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Culture War Roundup for the week of October 24, 2022

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I just created an account on The Motte to PM someone a question, and afterwards I started browsing through some links and found this post in the vault: Belief Against an Intelligence Gap / Why the Woke Won't Argue: A look at Turkheimer and HBD research.

Now, a year ago or so, I would probably have strongly agreed with this post. But recently, I've come to a totally different conclusion: HBDers tend to totally refuse to engage with basic principles of the debate. I say that as an HBDer who has started interacting with other HBDers, and correcting when they make mistakes. Two core examples I have in mind:

  1. Heritability simply does not mean what a lot of HBDers want it to mean - because of the phenotypic null hypothesis. You often see HBDers declare success when yet another twin study shows that yet another variable is highly heritable, or that there is a genetic correlation between two variables which are usually suggested to be causally linked to each other. In the latter case, I often see HBDers act as if the genetic correlation proves that there is genetic confounding between the two variables, which is a ridiculous suggestion if you think through the actual math. It's perfectly reasonable to say that the debate struggles with progressing because anti-HBDers aren't properly engaging with HBDers, but it would be a lie to also pretend that HBDers aren't also guilty of lack of thought and engagement.

  2. HBDers often signal-boost nonserious or dishonest studies. My go-to example of this is this study on effort and IQ, which claimed to find that effort does not matter for IQ scores. This obviously massively contradicts common sense, and indeed when I took a quick look at the study, its data actually totally supported the notion that effort matters for IQ, and it's merely that the researcher (who is a well-respected leading IQ researcher!) analyzed it wrong (see my analysis in the thread, or perform the analysis for yourself). The researcher still has not changed his mind on the flaws of it, and I regularly see the study pop up on my timeline. If HBDers are going to boost these kinds of studies and ignore critique of them, then why should anyone listen to HBDers?

So, what view would I suggest? A far more symmetric view: Leftist inclined people want to create racial equality of outcomes, and they therefore boost whichever kinds of rationalizations they can come up with for the achievability and justification of such equality. Rightist inclined people want to preserve racial inequality of outcomes, and they therefore boost whichever kinds of rationalizations they can come up with for the unachievability of equality and justification of inequality. There's some honest people on either side who have been swept up in the drama, but in terms of the direction of the energy which drives the whole debate, this is what lies underneath it.

Hi again. You may not know it, but the author of the text in the vault, JB, is a bit of a meme here, an avatar of pig-headed intransigence and hubris, which lends credence to your words. Nevertheless, I can't see how your arguments justify disagreeing with him on this issue and indeed coming to a «totally different conclusion».

If HBDers are going to boost these kinds of studies and ignore critique of them, then why should anyone listen to HBDers?

To begin with: because for most would-be listeners, supporting the opposite camp equals approval of one's family and one's people getting discriminated against (the nigh-inevitable alternative to HBD being acceptance of unredeemed racial guilt). Some are turned off by this; others are quite happy.

And because whatever the faults of HBDers, the other side remains epistemologically worse. Turkheimer may have some legitimate scientific argument against between-group genetic diffs on g; his bottom line was still arrived at through moralizing. «We can recognize a contention that Chinese people are genetically predisposed to be better table tennis players than Africans as silly, and the contention that they are smarter than Africans as ugly, because it is a matter of ethical principle that individual and cultural accomplishment is not tied to the genes in the same way as the appearance of our hair

HBD/Blank Slate is a political question more than it's a scientific one, a question of whether a civic religion founded on this stated promise of equal innate potential (or at least absence of substantial between-group differences) is needed for the prosperity of a polity and reduction in individual suffering; it's a question of oughts. Turkheimer et al. wear their oughts on their sleeves, adversarially, so it's a bit of a double standard to dunk on HBDers for failing or refusing to understand a peripheral aspect of «is».

Now to be clear, the faults of HBDers are not big. I have read a decent amount of your writing on the topic today, debate and adjacent content; the more I was reading, the stronger was the feeling that this'll be a fruitless debate. Your writing over the last year displays a trend towards isolated demands for rigor against HBD outlook (for unknown reasons that I assume, for now, are self-preservation and career strategy, a la Abdel The Backstabber, but might be just autistic perfectionism and purity spiraling; take your pick at which is less charitable). Your two examples aren't damning.

