4150 words

Introduction

It is claimed that genes (DNA sequences) have a special, privileged role in the development of all traits. But once we understand what genes do and their role in development, then we will understand that the role ascribed to genes by gene-selectionists and hereditarians outright fails. Indeed, the whole “nature vs nurture” debate implies that genes determine traits and that it’s possible to partition the relative contributions to traits in a genetic and environmental way. This, however, is far from reality (like heritability estimates).

DST isn’t a traditional scientific theory—it is more a theoretical perspective on developmental biology, heredity, and evolution, though it does make some general predictions (Griffiths and Hochman, 2015). But aspects of it have been used to generate novel predictions in accordance with the extended evolutionary synthesis (Laland et al, 2015).

Wilson (2018: 65) notes six themes of DST:

Joint determination by multiple causes

Development is a process of multiple interacting sources.

Context sensitivity and contingency

Development depends on the current state of the organism.

Extended inheritance

An organism inherits resources from the environment in addition to genes.

Development as a process of construction

The organism helps shape its own environment, such as the way a beaver builds a dam to raise the water level to build a lodge.

Distributed control

Idea that no single source of influence has central control over an organism’s development.

Evolution as construction

The evolution of an entire developmental system, including whole ecosystems of which organisms are parts, not just the changes of a particular being or population.

Genes (DNA sequences) as resources and outcomes

Hereditarians have a reductionist view of genes and what they do. Genes, to the hereditarian, are causes of not only development but of traits and evolution, too. However the hereditarian is sorely mistaken—there is no a priori justification for treating genes as privileged causes over and above other developmental resources (Noble, 2012). I take Noble’s argument there to mean that strong causal parity is true—where causal parity means that all developmental resources are on par with each other, with no other resource having primacy over another. They all need to “dance in tune” with the “music of life” to produce the phenotype, to borrow Noble’s (2006, 2017) analogy. Hereditarian dogma also has its basis in the neo-Darwinian Modern Synthesis. The modern synthesis has gotten causality in biology wrong. Genes are, simply put, passive, not active, causes:

Genes, as DNA sequences, do not of course form selves in any ordinary sense. The DNA molecule on its own does absolutely nothing since it reacts biochemically only to triggering signals. It cannot even initiate its own transcription or replication. … It would therefore be more correct to say that genes are not active causes; they are, rather, caused to give their information by and to the system that activates them. The only kind of causation that can be attributed to them is passive, much in the way a computer program reads and uses databases. (Noble, 2011)

These ideas, of course, are also against the claim that genes are blueprints or recipes, as Plomin (2018) claims in his most recent book (Joseph, 2022). This implies that they are context-independent; we have known for years that genes are massively context-sensitive. The line of argument that hereditarians push is that genes are context-insensitive, that is they’re context-independent. But since DNA is but one of the developmental resources the physiological system uses to create the phenotype, this claim fails. Genes are not causes on their own.

Behavioral geneticist and evolutionary psychologist J. P. Rushton (1997: 64) claims that a study shows that “genes are like blueprints or recipes providing a template for propelling development forward to some targeted endpoint.” That is, Rushton is saying that there is context-independent “information” in genes, and that genes, in essence, guide development toward a targeted endpoint. Noah Carl (2019) claims that the hereditarian hypothesis “states that these differences [in cognitive ability] are partly or substantially explained by genetics.” When he says the differences are “partly or substantially explained by genetics”, he’s talking about “cognitive ability” being caused by genes. The claim that genes cause (either partly or substantially) cognitive ability—and all traits, for that matter—fails and it fails since genes don’t do what hereditarians think they do. (Nevermind the conceptual reasons.) These claims are laughable, due to what Noble, Oyama, Moore and Jablonka and Lamb have argued. It is outright false that genes are like blueprints or recipes. Rushton’s is reductionist in a sociobiology-type way, while Plomin’s is reductionist in a behavioral genetic type way.

In The Dependent Gene, David Moore (2002: 81) talks about the context-dependency of genes:

Such contextual dependence renders untenable the simplistic belief that there are coherent, long-lived entities called “genes” that dictate instructions to cellular machinery that merely constructs the body accordingly. The common belief that genes contain context-independent “information”—and so are analogous to “blueprints” or “recipes”—is simply false.

