Not sure what you mean. Are you doing a definitional dispute about what counts as the "standard" definition of Bayesian networks?

Your linked paper is kind of long - is there a single part of it that summarizes the scoring so I don't have to read all of it?

Either way, yes, it does seem plausible that one could create a market structure that supports latent variables without rewarding people in the way I described it.

I'm not convinced Scott Alexander's mistakes page accurately tracks his mistakes. E.g. the mistake on it I know the most about is this one:

56: (5/27/23) In Raise Your Threshold For Accusing People Of Faking Bisexuality, I cited a study finding that most men’s genital arousal tracked their stated sexual orientation (ie straight men were aroused by women, gay men were aroused by men, bi men were aroused by either), but women’s genital arousal seemed to follow a bisexual pattern regardless of what orientation they thought they were - and concluded that although men’s orientation seemed hard-coded, women’s orientation must be more psychological. But Ozy cites a followup study showing that women (though not men) also show genital arousal in response to chimps having sex, suggesting women’s genital arousal doesn’t track actual attraction and is just some sort of mechanical process triggered by sexual stimuli. I should not have interpreted the results of genital arousal studies as necessarily implying attraction.

But that's basically wrong. The study found women's arousal to chimps having sex to be very close to their arousal to nonsexual stimuli, and far below their arousal to sexual stimuli.

I mean I don't really believe the premises of the question. But I took "Even if you're not a fan of automating alignment, if we do make it to that point we might as well give it a shot!" to imply that even in such a circumstance, you still want me to come up with some sort of answer.

I talk to geneticists (mostly on Twitter, or rather now BlueSky) and they don't really know about this stuff.

(Presumably there exists some standard text about this that one can just link to lol.)

I don't think so.

I'm still curious whether this actually happens.... I guess you can have the "propensity" be near its ceiling.... (I thought that didn't make sense, but I guess you sometimes have the probability of disease for a near-ceiling propensity be some number like 20% rather than 100%?) I guess intuitively it seems a bit weird for a disease to have disjunctive causes like this, but then be able to max out at the risk at 20% with just one of the disjunctive causes? IDK. Likewise personality...

For something like divorce, you could imagine the following causes:

• Most common cause is you married someone who just sucks
• ... but maybe you married a closeted gay person
• ... or maybe your partner was good but then got cancer and you decided to abandon them rather than support them through the treatment

The genetic propensities for these three things are probably pretty different: If you've married someone who just sucks, then a counterfactually higher genetic propensity to marry people who suck might counterfactually lead to having married someone who sucks more, but a counterfactually higher genetic propensity to marry a closeted gay person probably wouldn't lead to counterfactually having married someone who sucks more, nor have much counterfactual effect on them being gay (because it's probably a nonlinear thing), so only the genetic propensity to marry someone who sucks matters.

In fact, probably the genetic propensity to marry someone who sucks is inversely related to the genetic propensity to divorce someone who encounters hardship, so the final cause of divorce is probably even more distinct from the first one.

Ok, more specifically, the decrease in the narrowsense heritability gets "double-counted" (after you've computed the reduced coefficients, those coefficients also get applied to those who are low in the first chunk and not just those who are high, when you start making predictions), whereas the decrease in the broadsense heritability is only single-counted. Since the single-counting represents a genuine reduction while the double-counting represents a bias, it only really makes sense to think of the double-counting as pathological.

It would decrease the narrowsense (or additive) heritability, which you can basically think of as the squared length of your coefficient vector, but it wouldn't decrease the broadsense heritability, which is basically the phenotypic variance in expected trait levels you'd get by shuffling around the genotypes. The missing heritability problem is that when we measure these two heritabilities, the former heritability is lower than the latter.

If some amount of heritability is from the second chunk, then to that extent, there's a bunch of pairs of people whose trait differences are explained by second chunk differences. If you made a PGS, you'd see these pairs of people and then you'd find out how specifically the second chunk affects the trait.

This only applies if the people are low in the first chunk and differ in the second chunk. Among the people who are high in the first chunk but differ in the second chunk, the logarithm of their trait level will be basically the same regardless of the second chunk (because the logarithm suppresses things by the total), so these people will reduce the PGS coefficients rather than increasing the PGS coefficients. When you create the PGS, you include both groups, so the PGS coefficients will be downwards biased relative to $\gamma$.