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A fallacy is an error in reasoning that makes an argument invalid. The “interactionism fallacy” is the fallacy—coined by Gottfredson (2009)—that since genes and environment interact, that heritability estimates are not useful—especially for humans (they are for nonhuman animals where environments can be fully controlled; see Schonemann, 1997; Moore and Shenk, 2016). There are many reasons why this ‘fallacy’ is anything but a fallacy; it is a simple truism: genes and environment (along with other developmental products) interact to ‘construct’ the organism (what Oyama, 2000 terms ‘constructive interactionism—“whereby each combination of genes and environmental influences simultaneously interacts to produce a unique result“). The causal parity thesis (CPT) is the thesis that genes/DNA play an important role in development, but so do other variables, so there is no reason to privilege genes/DNA above other developmental variables (see Noble, 2012 for a similar approach). Genes are not special developmental resources and so, nor are they more important than other developmental resources. So the thesis is that genes and other developmental resources are developmentally ‘on par’.

Genes need the environment. Without the environment, genes would not be expressed. Behavior geneticists claim to be able to partition genes from environment—nature from nurture—on the basis of heritability estimates, mostly gleaned from twin and adoption studies. However, the method is flawed: since genes interact with the environment and other genes, how would it be possible to neatly partition the effects of genes from the effects of the environment? Behavior geneticists claim that we can partition these two variables. Behavior geneticists—and others—cite the “Interactionism fallacy”, the fallacy that since genes interact with the environment that heritability estimates are useless. This “fallacy”, though, confuses the issue.

Behavior geneticists claim to show how genes and the environment affect the ontogeny of traits in humans with twin and adoption studies (though these methods are highly flawed). The purpose of this “fallacy” is to disregard what developmental systems theorists claim about the interaction of nature and nurture—genes and environment.

Gottfredson (2009) coins the “interactionism fallacy”, which is “an irrelevant truth [which is] that an organism’s development requires genes and environment to act in concert” and the “two forces are … constantly interacting” whereas “Development is their mutual product.” Gottfredson also states that “heritability … refers to the percentage of variation in … the phenotype, which has been traced to genetic variation within a particular population.” (She also makes the false claim that “One’s genome is fixed at birth“; though this is false, see epigenetics/methylation studies.) Heritability estimates, according to Phillip Kitcher are “‘irrelevant’ and the fact that behavior geneticists persist

in using them is ‘an unfortunate tic from which they cannot free themselves’ (Kitcher,

2001: 413)” (quoted in Griffiths, 2002).

Gottfredson is engaging in developmental denialism. Developmental denialism “occurs when heritability is treated as a causal mechanism governing the developmental reoccurrence of traits across generations in individuals.” Gottfredson, with her “interactionism fallacy” is denying organismal development by attempting to partition genes from environment. As Rose (2006) notes, “Heritability estimates are attempts to impose a simplistic and reified dichotomy (nature/nurture) on non-dichotomous processes.” The nature vs nurture argument is over and neither has won—contra Plomin’s take—since they interact.

Gottfredson seems confused, since this point was debated by Plomin and Oyama back in the 80s (Plomin’s review of Oyama’s book The Ontogeny of Information; see Oyama, 1987, 1988; Plomin, 1988a, b). In any case, it is true that development requires genes to interact. But Gottfredson is talking about the concept of heritability—the attempt to partition genes and environment through twin, adoption and family studies (which have a whole slew of problems). For example, Moore and Shenk (2016: 6) write:

Heritability statistics do remain useful in some limited circumstances, including selective breeding programs in which developmental environments can be strictly controlled. But in environments that are not controlled, these statistics do not tell us much.

Susan Oyama writes in The Ontogeny of Information (2000, pg 67):

Heritability coefficients, in any case, because they refer not only to variation in genotype but to everything that varied (was passed on) with it, only beg the question of what is passed on in evolution. All too often heritability estimates obtained in one setting are used to infer something about an evolutionary process that occurred under conditions, and with respect to a gene pool, about which little is known. Nor do such estimates tell us anything about development.

