>First proving what % of intelligence is heritable is not the purpose of GWAS's.

And yet here we are on a thread about using a GWAS to prove what % of intelligence is heritable.

>If you are arguing that some people(maybe even a lot) misunderstand the definition of genetic causation in a similar way that you previously did, then that might be true.

My understanding isn't past tense. Here, allow me to illustrate why this makes no sense to me. Let's take what Gwern said above:

Are they genetic causation? Yes, because if you counterfactually changed the genes and nothing but the genes, you would get different outcomes. They are differences which make a difference.

But in my basketball example I could also say this:

Are they environmental causation? Yes, because if you counterfactually changed the environment and nothing but the environment, you would get different outcomes. They are differences which make a difference.

So we are going to take factors where both of those statements are true and still assert that they are genetically causal? That's incorrect.

>But when any experts, or any study talks about genetic causation they are using the definition the rest of us are using on the this thread.

The 'rest of us' in this thread are definitely not using the same language you use. Let's take a look at just the post author's comments:

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>The most iron-clad part of showing direct gene->trait causation is the 4 sibling-comparison studies

except it's not iron-clad at all and it doesn't show direct gene->trait causation.

>where you see whether you can predict the difference between 2 siblings; as they have identical ancestries, families, locations etc, their environments are near-identical in the first place

Their environments are not near-identical.

>No, it doesn't. It merely tells us that with the data up to now, we've reached 11% (up from, incidentally, ~0.3% just 5 years ago). It provides a very loose lower bound on genes.

Except you're telling me that not only is a GWAS not useful for this purpose but that even this number shouldn't be treated as a 'lower bound' but as a potential identifier to further study the genes identified. It would seem that this

>> Observational studies of this type cannot show causality
>They can: sibling comparisons.

Again, this quote appears to conflict with what you believe GWASs are capable of.

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Again, why are these falsehoods being spread around? Because of an (mis)understanding that 'genetic causation' as measured in the paper is not manipulatable by the environment. Except that it actually is. And a misunderstanding of what GWASs are good for.

>- Embryo selection

No it's not. GWASs don't understand what they're measuring and label the environmental as genetic biasing their measurements. Embryo selection is done the old-fashioned way looking for specific genetic variants that we understand through the use of other types of studies.

>- Tests to figure out risk for certain diseases for preventative purposes

Look at the use of GWASs in identifying schizophrenia. They typically fail to replicate. GWASs find genetic connections where none exist.

Take schizophrenia. It could be that we run a GWAS on schizophrenia and find some genetic similarities. Then we look at these similarities and find one of them is a cuddle gene. A cuddle gene what the heck? Well the cuddle gene makes you want to cuddle which makes their mothers more likely to own pets to cuddle which makes them more likely to own cats which increases their risk of exposure to toxoplasmosis which increases their of schizophrenia. Is that a genetic causation? Because the way genetic causation is actually being used in this thread really doesn't lead to that conclusion. It leads to the idea that the identified genes make you a little more unstable in a certain way, not that we could totally eliminate that element of genetic causation by just educating mothers.