Astral Codex Ten

ScienceDirect

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ScienceDirect

Article

ScienceDirect is a recurring publication in the Astral Codex Ten archive, appearing 2 times across 2 issues between February 02, 2023 and June 26, 2025. The archive places it in contexts such as “according to https://www.sciencedirect.com/science/article/pii/S1674927821001490”; “Sources: Generation Scotland: https://www.sciencedirect.com/science/article/pii/S0160289614000178?via%3Dihub”. It most often appears alongside Act Blue, ACXers, Aftab.

Metadata

  • Category: Publications
  • Mention count: 2
  • Issue count: 2
  • First seen: February 02, 2023
  • Last seen: June 26, 2025

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Source Context

Recovered passages from the original issue text. When the raw archive preserved outbound links inside the source passage, they are listed directly under the quote.

Mostly Skeptical Thoughts On The Chatbot Propaganda Apocalypse
February 02, 2023 · Original source
On the 'disinformation vs. establishment bot' question, check out bots interacting with climate change: 83.1% of bot tweets support activism, 16.9% skepticism according to https://www.sciencedirect.com/science/article/pii/S1674927821001490 .
Inline links: https://www.sciencedirect.com/science/article/pii/S1674927821001490
Missing Heritability: Much More Than You Wanted To Know
June 26, 2025 · Original source
Are these two cuties monozygotic or dizygotic? Are you sure? (answer) 2: Fraternal And Identical Twins Have Equally Concordant Uterine Environments: Fraternal twins have different sacs in the uterus and use different placentas. Most identical twins share a placenta, and some share an amniotic sac. If trait similarity is caused by sharing a placenta or sac (maybe because the placenta is defective, the fetal brain is starved of nutrients, and so the person has a lower IQ when they grow up), twin studies would falsely read this identical-fraternal difference as genetic. Luckily this is easy to study; not all identical twins share a placenta or sac, so you can cleanly separate the effect of uterine environment from genetics. If you measure enough traits, you can find small deviations in some, but it’s not clear whether this is just multiple testing, and in any case the deviations are small. The best studies suggest this chips off somewhere between 0 - 3% from heritability estimates9. 3: There is little assortative mating: We discussed this one above in the earlier section on GWAS - smart/pretty/kind/whatever people tend to marry other smart/pretty/kind/whatever people. Why would this bias twin study results? Identical twins share 100% of their genes. Fraternal twins ought to share 50% of their genes - but they get half their genes from their mother, and half from their father. In the degenerate case where the mother and father have exactly the same genes (“would you have sex with your clone?”) even fraternal twins will be extremely similar (although not quite identical, since they’ll get different alleles from each clone). In the more plausible case where mothers and fathers are just a little more alike than chance (eg because smart people tend to marry other smart people), fraternal twins will share a genetic tendency towards a trait somewhat more than their 50% shared genes suggest. Since this makes fraternal twin pairs more (genetically) like identical twin pairs, and twin studies assess heritability as the difference in fraternal-identical-twin-pair concordance, this bias would make twin studies underestimate heritability. But this is the opposite of what you would need to “discredit” twin studies - if this bias is true, then everything is more genetic than twin studies think. And unlike the previous two biases, this one seems real and important, so much so that when you adjust for it, the heritability of educational attainment rises from ~40% to ~50%. I’m only mentioning this one here because some anti-hereditarians argue that you can’t trust twin studies because of assortative mating, without mentioning that this can only bias them down. 4: Population stratification: This is often large and worth worrying about, but it applies to identical and fraternal twin pairs equally, and doesn’t bias twin study heritability estimates much (though it might shift the balance between shared and non-shared environment). See eg the sentence around footnote 30 here. 5: Non-additive / “interaction” effects: These are theoretically interesting, but all research thus far has found they are minimal (1, 2). Some experts think this may miss rarer or harder-to-find interactions; we’ll return to this later. 