Characters are produced by the interaction of nongenetic and genetic factors. The biological flaw, as Moore and Shenk note, throw a wrench into the claims of Gottfredson and other behavior geneticists. Phenotypes are ALWAYS due to genetic and nongenetic factors interacting. So the two flaws of heritability—the environmental and biological flaw (Moore and Shenk, 2016)—come together to “interact” to refute such simplistic claims that genes and environment—nature and nurture—can be separated.

For instance, as Moore (2016) writes, though “twin study methods are among the most powerful tools available to quantitative behavioral geneticists (i.e., the researchers who took up Galton’s goal of disentangling nature and nurture), they are not satisfactory tools for studying phenotype development because they do not actually explore biological processes.” (See also Richardson, 2012.) This is because twin studies ignore biological/developmental processes that lead to phenotypes.

Gamma and Rosenstock (2017) write that the concept of heritability that behavioral geneticists use is “is a generally useless quantity” while “the behavioral genetic dichotomy of genes vs environment is fundamentally misguided.” This brings us back to the CPT; there is causal parity to all processes/interactants that form the organism and its traits, thus the concept of heritability that behavioral geneticists employ is a useless measure. Oyama, Griffiths, and Gray (2001: 3) write:

These often overlooked similarities form part of the evidence for DST’s claim of causal parity between genes and other factors of development. The “parity thesis” (Griffiths and Knight 1998) does not imply that there is no difference between the particulars of the causal roles of genes and factors such as endosymbionts or imprinting events. It does assert that such differences do not justify building theories of development and evolution around a distinction between what genes do and what every other causal factor does.

Behavior geneticists’ endeavor, though, is futile. Aaron Panofsky (2016: 167) writes that “Heritability estimates do not help identify particular genes or ascertain their functions in development or physiology, and thus, by this way of thinking, they yield no causal information.” (Also see Panofsky, 2014; Misbehaving Science: Controversy and the Development of Behavior Genetics.) So, the behavioral genetic method of partitioning genes and environment does not—and can not—show causation for trait ontogeny.

Now, while people like Gottfredson and others may deny it, they are genetic determinists. Genetic determinism, as defined by Griffiths (2002) is “the idea that many significant human characteristics are rendered inevitable by the presence of certain genes.” Using this definition, many behavior geneticists and their sympathizers have argued that certain traits are “inevitable” due to the presence of certain genes. Genetic determinism is literally the idea that genes “determine” aspects of characters and traits, though it has been known for decades that it is false.

Now we can take a look at Brian Boutwell’s article Not Everything Is An Interaction. Boutwell writes:

Albert Einstein was a brilliant man. Whether his famous equation of E=mc2 means much to you or not, I think we can all concur on the intellectual prowess—and stunning hair—of Einstein. But where did his brilliance come from? Environment? Perhaps his parents fed him lots of fish (it’s supposed to be brain food, after all). Genetics? Surely Albert hit some sort of genetic lottery—oh that we should all be so lucky. Or does the answer reside in some combination of the two? How very enlightened: both genes and environment interact and intertwine to yield everything from the genius of Einstein to the comedic talent of Lewis Black. Surely, you cannot tease their impact apart; DNA and experience are hopelessly interlocked. Except, they’re not. Believing that they are is wrong; it’s a misleading mental shortcut that has largely sown confusion in the public about human development, and thus it needs to be retired. […] Most traits are the product of genetic and environmental influence, but the fact that both genes and environment matter does not mean that they interact with one another. Don’t be lured by the appeal of “interactions.” Important as they might be from time to time, and from trait to trait, not everything is an interaction. In fact, many things likely are not.

I don’t even know where to begin here. Boutwell, like Gottfredson, is confused. The only thing that needs to be retired because it “has largely sown confusion in the public about human development” is, ironically, the concept of heritability (Moore and Shenk, 2016)! I have no idea why Boutwell claimed that it’s false that “DNA and experience [environment] are hopelessly interlocked.” This is because, as Schneider (2007) notes, “the very concept of a gene requires an environment.” Since the concept of the gene requires the environment, how can we disentangle them into neat percentages like behavior geneticists claim to do? That’s right: we can’t. Do be lured by the appeal of interactions; all biological and nonbiological stuff constantly interacts with one another.

