who am I?

A statistical-significance threshold is irrelevant NHST mumbo-jumbo. What you care about is posterior probability of the causal variant's effect being above the cost-safety threshold, whatever that may be, but which will have nothing at all to do with 'genome-wide statistical significance'.

I'm aware of this, but if you're just indiscriminately shoveling heaps of edits into someone's genome based on a GWAS with too low a sample size to reveal causal SNPs for the desired trait, you'll be editing a whole bunch of what are actually tags, a whole bunch of things that are related to independent traits other than intelligence, and a whole bunch of random irrelevant alleles that made it into your... (read more)

I might end up eating my words on the delivery problem. Something has just come out a few days ago that renewed a bit of my optimism, see here. According to the findings in this pre-print, it is possible to shield AAVs from the immune system using protein vaults that the immune system recognizes as self. It is not perfect though; although VAAV results in improved transduction efficiency even in the presence of neutralizing antibodies, it still only results in transduction of ~4% of cells if neutralizing antibodies are present. This means you'd need to cross your fingers and hope that 1) the patient doesn't already have naturally extant neutralizing antibodies and... (read more)

The SAT is heavily g-loaded: r = .82 according to Wikipedia, so ~2/3 of the variance is coming from g, ~1/3 from other stuff (minus whatever variance is testing noise). So naively, assuming no noise and that the genetic correlations mirror the phenotype correlations, if you did embryo selection on SAT, you'd be getting .82*h_pred/sqrt(2) SDs g and .57*h_pred/sqrt(2) SDs 'other stuff' for every SD of selection power you exert on your embryo pool (h_pred^2 is the variance in SAT explained by the predictor, we're dividing by sqrt(2) because sibling genotypes have ~1/2 the variance as the wider population). Which is maybe not good; maybe you don't want that much of the

The problem could potentially be solved by conducting GWASes that identify the SNPs of things known to correlate with the proxy measure other than intelligence and then subtracting those SNPs, but like you mention later in your reply, the question is what approach is faster and/or cheaper. Unless there is some magic I don't know about with GSEM, I can't see a convincing reason why it would have intelligence SNPs buoy to the top of lists ranked on the basis of effect size, especially with the sample size we would likely end up working with (<1 million). If you don't know what SNPs contribute to intelligence versus something else, applying a flat... (read more)

I am more optimistic than you here. I think it is enough to get people who have already gotten their genomes sequenced through 23&Me or some other such consumer genomics service to either take an online IQ test or submit their SAT scores. You could also cross-check this with other data such people submit to validate their answer and determine whether it is plausible.

I think this could potentially be done for a few million dollars rather than 50. In fact companies like GenomeLink.io already have these kind of third party data analysis services today.

Also, we aren't limited to western countries. If China or Taiwan or Japan or any other country creates a

Me: "I don't think this therapy as OP describes it is possible for reasons that have already been stated by HiddenPrior and other reasons"

kman: "Can you elaborate on this? We'd really appreciate the feedback."

Considering the enormity of my response, I figured I would post it in a place that is more visible to those interested. First I'd like to express my gratitude for you and GeneSmith's goal and motivation; I agree that without some brain-machine interface solution, intelligence enhancement is certainly the way forward for us if we'd like to not only keep up with AI, but also break through the intellectual soft caps that have led to plateauing progress in many... (read 1444 more words →)

Yes, as someone who has worked both in CS and in neuroscience at the graduate level, I probably do know far more than you about this topic. At the risk of sounding more polemic than I am, it's posts like yours and others that make excessively reductive inferences about neurons and the brain that invariably end up polluting discussions of this topic and turn it into an unproductive cesspool of ML people offering their two-cents for topics they don't understand (most of the replies to the original post being the cases in point).

I will grant you that it is indeed possible that we don't understand enough about the brain to be confident... (read 378 more words →)

This reply is hilarious in the context of your first one. At first you confidently assert that changing genes in the brain won't do anything to an adult, followed by your statement that "we understand still far too little of how brains work" to know what's going to happen following such a therapy along with other predictions like total memory erasure. Which is it?

While the vast majority of neurons are subject to mitotic arrest after adolescence, gene expression, the regulation of gene expression, and morphological/biochemical restructuring of individual neurons (plasticity) doesn't stop until you're dead. Additionally, there's no reason to rule out the possibility of genome changes in adolescence leading to macroscopic... (read more)