Astral Codex Ten

RDR

5 min read

RDR

Article

RDR is a recurring concept in the Astral Codex Ten archive, appearing 2 times across 2 issues between June 26, 2025 and July 03, 2025. The archive places it in contexts such as “RDR also doesn’t include much variance caused by statistical interactions between genes”; “Why did the Iceland study find significantly lower numbers for Sib-Regression/RDR than twin studies for almost every trait?”; “In the GWAS (and RDR) model, AxA and AxC get counted as E”. It most often appears alongside Arthur Jensen, Awais Aftab, Cremieux.

Metadata

  • Category: Concepts
  • Mention count: 2
  • Issue count: 2
  • First seen: June 26, 2025
  • Last seen: July 03, 2025

Appears In

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.

Missing Heritability: Much More Than You Wanted To Know
June 26, 2025 · Original source
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: here, 13
Why did the Iceland study find significantly lower numbers for Sib-Regression/RDR than twin studies for almost every trait? (hilariously, not for educational attainment with Sib-Regression this time, although I suspect this is just the big margin of error and the real number is commensurate with the other traits studied)
Highlights From The Comments On Missing Heritability
July 03, 2025 · Original source
Take the peanut allergy example [from a paywalled post of Lyman Stone’s]. Let's say in order to develop an allergy you need a mutation in the PNUT gene AND ALSO grow up in a household with [ed: possibly this should be “without”] early exposure to nuts (no Bamba!); that's a gene-environment interaction. For MZ twins, they will always share PNUT mutant (or wildtype) and 100% of their household exposure, so they'll be perfectly correlated on allergy; for DZ twins, they will share PNUT mutations half the time and 100% of their household exposure, so their correlation drops in half. So the twin study will tell you allergy is a 100% heritable trait. Now we test the PNUT variant in a GWAS, the first thing you do is throw away all the relatives (i.e. take one of each twin). Some people will be PNUT mutants and grow up in a household with no exposure and be allergy free, some will be PNUT mutants with exposure and will have allergy (and vice versa for the non-carriers). The resulting correlation between PNUT mutation and allergy will be low, so the heritability estimate will be <100%. TLDR: in the ACE twin model (and sib-reg), AxA and AxC interactions get counted as A. In the GWAS (and RDR) model, AxA and AxC get counted as E. In my opinion AxA could plausible be considered "heritability" in the sense that it only relies on genes, but AxC cannot.