Your thread on effort and application of instrumental variables seems to sidestep the problem of scores influencing perception of effort, and anyway it doesn't affect the debate in absence of good evidence for differences in incentives&effort (and, well, whatever happens with low-stakes online IQ testing, people try «as hard as they can» in contexts relevant for long-term life outcomes or even on serious IQ tests).

Your triumphant post on the environmental null hypothesis is… inconclusive, since it doesn't bother comparing models following from theories on their predictive merits (and also other twins and pedigree schemes). You can't just «call» ENH like you so often do on Twitter, and certainly can't just assume that nobody accounts for measurement error, that all causal effects will generate genetic correlations, and thus that the usual HBDer touting of gen correlations/gen confounding is invalid. Take any actually published model emphasizing environment (i.e. an X factor creating race differences – I mean, okay, the gay-bullying-mental illness stuff at least proposes a half-legible causal pathway), and subject it to scrutiny next to a genetics-first one – most likely, it'll fall apart first.

Like Bryan Pesta's career did: it took years of digging by concerned people, but this HBDer got caught on a technicality and made unemployable. He had tenure, too. As for the non-tenured faculty, we can have Turkheimer spell it out. Like Bird says, there is reason to be optimistic about the eventual result of such policies:

Over the last decade the Pioneer Fund appears to have emptied most of its accounts and is at a low level of activity, and the Ulster Institute is similarly operating on slim budgets (Saini, 2019). […] Instead of Nobel Laureates and respected tenure track faculty, the new generation of race scientists on the Pioneer Fund dole are untrained post-graduates.

So there's no money in it; databases are getting closed off too; getting published is near-impossible (note that all those would-be publications deal with weaknesses of HBD research program that you lament). The paradigm is shriveling up and dying (though Hyde would beg to differ). HBDers' incompetence is the intended outcome of censorship. In time, you'll have every self-respecting scientist firmly in the blank slate camp; forget structural equation modeling, unrepentant HBDers won't understand trivial correlation coefficients, and will be wholly undeserving of attention. Won't this make your argument so much stronger? And I think this means your argument is ultimately uninteresting, as far as science or policy are concerned.

So, what view would I suggest? A far more symmetric view: Leftist inclined people want to create racial equality of outcomes, and they therefore boost whichever kinds of rationalizations they can come up with for the achievability and justification of such equality. Rightist inclined people want to preserve racial inequality of outcomes, and they therefore boost whichever kinds of rationalizations they can come up with for the unachievability of equality and justification of inequality.

You seem to use a coarse-grained notion of politics involved, in stark contrast to your (not necessarily correct but hard-to-critique*) analysis of the technical side. Most «HBDers» are the opposite: laymen beliefs both in the heritability of human behavioral traits and in between-group differences owing to genetics overwhelmingly come from raw life experience, not from data analysis and literature; approval of papers is driven by priors and the general vibe. Likewise comes the understanding of political implications; the sense of unfairness in this debate; and the will to signal-boost arguments-like-soldiers of your allies. This sounds low-IQ, and it is, but consilience can be pretty powerful, and HBD is anything if not consilient; so they're justified in not worrying a lot about minor nitpicks.

As for what happens on the other side – let's say that your model doesn't follow from your text and may conflict with the data. Emil sums it up nicely:

Leftists prefer studies where groups are equal, and if not, then where Africans do better. Moderates and conservatives both show a preference for equal-outcomes, and if not, then Europeans do better. As such, based on these results one might say that leftists show pro-African or anti-European preference, and moderates/conservatives show pro-European or anti-African preference. […] The leftist effect was very clear showing up 19 out of 20 times with effects against Europeans and against men. So pray you don't do any research that makes these groups look good and have leftist readers!

