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To be blunt: «Phenotypic null hypothesis [for the genetics of personality]» is a 2013 review paper by Eric Turkheimer, with 162 citations.
Turkheimer, like Lewontin before him with his «apportionment» and, more to the point, with his corn plants (cited by Ned Block here), is making a mountain out of a common-sensical molehill, in his case to bury the monster of HBD implications that have sprang forth (as he asserts, unreasonably) from his own First Law that he now seeks to reframe (as much is stated in the paper). Moreover, you both are sufficiently obscurantist and informal that it's hard to tell if you're gesturing at the same mountain:
vs yours:
Ok, and?
….The problem you talk about in your Substack post is real, although not nearly as damaging with regards to the sort of HBD beliefs most salient in the culture war and pro/anti-HBD debate (i.e. not the issue of bullied gays) as one could assume from careless reading of your initial post. (Besides, we have plenty of data such as admixture and, as of late, GWAS confirming simple additive model for the group difference – qualitatively similar to the case of height, not similar to gay-bullying and personality research). Measurement error is a fundamental problem; though as better-informed people remind us, there are methods, e.g. common pathway models, which help against it, and HBD research using those methods has yielded largely the same conclusions. It is also possible to directly test for AE vs ACE, precluding the sort of erroneous assumptions you warn against.
This is what is recommended is a textbook, literally, in crypto-HBDer Plomin's «Behavioral Genetics» 2012 edition (that is, anticipating Turkheimer's paper by a year). Consider p.157:
Or in a section about model fitting, pp. 380-390:
Plomin practices what he preaches, too – here's an example of a paper.
So yeah, those are real problems with real countermeasures. «Phenotypic null hypothesis» is a meme, and there are apparently only two people forcing this meme.
Again, what Turkheimer is doing here is not different from Lewontin's tricks, which are known to have been motivated by politics. It's uncanny how similar these situations are. In the entry-level «Making sense of Heritability, pp. 60:-62:
By all means, do promote statistical literacy and demand intellectual honesty among HBDers, do shame us for our sloppiness. Keep discussing this in terms of phenotypic null hypothesis, if you must. But do not gaslight. This argument, and in this specific formulation, is not Behavioral Genetics 101, but your recent contribution to the debate, and it's more of a rhetorical nature.
Ok, so regarding this paper:
According to Plomin, the goal of the paper is to test the plausibility of evolutionary theories are about environmental sensitivity by using twin studies to look for heritability:
This is very much the sort of nonsense the phenotypic null hypothesis is an objection to. Everything is heritable, and we have good theoretical understanding of why that is. It is thus of no evidentiary value to find that things are heritable, and this shouldn't be treated as a confirmation of evolutionary theories, which destroys the whole point of the paper.
Not so relevant to the phenotypic null hypothesis and I haven't looked at this in detail as it's a citation of a different study, but the cited study makes me suspicious: They didn't find any main effect of the treatment, so this was a subgroup analysis of exactly the sort that Scott Alexander has warned me about.
I acknowledge that common pathway models/factor models can control for some types of measurement error in some scenarios, but it doesn't really seem to work for personality traits (and therefore not for HSC either, unless HSC is an unusual personality trait). The appropriate way to do this for personality data is multi-informant data, which tends to lead to way higher heritabilities for personality, indicating that a substantial proportion of the nonshared environment component is measurement error, even with naive common pathways.
Plomin finds that all the "good" personality traits are correlated, i.e. emotional stability, extraversion, openness, conscientiousness and agreeableness are all positively correlated with each other. The model he chooses to apply to those correlations assumes that these correlations are substantive, but I believe that is an inappropriate model.
Correlations between the Big Five personality traits within a single rater appear to reflect a "Halo"/"social desirability" bias factor. The way we can tell this is because it fails to correlate across informants. I.e. while it's true that you rating yourself as more extraverted correlates with you rating yourself as more conscientious, you rating yourself as more extraverted does not correlate with others rating you as more conscientious. See for instance this paper.
Also I believe it's well-established that the different subscales of HSC differ from each other in their correlations with the Big Five, and indeed he replicates that finding in the study. However, this pattern of correlations is incompatible with the notion that the correlations between HSC subscales and Big Five is mediated by the HSC common pathway, which makes his later models very strange.
In conclusion, the Plomin study you linked is a fractal of bad study design. In many ways it's a good example of the necessity to further popularize the phenotypic null hypothesis. However, the study also has severe flaws beyond the phenotypic null hypothesis. This is cruxy to me: if you can convince me that Plomin's study is good, then I will likely grant that I was wrong about my point about the phenotypic null hypothesis, but conversely I think Plomin's study is really bad and I think Turkheimer has to deal with an endless stream of studies that are equally as bad as Plomin's here, so I think this serves as an excellent case study that explains why Turkheimer is so bothered by behavioral genetics.
I rest my case.
Wait is the study even by Plomin? The authors listed are:
None of whom seem to be Plomin.
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I don't have time to respond to this right now, as I'm on my phone, but just quickly skimming it, it looks cruxy to me. I will respond once I get home.
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I'm not claiming it to be damaging to HBD beliefs, I'm claiming it to be damaging to certain types of arguments and findings HBDers often make. There can be bad arguments for correct conclusions, and people who make those arguments should stop making them because it introduces noise and makes it harder to find the good arguments.
Again I posted various examples of people not properly applying the phenotypic null hypothesis. Let's zoom into one of them to understand the problem:
https://twitter.com/tailcalled/status/1475441032292667394
If one doesn't understand the phenotypic null hypothesis, then this is an exciting study. Researchers have shown jealousy and restricted sociosexuality to be genetic! And to be biologically linked to each other! In the past I would have been really interested in these sorts of results, as tying into all sorts of evo psych theories.
However, when appreciating the phenotypic null hypothesis, it's a boring study. What are we even supposed to learn from it? Obviously these variables are going to be heritable and genetically correlated, but this doesn't really tell us much.
If you disagree with this notion, then feel encouraged to make your case for why this is such an important and meaningful finding.
I don't think Turkheimer is being an obscurantist here. He's a leading behavior geneticist and an editor for a behavior genetics journal; he has to deal with an endless stream of papers that proudly talk about how they've shown this and that to be genetic. He's got excellent reasons to try to make people accept the phenotypic null hypothesis, since it's a huge piece of missing knowledge.
But these models are rarely used. Even from the "better-informed people", I have had trouble getting it for e.g. testing the causal effect of g.
This is badly powered when C is smallish, e.g. try computing the power requirement for C^2=0.01.
I don't see how GWAS additivity defends personality research, can you expand? In particular I don't see how phenotypic null hypothesis predicts nonadditivity.
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