing about the challenges interpreting the results here: https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1008222). Hill et al. is the paper that relies on kinship models I talked about in the article (
https://theinfinitesimal.substack.com/i/148251755/what-about-kinship-studies-why-do-we-need-to-control-for-relatedness ), it is again not a within-family study and so in the presence of indirect effects it becomes hugely inflated and is uninterpretable. Part of the reason these studies are still coming out is the data and methods are available, so people will run them. The other part is that the understanding of indirect effects and within-family analyses is still fairly new, and most of these studies (Hill and Wainschtein) were conducted before these issues were even known.
There have not been any surveys of experts on this topic that I'm aware of. To be honest, even though I find the question fascinating from a meta-science perspective, it's not one that geneticists care all that much about. Even if rare variants explain very little heritability, people will still run whole-genome studies because finding *any* rare variants can point to useful mechanisms. Most likely in the next few years there will be enough sibling data to get precise within-family estimates -- reproducing the Young/RDR analysis a few more times -- and put the question to rest from the molecular genetics side. Whether that becomes the consensus more broadly we will have to see.
Thanks for the thoughtful and comprehensive reply! You've given me alot to think about. A few quick thoughts. In trying to make sense of this debate, I listened to Alexander Young talk about his own research.
https://www.youtube.com/watch?v=qeTSmMOm7CM
At least in this interview, he had a different interpretation than you seem to have. He said that the jury is still out on whether his study or the twin studies are closer to the truth, and he suggested that the truth is probably somewhere in the middle. In any event, he apparently doesn't think that the missing heritability problem has been definitively solved. In fact, he suggests that rare variants may have an important role to play. Perhaps he's wrong about his own research, but I thought this was interesting.
My heuristic/bias is that I'm wary about relying on any individual study to arrive at a conclusion on this issue. And I find that I remain confused about this debate!
I think it is true that "the jury is still out" on this question because people are clearly still debating it. Certainly twin researchers have not abandoned their work and continue to publish twin study estimates of heritability as if they are highly precise. You should not rely on a single study, but in the post I talked about a convergence of multiple studies that are consistent with the RDR estimate: Young 2018 (RDR); Bingley 2023 (twin study with equal environment assumption relaxed), Weiner 2023 (rare burden heritability), Schoech 2019 (low frequency variant analysis), and Chen 2023 (direct rare burden scan). As far as I am aware no one has identified any fundamental flaws in these analyses or conducted independent studies that refute them. So I think the preponderance of evidence continues to be support the Young et al. RDR findings.
Great, thank you. One remaining question I have is about the studies of rare variants that you cite in your last comment. Earlier, you said that other studies of rare variants at the population level "are estimates in the population rather than within families, so are still susceptible to all of the issues of environmental confounding and population structure." Would this same concern apply to some of the studies that you cited in your above comment? I'm not sure why these studies escape these problems. I may very well be missing something, but most of these studies don't seem to use within-family data.
Good point and it is study specific. Young is within family obviously. Bingley is a twin study. Weiner accounts for population structure but not indirect effects. Schoech + Chen is susceptible to both. However, the studies that do not account for environmental confounding (Weiner, Schoech, Chen) all demonstrate that the contribution from rare variants is already low, so it would only expected to be even lower if this extra confounding was removed. In contrast, a study like Hill et al. estimates the kinship "heritability" for a phenotype could be high, but uses an estimator that can be inflated by 2x or 3x by indirect effects. Upward bias in the rare variant studies only makes the finding that rare variants explain very little heritability more striking.
I read through both articles, though in this one I skipped over some sections, and I did not see a lot of discussion on IQ test design itself and the variability it can introduce (e.g., SAT vs Raven's). You do mention how tests are normalized to a population, but I didn't see anything discussing how many "IQ" tests have strong assumptions about education/culture baked into the tests themselves.
The worst I have seen of this is people calling the SAT an "IQ test" because it is "correlated with positive life outcomes", even though it is essentially a knowledge test at best, memorization test at worst.
Has any of the types of analysis you discuss been done on a limited dataset that tries to only use tests with as little dependence on life experience as possible (like Raven's)? An ideal test seems like one you can give to a child that is old enough to see and point at things and can understand the concept of "correct answer", but otherwise has no educational/cultural history. If so, do the results come out the same?
I agree that IQ tests have very strong assumptions and it is difficult to make any definitive statements because the tests can be very different. Even though they are not intended to test "general knowledge" they are often still highly correlated with culturally-specific questions: http://gusevlab.org/projects/hsq/#h.pqhr9q81wgd5
I talk about measurement error a bit at the end here:
https://theinfinitesimal.substack.com/i/148251755/what-about-measurement-error
I've yet to see an example where GWAS heritability increased substantially because a better IQ test was used. In instances where people have looked at more "fluid" like subtests, like memory or reaction time, the heritability of those is *much* lower than that of an overall IQ test or a general factor. For example, see Supp Table 2 of https://pubmed.ncbi.nlm.nih.gov/32895543/, where the Verbal Numeric Reasoning test (which includes general knowledge / SAT-type questions) has much higher heritability than all of the more basic subtests. We do not have direct effect estimates for these subtests but in general it looks like the less cultural a test is, the less heritable it is.
Right, one cold hard truth is that we currently do not have any methods or data to outperform the prediction accuracy set by the GWAS heritability + the rare burden heritability. Even for people who believe there is missing heritability still out there, we would not currently have any way to leverage it for prediction. I do think the broader biological questions of how much rare variant heritability there is in truth and how much Gene-Environment interaction are interesting, of course.