6: “Genetic nurture”, parent-to-child Mentioned above: if there is a gene for reading books to kids, and reading books raises IQ, it will look like a “gene for IQ”. This isn’t as relevant to twin study estimates of heritability, since both identical twins and fraternal twins are equally related to their parents, and any trait caused by genetic nurture wouldn’t differ between them (and therefore would not falsely appear heritable in this design). Rather, they would appear as shared environment. 7: “Genetic nurture”, sibling-to-sibling That is, suppose your sibling’s traits influence your own development. For example, suppose your sibling has a gene that makes them sabotage your schoolwork, causing you to fail and drop out of school early. An identical twin would share this gene with their sibling more often than a fraternal twin, making it look like a “gene for doing badly at school” (since the people who have it do worse at school than those who don’t). Why are we even talking about this? Do we really think it’s a big part of the variance in behavioral traits? Challenging twin study heritability estimates through this route requires inhabiting a weird no-man’s-land where otherwise-invisible genetic and environmental pathways suddenly flare up when you say the magic words “it was done by a sibling”. For example, this requires a strong effect of shared environment - that is, your educational attainment has to depend on whether you’re being sabotaged or not. But in general, shared environmental effects are weak. And it requires a strong effect of genes - that is, this mechanism only works if your sibling’s tendency to sabotage you is highly genetically determined. But we’re deploying this claim to deny that traits like IQ or educational attainment are highly genetically determined. So to get much out of this, the tendency to sabotage siblings would have to be more genetic than other behavioral traits! The reason this convoluted possibility gets brought up so often is that, unlike the more plausible parent-to-child genetic nurture, twin studies can’t rule it out. So if you really want to deny twin studies, this is one of your best bets. But when investigated, this has effects indistinguishable from zero. I’ve been a bit mean in this whole section, because people really like to dismiss twin studies as “Oh, don’t you know, those depend on assumptions, I bet you never considered that assumptions might be wrong”, and then Gish Gallop you with different assumptions until you give up. But scientists have actually done a lot of really good work checking the assumptions and they mostly hold. An alternative way of validating twin studies (brought up by Noah Carl in this article) is to check them against their close cousins, adoption studies and pedigree studies. Pedigree studies investigate large family trees, and check how trait similarity decreases with genetic distance. They avoid twin specific biases (like different treatment of fraternal vs. identical twin pairs, or different prenatal environments), while adding others like assortative mating. Here are the heritabilities of IQ and EA found in pedigree studies10 (see footnote for sources and caveats, and see also here and here for somewhat similar designs): Adoption studies investigate whether adoptees’ traits are more correlated with their adoptive or biological parents. They avoid a large swathe of biases, at the risk of introducing new adoption-related biases of their own (like the possibility that agencies deliberately place adoptive children with parents who are culturally or behaviorally similar, or the possibility that adoptees were adopted late enough to still get some shared environment from their biological parents). Here are the findings of some of the largest and best11: Both straightforwardly confirmed the larger heritability numbers found in twin studies. I would add the evidence from some less formal “adoption studies”12. During residency, I spent a few months working in a child psychiatric hospital for the worst of the worst - kids who committed murder or rape or something before age 18. Many of these children had similar stories: they were taken from their parents just after birth because the parents were criminals/drug addicts/in jail/abusing them. Then they were adopted out to some extremely nice Christian family whose church told them that God wanted them to help poor little children in need. Then they promptly proceeded to commit crime / get addicted to drugs / go to jail / abuse people, all while those families’ biological children were goody-goodies who never got so much as a school detention. When I met with the families, they would always be surprised that things had gone so badly, insisting that they’d raised them exactly like their own son/daughter and taught them good Christian morals. I had to resist