Call me a misanthrope, but it's a priori implausible for people en masse to have consistent abstract preferences such as «equality» and «inequality». Equality is an obvious compromise; beyond that, people just root for the team and want their side to be on top or at least not trampled upon. Bluntly, white «rightists» want to not be punished for the underperformance of Blacks, and thus prefer an HBD narrative that puts them solidly below some groups, above others, and absolves them of their purported sin of systemic racism. «Leftists» have other ideas, so they obstruct research into between-groups genetic differences and enforce the conclusion of racism being the leading causal explanation by fiat.

But this obstruction, when perpetrated by knowledgeable people such as Kaplan or Turkheimer or Rutherford, is telling enough, and cancels out all incompetence HBDers and even run-of-the-mill racists may show.

*my impression of the topic is still best described in this quote:

[…] Well, OK, I could believe that; visible traits consistent over entire populations like skin color might differ systematically because of sexual selection or something, but why not leave IQ following the exact same bell curve in each population? There was no specific thing here that made me start to wonder, more a gradual undermining (Gould’s work like The Mismeasure of Man being completely dishonest is one example - with enemies like that…) as I continued to read studies and wonder why Asian model minorities did so well, and a lack of really convincing counter-evidence like one would expect the last two decades to have produced - given the politics involved - if the idea were false. And one can always ask oneself: suppose that intelligence was meaningful, and did have a large genetic component, and the likely genetic ranking East Asians > Caucasian > Africans; in what way would the world, or the last millennium (eg the growth of the Asian tigers vs Africa, or the different experiences of discriminated-against minorities in the USA), look different than it does now?

It’s worth noting that the IQ wars are a rabbit hole you can easily dive down. The literature is vast, spans all sorts of groups, all sorts of designs, from test validities to sampling to statistical regression vs causal inference to forms of bias; every point is hotly debated, the ways in which studies can be validly critiqued are an education in how to read papers and look for how they are weak or make jumps or some of the data just looks wrong, and you’ll learn every technical requirement and premise and methodological limitation because the opponents of that particular result will be sure to bring them up if it’ll at all help their case.

In this respect, it’s a lot like the feuds in biblical criticism over issues like whether Jesus existed, or the long philosophical debate over the existence of God. […]

But having said that, and admiring things like Plantinga’s free will defense, and the subtle logical issues in formulating it and the lack of any really concrete evidence for or against Jesus’s existence, do I take the basic question of God seriously? No. The theists’ rearguard attempts and ever more ingenious explanations and indirect pathways of reasons and touted miracles fundamentally do not add up to an existing whole. The universe does not look anything like a omni-benevolent/powerful/scient god was involved, a great deal of determined effort has failed to provide any convincing proof, there not being a god is consistent with all the observed processes and animal kingdom and natural events and material world we see, and so on. The persistence of the debate reflects more what motivated cognition can accomplish and the weakness of existing epistemology and debate.[…]

I don’t know when the definitive paper will come out, if it’ll be this year, or by 2020, although I would be surprised if there was still nothing by 2030; but it will happen and it will happen relatively soon (for a debate going on for the past century or more). Genome sequencing is simply going to be too cheap for it to not happen.

Incidentally, this can no longer be found on the author's website.

The manner is recognizable enough, of course.

Phenotypic null hypothesis isn't an obscure methodological limitation, it is a fundamental property of concepts like "heritability" and "genetic correlation" which can easily be derived in simulation studies. If you don't understand how it works then you shouldn't use concepts like heritability and genetic correlation at all in the first place.

Phenotypic null hypothesis isn't an obscure methodological limitation, it is a fundamental property of concepts like "heritability" and "genetic correlation"

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:

The phenotypic null hypothesis integrates what we have learned from multivariate behavior genetics: Until demonstrated otherwise, complex heritable behavioral traits should be the result of psychological processes defined at a high level of analysis, rather than at the level of genes or neurons. Although such complex traits are never independent of genetic variation, they cannot be defined by genetic processes. Genes and behavior are a single entity, a single organism observed at two levels of analysis. Some traits are better understood using low-level concepts (genes, neurons, structures), whereas others require high-level constructs (organizations, algorithms, beliefs).

vs yours:

Put simply, the phenotypic null hypothesis is this: Heritability tells you that if you go up through the chain of causation, then you will often end up with genes. However, there may be many ways that variables can be connected to each other, and there’s no particular reason to expect that every step along the chain of causation from genes to outcomes is best thought of as biological.