Boutwell’s claims are nonsense. It would be worth it to quote Richard Lewontin’s forward in the 2000 2nd edition of Susan Oyama’s The Ontogeny of Information (emphasis Lewontin’s):

Nor can we partition variation quantitatively, ascribing some fraction of variation to genetic differences and the remainder to environmental variation. Every organism is the unique consequence of the reading of its DNA in some temporal sequence of environments and subject to random cellular events that arise because of the very small number of molecules in each cell. While we may calculate statistically an average difference between carriers of one genotype and another, such average differences are abstract constructs and must not be reified with separable concrete effects of genes in isolation from the environment in which the genes are read. In the first edition of The Ontogeny of Information Oyama characterized her construal of the causal relation between genes and environment as interactionist. That is, each unique combination of genes and environment produces a unique and a priori unpredictable outcome of development. The usual interactionist view is that there are separable genetic and environmental causes, but the effects of these causes acting in combination are unique to the particular combination. But this claim of ontogenetically independent status of the causes as causes, aside from their interaction in the effects produced, contradicts Oyama’s central analysis of the ontogeny of information. There are no “gene actions” outside environments, and no “environmental actions” can occur in the absence of genes. The very status of environment as a contributing cause to the nature of an organism depends on the existence of a developing organism. Without organisms there may be a physical world, but there are no environments. In like the manner no organisms exist in the abstract without environments, although there may be naked DNA molecules lying in the dust. Organisms are the nexus of external circumstances and DNA molecules that make these physical circumstances into causes of development in the first place. They become causes only at their nexus, and they cannot exist as causes except in their simultaneous action. That is the essence of Oyama’s claim that information comes into existence only in the process of ontogeny. (Oyama, 2000: 16)

There is an “interactionist consensus” (see Oyama, Griffiths, and Grey, 2001; What is Developmental Systems Theory? pg 1-13): the organism and the suite of traits it has is due to the interaction of genetic/environmental/epigenetic etc. resources at every stage of development. Therefore, for organismal development to be successful, it always requires the interaction of genes, environment, epigenetic processes, and interactions between everything that is used to ‘construct’ the organism and the traits it has. Thus “it makes no sense to ask if a particular trait is genetic or environmental in origin. Understanding how a trait develops is not a matter of finding out whether a particular gene or a particular environment causes the trait; rather, it is a matter of understanding how the various resources available in the production of the trait interact over time” (Kaplan, 2006).

Lastly, I will shortly comment on Sesardic’s (2005: chapter 2) critiques on developmental systems theorists and their critique of heritability and the concept of interactionism. Sesardic argues in the chapter that interaction between genes and environment, nature and nurture, does not undermine heritability estimates (the nature and nurture partition). Philosopher of science Helen Longino argues in her book Studying Human Behavior (2013):

By framing the debate in terms of nature versus nurture and as though one of these must be correct, Sesardic is committed to both downplaying the possible contributions of environmentally oriented research and to relying on a highly dubious (at any rate, nonmethodological) empirical claim.

In sum, the “interactionist fallacy” (coined by Gottfredson) is not a ‘fallacy’ (error in reasoning) at all. For, as Oyama writes in Evolution’s Eye: A Systems View of the Biology-Culture Divide “A not uncommon reaction to DST is, ‘‘That’s completely crazy, and besides, I already knew it” (pg 195). This is exactly what Gottfredson (2009) states, that she “already knew” that there is an interaction between nature and nurture; but she goes on to deny arguments from Oyama, Griffiths, Stotz, Moore, and others on the uselessness of heritability estimates along with the claim that nature and nurture cannot be neatly partitioned into percentages as they are constantly interacting. Causal parity between genes and other developmental resources, too, upends the claim that heritability estimates for any trait make sense (not least for how heritability estimates are gleaned for humans—mostly twin, family, and adoption studies). Developmental denialism—what Gottfredson and others often engage in—runs rampant in the “behavioral genetic” sphere; and Oyama, Griffiths, Stotz, and others show how we should not deny development and we should discard with these estimates for human traits.

Heritability estimates imply that there is a “nature vs nurture” when it is “nature and nurture” which are constantly interacting—and, due to this, we should discard with these estimates due to the interaction of numerous developmental resources; it does not make sense to partition an interacting, self-organizing developmental system. Claims from behavior geneticists—that genes and environment can be separated—are clearly false.