Genes are always expressed in context and cannot be divorced from said context, like hereditarians attempt using heritability analyses. Phenotypes aren’t “in the genes”, they aren’t innate. They develop through the lifespan (Blumberg, 2018).

Causal parity and hereditarianism

Hereditarianism can be said to be a form of genetic reductionism (and mind-brain identity). The main idea of reductionism is to reduce the whole to the sum of its parts and then analyze those parts. Humans (the whole) are made up of genes (the parts), so to understand human behavior, and humans as a whole, we must then understand genes, so the story goes.

Cofnas (2020) makes several claims regarding the hereditarian hypothesis and genes:

But if we find that many of the same SNPs predict intelligence in different racial groups, a risky prediction made by the hereditarian hypothesis will have passed a crucial test.

…

But if work on the genetics and neuroscience of intelligence becomes sufficiently advanced, it may soon become possible to give a convincing causal account of how specific SNPs affect brain structures that underlie intelligence (Haier, 2017). If we can give a biological account of how genes with different distributions lead to race differences, this would essentially constitute proof of hereditarianism. As of now, there is nothing that would indicate that it is particularly unlikely that race differences will turn out to have a substantial genetic component. If this possibility cannot be ruled out scientifically, we must face the ethical question of whether we ought to pursue the truth, whatever it may be.

Haier is a reductionist of not only the gene variety but the neuro variety—he attempts to reduce “intelligence” to genes and neurology (brain physiology). I have though strongly criticized the use of fMRI neuroimaging studies regarding IQ; cognitive localizations in the brain are untenable (Uttal, 2001, 2011) and this is because mind-brain identity is false.

Cofnas asks “How can we disentangle the effects of genes and environment?” and states the the behavioral geneticist has two ways—correlations between twins and adoptees and GWAS. Unfortunately for Cofnas, twin and adoption studies show no such thing (see Ho, 2013), most importantly because the EEA is false (Joseph, 2022a, b). GWAS studies are also fatally confounded (Janssens and Joyner, 2019) and PGS doesn’t show what behavioral geneticists need it to show (Richardson, 2017, 2022). The concept of “heritability” is also a bunk notion (Moore and Shenk, 2016). (Also see below for further discussion on heritability.) At the end of the day, we can’t do what the hereditarian needs to be done for their explanations to hold any water. And this is even before we look at the causal parity between genes and other developmental resources. Quite obviously, the hereditarian hypothesis is a gene-centered view, and it is of course a reductionist view. And since it is a reductionist, gene-centered view, it is then false.

Genetic, epigenetic, and environmental factors operate as a system to form the phenotype. Since this is true, therefore, both genetic and epigenetic determinism is false (also see Wagoner and Uller, 2015). It’s false because the genes one is born with, or develops with, don’t dictate or determine anything, especially not academic achievement as hereditarian gene-hunters would so gleefully claim. And one’s early experience need not dictate an expected outcome, since development is a continuous process. Although, that does not mean that environmental maladies that one experiences during childhood won’t have lasting effects into adulthood due to possibly affecting their psychology, anatomy or physiology.

The genome is responsive, that is, it is inert before it is activated by the physiological system. When we put DNA in a petri dish, it does nothing. It does nothing because DNA cannot be said to be a separate replicator from the cell (Noble, 2018). So genes don’t do anything independent of the context they’re in; they do what they do DUE TO the context they’re in. This is like Gottlieb’s (2007) probabilistic epigenesis, where the development of an organism is due to the coaction of irreducible bidirectional biological and environmental influences. David S. Moore, in The Developing Genome: An Introduction to Behavioral Epigenetics states this succinctly:

Genes—that is, DNA segments—are always influenced by their contexts, so there is never a perfect relationship between the presence of a gene and the ultimate appearance of a phenotype. Genes do not determine who we become, because nongenetic factors play critical roles in trait development; genes do what they do at least in part because of their contexts.

