Hi, I'm Scott Alexander and I will now explain why every disease is in fact just poor genetics by using play-doh statistics to sorta refute a super specific point about schizophrenia heritability.
edited to add tl;dr:
Siskind seems ticked off because recent papers on the genetics of schizophrenia are increasingly pointing out that at current miniscule levels of prevalence, even with the commonly accepted 80% heritability, actually developing the disorder is all but impossible unless at least some of the environmental factors are also in play. This is understandably very worrisome, since it indicates that even high heritability issues might be solvable without immediately employing eugenics.
Also notable because I don't think it's very often that eugenics grievances breach the surface in such an obvious way in a public siskind post, including the claim that the whole thing is just HBD denialists spreading FUD:
People really hate the finding that most diseases are substantially (often primarily) genetic. There’s a whole toolbox that people in denial about this use to sow doubt. Usually it involves misunderstanding polygenicity/omnigenicity, or confusing GWAS’ current inability to detect a gene with the gene not existing. I hope most people are already wise to these tactics.
Just like neuroscientists try to read out and decode the memories inside a living brain, we can now read and write (a little bit…) the anatomical goals and memories of the collective intelligence of morphogenesis.
The first time I presented this at a conference – genetically wild-type worms with a drastically different, rewritten, permanent, target morphology – someone stood up and said that this was impossible and “those animals can’t exist”. Here’s a video taken by Junji Morokuma, of them hanging out.
I was hoping someone more knowledgeable on the subject might have chimed in to provide some context by now, like are bioelectric circuits legit or is this sheldrake all over again, and why can't I find anything on the very interesting phenomenon of deer antlers maintaining acquired deformities between fall off and growth cycles, and apparently trophic memory is an hapax legomenon to your linked article according to google.
Feel free to ask Michael in the comments of his blog, he frequently replies, helpfully, with references.
I mean all science is tentative, so skepticism is healthy.
Like in the deer, the large-scale target morphology can be revised – the pattern memory re-written – by transient physiological experience. The genetics sets the hardware with a default pattern outcome, but like any good cognitive system, it has a re-writable memory that learns from experience.