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:

«In addition, recent work suggests that careful attention should be paid to claims of causality, measurement error, and environmental factors that can influence both the endophenotype and the final outcome (Kendler & Neale, 2010). … Another issue is that the goal of behavioral genetics is to understand pathways among genes, brain, and behavior. Genes found to be associated with brain phenotypes are important in terms of the brain level of analysis, but their usefulness for behavioral genetics depends on their relationship with behavior (Rasetti & Weinberger, 2011). In other words, when genes are found to be associated with brain traits, the extent to which the genes are associated with behavioral traits needs to be assessed rather than assumed».

Or in a section about model fitting, pp. 380-390:

« Although we will not follow the proof here, researchers have demonstrated that we cannot ask about additive genetic effects, dominance genetic effects, and shared environmental effects simultaneously if the only information we have is from MZ and DZ twins reared together. In virtually every circumstance, we will wish to retain the nonshared environmental variance component in the model. We wish to retain it partly because random measurement error is modeled as a nonshared environmental effect and we do not wish to have a model that assumes no measurement error (it is unlikely to fit very well). Most commonly, we would then model additive genetic variance and shared environmental variance. As mentioned earlier, such a model is called the ACE model […] Table A.2 shows that the AE model is unable to account for this particular set of observed values. Such a model is said to be underidentified. This condition is not necessarily problematic: In general, underidentified models are to be favored. Because a saturated model will always be able to fit the observed data perfectly, the goodness of fit does not really mean anything. However, if an underidentified model does fit the data, then we should take notice—it is not fitting out of mere statistical necessity».

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:

Lewontin’s criticism of ANOVA is often presented as making a purely the- oretical point about inherent limitations in any attempt to derive causal conclusions from statistical data by using the analysis of variance. This interpretation is supported by the way he himself describes the upshot of his argument at the outset: “I will begin by saying some very obvious and elementary things about causes, but I will come thereby to some very annoying conclusions” … The strange thing about (a) is that, despite defending an extreme methodological claim that measurement of human norms of reaction is impossible, Lewontin neither discusses nor so much as mentions what were then most important contributions to the literature on that issue. At the time, the most sophisticated analysis of methodological prob- lems in human behavior genetics was undoubtedly the paper by Jinks and Fulker (1970), which was an important step in the development of powerful model-fitting methods that dominate the contemporary scene. Moreover, John Jinks and David Fulker did suggest how G–E interac- tions could be empirically detected without testing the same genotype in a variety of environments (see below), which directly contradicted Lewontin’s impossibility claim. It is hard to explain why Lewontin fails to address their argument, or at least inform the reader about this “landmark paper”…

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:

Plomin practices what he preaches, too – here's an example of a 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:

According to the recent evolutionary-inspired theories (i.e., differential susceptibility [1], biological sensitivity to context [2]), humans, like many other species [3], differ substantially in their sensitivity to contextual factors, with some more susceptible to environmental influences than others. Importantly, these theories suggest that heightened sensitivity predicts both the reactivity to adverse contexts as well as the propensity to benefit from supportive features of positive environments. In other words, sensitivity is proposed to influence the impact of environmental influences in a “for better and for worse” manner [4]. These prominent theories converge on the proposition that genetic factors play a significant role in individual differences in Environmental Sensitivity (ES) [1, 2, 5].

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.

For example, children who scored higher on the HSC scale were found to benefit significantly more than less sensitive children from schoolbased resilience [16]

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.

[common pathway model for HSC]

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.

[correlation matrix for personality traits]

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:

Elham Assary, Helena M. S. Zavos, Eva Krapohl, Robert Keers & Michael Pluess

None of whom seem to be Plomin.

Plomin practices what he preaches, too – here's an example of a paper.

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.

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.

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.

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).

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.

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,

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.

It is also possible to directly test for AE vs ACE

This is badly powered when C is smallish, e.g. try computing the power requirement for C^2=0.01.

(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)

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.