What he means by “critical roles in trait development” is clear if one understands Developmental Systems Theory (DST). DST was formulated by Susan Oyama (1985) in her landmark book “The Ontogeny of Information. In the book, she argues that nature and nurture are not antagonistic to each other, they are cooperative in shaping the development of organisms. Genes do not play a unique informational role in development. Thus, nature vs. nurture is a false dichotomy—it’s nature interacting with nurture, or GxE. This interactionism between nature and nurture—genes and environment—is a direct refutation of hereditarianism. What matters is context, and the context is never independent from what is going on during development. Genes aren’t the units of selection, the developmental system is, as Oyama explains in Evolution’s Eye:

If one must have a “unit” of evolution, it would be the interactive developmental system: life cycles of organisms in their niches. Evolution would then be change in the constitution and distribution of these systems (Oyama, 2000b)

Genes are important, of course, for the construction of the organism—but so are other resources. Without genes, there would be nothing for the cell to read to initiate transcription. However, without the cellular environment, we wouldn’t have DNA. Lewontin puts this wonderfully in the introduction to the 2000 edition of Ontogeny:

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 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. (2000, 15-16)

Genes aren’t causes on their own, they are resources for development. And being resources for development, they have no privileged level of causation over other developmental resources, such as “methylation patterns, membrane templates, cytoplasmic gradients, centrioles, nests, parental care, habitats, and cultures” (Griffiths and Stotz, 2018). All of these things, and more of course, need to work in concert with each other.

Indeed, this is the causal parity argument—the claim that genes aren’t special developmental resources, that they are “on par” with other developmental resources (Griffiths and Gray, 1994; Griffiths and Stotz, 2018). Gene knockout studies show that the loss of a gene can be compensated by other genes—which is known as “genetic compensation.” None of the developmental resources play a more determinative role than other resources (Noble, 2012; Gamma and Liebrenz, 2019). This causal parity, then, has implications for thinking about trait ontogeny.

The causal parity of genes and other developmental factors also implies that genes cannot constitute sufficient causal routes to traits, let alone provide complete explanations of traits. Full-blown explanations will integrate various kinds of causes across different levels of organizational hierarchy, and across the divide between the internal and the external. The impossibly broad categories of nature vs. nurture that captured the imagination of our intellectual ancestors a century ago are no longer fit for the science of today. (Gamma and Liebrenz, 2019)

Oyama (2000a 40) articulates the casual parity thesis like this:

What I am arguing for here is a view of causality that gives formative weight to all operative influences, since none is alone sufficient for the phenomenon or for any of its properties, and since variation in any or many of them may or may not bring about variation in the result, depending on the configuration of the whole.

While Griffiths and Hochman (2015) formulate it like this:

The ‘parity thesis’ is the claim that if some role is alleged to be unique to nucleic acids and to justify relegating nongenetic factors to a secondary role in explaining development, it will turn out on closer examination that this role is not unique to nucleic acids, but can be played by other factors.

Genes are necessary pre-conditions for trait development, just as the other developmental resources are necessary pre-conditions for trait development. No humans without genes—this means that genes are necessary pre-conditions. If genes then humans—this implies that genes are sufficient for human life, but they are but one part of what makes humans human, when all of the interactants are present, then the phenotype can be constructed. So all of the developmental resources interacting are sufficient.

The nature vs. nurture dichotomy can be construed in such a way that they are competing explanations. However, we now know that the dichotomy is a false one and that the third way—interactionism—is how we should understand development. Despite hereditarian protestations, DST/interactionism refutes their claims. The “information” in the genes, then, cannot explain how organisms are made, since information is constructed dialectically between the resources and the system. There are a multiplicity of causal factors that are involved in this process, and genes can’t be privileged in this process. Thus the phrase “genetic causation” isn’t a coherent concept. Moreover, DNA sequences aren’t even coherent outside of cellular context (Noble, 2008).

