.I don't think this is anything too different from what I said in my post.
All genes are genes for something. Therefore, all genetic conditions will be conditions where the genes cause something that cause the disorder.
The two examples I gave were that cystic fibrosis, a classic genetic disease, is also a disease of lung mucus. And that if there were some virus where likelihood of getting it was 100% genetic, it would look like a 100% genetic condition.
I described this a bit in Argument 6B, "Genes could just be a proxy for some more satisfying cause of schizophrenia", and partly in the subsequent Open Thread, where I said that "part of my argument is that there may never be a satisfying unitary story of schizophrenia (any more than there will be a satisfying unitary story of what causes kidney disease), so instead of treating genes as the IOU for the satisfying story downstream of the genes, we should just go with the genes."
In terms of the schizotypy connection, the paper you cite finds many detrimental facets of negative schizotypy, but beneficial aspects of positive schizotypy (some of which I'm not impressed by; they seem to be things like "if they're in a cult, they're happier with the cult" and "sometimes the hallucinations say nice things to them"). But my impression is that in general, negative schizotypy is genetically correlated with schizophrenia, but positive schizotypy mostly isn't. See eg https://www.frontiersin.org/journals/psychiatry/articles/10.3389/fpsyt.2015.00143/full
"While positive schizotypy is the underlying dimension explaining psychotic features, it is not necessarily related to Krankheitswert. Negative schizotypy, however, appears closely related to schizophrenia regarding its heritability"
"These results provide genetic evidence in support of the spectrum model of schizophrenia, and support the view that negative and disorganised symptoms may have greater genetic basis than positive symptoms, making them better indices of familial liability to schizophrenia"...We further note that the association of SCZ PRS with only the negative dimension of schizotypy is in agreement with previous epidemiological findings that show familial predisposition to SCZ in the relatives of probands without a history of a psychotic episode is likely to be better indexed by the negative symptoms."
A simpler test of your thesis is whether schizophrenia risk is associated with creativity directly. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4590283/ looks at this and finds yes, but weakly. Given the polygenic scoring ability we actually have, someone in the 99.9th percentile of schizophrenia risk is about 0.2 percentage points more likely to have a creative job than someone at the median. Given hypothetical perfect scoring ability, it's 1.75 pp (these look larger as relative effects, 20% and 175% respectively). I'm not sure how much this actually reflects increased creativity compared to less suitability for other jobs and/or more interest in creative ones. I think profession in this study was something like self-rated; there are lots of schizophrenic-seeming people who think they're musicians, artists, and writers; but fewer who have convinced others.
It's implausible that any substantial portion of the population will be selected for low schizophrenia risk, because even if everyone in the population opts for polygenic selection, most people will be selecting for other things like low diabetes risk or whatever. The people most likely to select for low schizophrenia risk would be people in families with high likelihood of schizophrenia, or people who incidentally notice that one of their eggs has very high schizophrenia risk.
So the way I would think about this is that now when polygenic scores are weak, given the weak schizophrenia->creativity correlation, nothing we do to imputed schizophrenia risk can affect creativity much. Later, when polygenic scores are strong, we'll be able to identify embryos at very high risk to actually get schizophrenia, without lowering overall risk significantly on a population-wide level (and in fact we won't want to, since if the kid probably won't get schizophrenia we'd rather use that selection ability to prevent heart attacks or whatever).
.I don't think this is anything too different from what I said in my post.
All genes are genes for something. Therefore, all genetic conditions will be conditions where the genes cause something that cause the disorder.
The two examples I gave were that cystic fibrosis, a classic genetic disease, is also a disease of lung mucus. And that if there were some virus where likelihood of getting it was 100% genetic, it would look like a 100% genetic condition.
I described this a bit in Argument 6B, "Genes could just be a proxy for some more satisfying cause of schizophrenia", and partly in the subsequent Open Thread, where I said that "part of my argument is that there may never be a satisfying unitary story of schizophrenia (any more than there will be a satisfying unitary story of what causes kidney disease), so instead of treating genes as the IOU for the satisfying story downstream of the genes, we should just go with the genes."
In terms of the schizotypy connection, the paper you cite finds many detrimental facets of negative schizotypy, but beneficial aspects of positive schizotypy (some of which I'm not impressed by; they seem to be things like "if they're in a cult, they're happier with the cult" and "sometimes the hallucinations say nice things to them"). But my impression is that in general, negative schizotypy is genetically correlated with schizophrenia, but positive schizotypy mostly isn't. See eg https://www.frontiersin.org/journals/psychiatry/articles/10.3389/fpsyt.2015.00143/full
"While positive schizotypy is the underlying dimension explaining psychotic features, it is not necessarily related to Krankheitswert. Negative schizotypy, however, appears closely related to schizophrenia regarding its heritability"
...and https://www.cambridge.org/core/services/aop-cambridge-core/content/view/47381AEC2205356A81390D3D214CF4B9/S0007125022001799a.pdf/relationship_between_polygenic_risk_scores_and_symptom_dimensions_of_schizophrenia_and_schizotypy_in_multiplex_families_with_schizophrenia.pdf
"These results provide genetic evidence in support of the spectrum model of schizophrenia, and support the view that negative and disorganised symptoms may have greater genetic basis than positive symptoms, making them better indices of familial liability to schizophrenia"...We further note that the association of SCZ PRS with only the negative dimension of schizotypy is in agreement with previous epidemiological findings that show familial predisposition to SCZ in the relatives of probands without a history of a psychotic episode is likely to be better indexed by the negative symptoms."
A simpler test of your thesis is whether schizophrenia risk is associated with creativity directly. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4590283/ looks at this and finds yes, but weakly. Given the polygenic scoring ability we actually have, someone in the 99.9th percentile of schizophrenia risk is about 0.2 percentage points more likely to have a creative job than someone at the median. Given hypothetical perfect scoring ability, it's 1.75 pp (these look larger as relative effects, 20% and 175% respectively). I'm not sure how much this actually reflects increased creativity compared to less suitability for other jobs and/or more interest in creative ones. I think profession in this study was something like self-rated; there are lots of schizophrenic-seeming people who think they're musicians, artists, and writers; but fewer who have convinced others.
It's implausible that any substantial portion of the population will be selected for low schizophrenia risk, because even if everyone in the population opts for polygenic selection, most people will be selecting for other things like low diabetes risk or whatever. The people most likely to select for low schizophrenia risk would be people in families with high likelihood of schizophrenia, or people who incidentally notice that one of their eggs has very high schizophrenia risk.
So the way I would think about this is that now when polygenic scores are weak, given the weak schizophrenia->creativity correlation, nothing we do to imputed schizophrenia risk can affect creativity much. Later, when polygenic scores are strong, we'll be able to identify embryos at very high risk to actually get schizophrenia, without lowering overall risk significantly on a population-wide level (and in fact we won't want to, since if the kid probably won't get schizophrenia we'd rather use that selection ability to prevent heart attacks or whatever).