the urge to shove a pile of twin studies in their face. This has left me convinced that behavioral traits are highly heritable to a level that it would be hard for any study to contradict. Ultimate source here. Although the study is confusing about this, I think it’s trying to say that almost 90% of subjects were adopted before age 2. But I don’t think studies do contradict this. Given the degree to which their assumptions have been validated, and the level of confirmation from pedigree and adoption studies, I think they have earned a presumption of accuracy. Doubting the twin studies doesn’t seem like a promising route to reconciling the twin-vs-Sib-Regression/RDR discrepancy. What’s Going On? (Part 2: Is Something Wrong With Sib-Regression And RDR?) Sib-Regression is a clever way of avoiding most biases. Its independent variable - the degree to which some sibling pairs end up with slightly more shared genes than others - is even more random and exogenous than the difference between fraternal and identical twins. It can sometimes have biases related to assortative mating (which would falsely push heritability down), but otherwise it’s pretty good. RDR has many of the same advantages, and allows more diverse relationships and so larger sample sizes. It’s hard to think of ways these methods could be wildly off. There is one caveat: although RDR includes most of the rare and structural variants missed by GWAS, in theory it can miss certain ultra-rare variants which are so uncommon that they aren’t shared between some of the relative pairs used in RDR. De novo variants that occurred during the subject’s own conception would be in this category, if the subject didn’t have children or didn’t pass on that gene13. This seems like a pretty small subcategory of genetic variation, and I wouldn’t normally expect that much of importance to be hiding here, but maybe it’s more important than it seems. RDR also doesn’t include much variance caused by statistical interactions between genes. Although we said above that these are usually found to be insignificant, they might be more important in a trait like intelligence that has been under recent evolutionary selection that lops off easily-detectable sources of variance and leaves only the weird obscure ones behind. There’s limited ability for classical Mendelian dominance to affect common variants, but more complicated genetic interactions might still prove important. Overall these are strong methods, and their failure to converge is troubling. If forced to explain them away, we might tell a story like: So far, there is only one RDR study and a few Sib-Regression studies, so we should wait for more data before updating too hard.
Inline links: answer, The best studies, 9, seems real and important, here, 1, 2, when investigated, in this article, 10, here, here, https://substackcdn.com/image/fetch/$s_!b3LF!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2Fc094f9c0-4c71-48cf-89dc-615498d94812_483x51.png, 11, https://substackcdn.com/image/fetch/$s_!XFWU!,f_auto,q_auto:good,fl_progressive:steep/https%3A%2F%2Fsubstack-post-media.s3.amazonaws.com%2Fpublic%2Fimages%2F85f433e5-d141-47b7-8dc5-2271925032e9_483x102.png, 12, https://x.com/cremieuxrecueil/status/1935731422205010135, here, 13
Generation Scotland: https://www.sciencedirect.com/science/article/pii/S0160289614000178?via%3Dihub . See also https://www.nature.com/articles/s41380-017-0005-1.pdf, page 2353, "The genetic results . . . are similar to the heritability estimates derived using the traditional pedigree study design in the same data set, which found a heritability estimate of 54% for g and 41% for education."
Inline links: https://www.sciencedirect.com/science/article/pii/S0160289614000178?via%3Dihub, https://www.nature.com/articles/s41380-017-0005-1.pdf
Minnesota transracial: https://sci-hub.st/https://www.sciencedirect.com/science/article/abs/pii/016028969390018Z, page 547, "adoptive fathers' and mothers' correlations with their biological offspring at Time 1 were .25 and .40; with their trans-racially adopted children, .08 and .14 (h 2 = .34 ± .29 and .52 --- .26, respectively). At Time 2, the corresponding correlations were .13 and .45 for biological children; .21 and .21 for adoptees (h 2 = - . 16 ± .29 and .48 ± .25, respectively). o3 advised me to take the maternal correlation since there were too few fathers to give meaningful results (as indicated by the negative heritability at time 2). Because this required a design choice (throwing out the paternal data) I’ve listed it in gray as less trustworthy than some of the other estimates. Reversing this design choice would lower the estimate.
Inline links: https://sci-hub.st/https://www.sciencedirect.com/science/article/abs/pii/016028969390018Z