Griffiths and Stotz (2018) put the parity argument like this:

In The Ontogeny of Information Oyama pioneered the parity argument, or the ‘parity thesis’, concerning genetic and environmental causes in development (see also Griffiths and Gray 1994; Griffiths and Gray 2005; Griffiths and Knight 1998; Stotz 2006; Stotz and Allen 2012). Oyama relentlessly tracked down failures of parity of reasoning in earlier theorists. The same feature is accorded great significance when a gene exhibits it, only to be ignored when a non-genetic factor exhibits it. When a feature thought to explain the unique importance of genetic causes in development is found to be more widely distributed across developmental causes, it is discarded and another feature is substituted. Griffiths and Gray (1994) argued in this spirit against the idea that genes are the sole or even the main source of information in development. Other ideas associated with ‘parity’ are that the study of development does not turn on a single distinction between two classes of developmental resources, and that the distinctions useful for understanding development do not all map neatly onto the distinction between genetic and non-genetic.

Shea (2011) tries to argue that genes do have a special role, and that is to transport information. Genes are, of course, inherited, but so is every other part of the system (resources). Claiming that there is information “in the genes” is tantamount to saying that there is a special role for DNA in development. But, as I hope will be clear, this claim fails due to the nature of DNA and its role in development.

This line of argument leads to one clear conclusion—genes are followers, they are not leaders; most evolution begins with environmentally-mediated phenotypic change, and then genetic changes occur (West-Eberhard, 2003). Ho and Saunders (1979) state that variation in organisms is constructed during development due to an interaction between genetic and non-genetic factors. That is, they follow what is needed to do by the developmental system, they aren’t leading development, they are but one party in the whole symphony of development. Development can be said to be irreducible, so we cannot reduce development to genes or anything else, as all interactants need to be present for development to be carried out. Since genes are activated by other factors, it is incoherent to talk of “genetic causes.” Genes affect the phenotype only when they are expressed, and other resources, too, affect the phenotype this is, ultimately, an argument genes against as blueprints, codes, recipes, or any other kind of flowery language one can used to impute what amounts to intention to inert DNA.

Even though epigenetics invalidates all genetic reductionism (Lerner and Overton, 2017), genetic reductionist ideas still persist. They give three reasons why genetic reductionist ideas still persist despite the conceptual, methodological, and empirical refutations. (1) Use of terms like “mechanism”, “trait”, and “interaction”; (2) constantly shifting to other genes once their purported “genes for” traits didn’t workout;  and (3) they “buried opponents under repetitive results” (Panofsky, quoted in Lerner and Overton, 2017). The fact of the matter is, there are so many lines of evidence and argument that refute hereditarian claims that it is clear the only reason why one would still be a hereditarian in this day and age is that they’re ignorant—that is racist.

Genes, that is, are servants, not masters, of the development of form and individual differences. Genes do serve as templates for proteins: but not under their own direction. And, as entirely passive strings of chemicals, it is logically impossible for them to initiate and steer development in any sense. (Richardson, 2016)

DST and hereditarian behavioral genetics

I would say that DST challenges three claims from hereditarian behavioral genetics (HBG hereafter):

(1) The claim that we can neatly apportion genes and environment into different causes for the ontogeny of traits;

(2) Genes are the only thing that are inherited and that genes are the unit of selection and a unique—that is, special and privileged cause over and above other resources;

(3) That genes vs environment, blank skate vs human nature, are a valid dichotomy.

(1) HBG needs to rely on the attempting to portion out causes of traits into gene and environmental causes. The heritability statistic presumes additivity, thy is, it assumes no interaction. This is patently false. Charney (2016) gives the example of schizophrenia—it is claimed that 50 percent of the heritability of schizophrenia is accounted for by 8000 genes, which means that each SNP accounts for 1/8000 of the half of the heritability. This claim is clearly false, as genetics aren’t additive, and the additivity assumption precludes the interaction of genes with genes, and environment, which create new interactive environments. Biological systems are not additive, they’re interactive. Heritability estimates, therefore, are attempts at dichotomizing what is not dichitomizable (Rose, 2005).

An approach that partitions variance into independent main effects will never resolve the debate because, by definition, it has no choice but to perpetuate it. (Goldhaber, 2012)

This approach, of course, is the approach that attempts to partition variance into G and E components. The assumption is that G and E are additive. But as DST theorists have argued for almost 40 years, they are not additive, they are interactive and so not additive, therefore heritability estimates fail on conceptual grounds (as well as many others). Heritability estimates have been—and continue to today—been at the heart of the continuance of the nature vs nurture distinction, the battle, if you will. But if we accept Oyama’s causal parity argument—and due to the reality of how genes work in the system, I see no reason why we shouldn’t—then we should reject hereditarianism. Hereditarians have no choice but to continue the false dichotomy of nature vs nurture. Their “field” depends on it. But despite the fact that the main tool for the behavioral geneticist lies on false pretenses (twin and adoption studies), they still try to show that heritability estimates are valid in explaining trait variation (Segalowitz, 1999; Taylor, 2006, 2010).

(2) More than genes are inherited. Jablonka and Lamb (2005) argue that there are four dimensions—interactants—to evolution: genetic, epigenetic, behavioral, and symbolic. They show the context-dependency of the genome, meaning that genotype does not determine phenotype. What does determine the phenotype, as can be seen from the discussion here, is the interacting of developmental resources in development. Clearly, there are many other inheritance systems other than genes. There is also the fact that the gene as popularly conceived does not exist—so it should be the end of the gene as we know it.

(3) Lastly, DST throws out the false dichotomy of genes and environment, nature and nurture. DST—in all of its forms—rejects the outright false dichotomy of nature vs nurture. They are not in a battle with each other, attempting to decide who is to be the determining factor in trait ontogeny. They interact, and this interaction is irreducible. So we can’t reduce development to genes or environment (Moore, 2016) Development isn’t predetermined, it’s probabilistic. The stability of phenotypic form isn’t found in the genes (Moore and Lickliter, 2023)

Conclusion

Genes are outcomes, not causes, of evolution and they are not causes of trait ontogeny on their own. The reality is that strong causal parity is true, so genes cannot be regarded as a special developmental resource from other resources—that is, genes are not privileged resources. Since they are not privileged resources, we need to, then, dispense with any and all concepts of development that champion genes as being the leader of the developmental process. The system is, not genes, with genes being but one of many of the interactants that shape phenotypic development.

By relying on the false narrative that genes are causes and that they cause not only our traits but our psychological traits and what we deem “good” and “bad”, we would then be trading social justice for hereditarianism (genetic reductionism).

These recommended uses of bad science reinforce fears of institutionalized racism in America and further the societal marginalization of minority groups; these implications of their recommendations are never publicly considered by those who promulgate these flawed extensions of counterfactual genetic reductionism. (Lerner, 2021)

Such [disastrous societal] applications can only rob people of life chances and destroy social justice. Because developmental science has the knowledge base to change the life course trajectories of people who are often the targets of genetic reductionist ideas, all that remains to eradicate genetic reductionism from scientific discussion is to have sufficient numbers of developmental scientists willing to proclaim loudly and convincingly that the naked truth is that the “emperor” (of genetic reductionism) has no clothes. (Lerner, 2021: 338)

Clearly, hereditarians need the nature vs nurture debate to continue so they can push their misunderstandings about genes ans psychology. However, given our richer understanding of genes and how they work, we now know that hereditarianism is untenable, and DST conceptions of the gene and development as a whole have led us to that conclusion. Lerner (2017) stated that as soon as the failure of one version of genetic reductionism is observed, another one pious up—making it like a game of whack-a-mole.

The cure to hereditarian genetic reductionism is a relational developmental systems (RDS) model. This model has its origins with Uri Bronfenbrenner’s ecological systems theory (Bronfenbrenner and Ceci, 1994; Ceci, 1996; Patel, 2011; Rosa and Tudge, 2013. Development is about the interacting and relation between the individual and environment, and this is where RDS theory comes in. Biology, physiology, culture, and history are studied to explain human development (Lerner, 2021). Hereditarian ideas cannot give us anything like what models derived from developmental systems ideas can. An organism-environment view can lead to a more fruitful, and the organism and environment are inseparable (Jarvilehto, 1998; Griffiths and Gray, 2002). And it is for these reasons, including many, many more, that hereditarian genetic reductionist ideas should become mere sand in the wind.

Having said all that, here’s the argument:

P1: If hereditarianism is true, then strong causal parity is false.

P2: Strong causal parity is true.

C: Therefore hereditarianism must be false.