In the year 2000, psychologist Erik Turkheimer proposed three “laws of behavioral genetics” (LoBG hereafter):
● First Law. All human behavioral traits are heritable.
● Second Law. The effect of being raised in the same family is smaller than the effect of genes.
● Third Law. A substantial portion of the variation in complex human behavioral traits is not accounted for by the effects of genes or families. (Turkheimer, 2000: 160)
In March of 2021, I asked Turkheimer how he defined “law.” He responded: “With tongue in cheek. In fact, it’s a null hypothesis: an expected result when nothing in particular is going on.“
In 2015, Chabris et al (2015) proposed a 4th “law”, that a typical behavioral trait is associated with many variants which each explain a small amount of behavioral variability. They state that the “4th law” explains the failure of candidate gene studies and also the need for higher sample sizes in GWA studies. (It seems they are not aware that larger sample sizes increase the probability of spurious correlations—which is all GWA studies are; Claude and Longo, 2016; Richardson, 2017; Richardson and Jones, 2019) Nice ad hoc hypothesis to save their thinking.
One huge proponent of the LoBG is JayMan, who has been on a crusade for years pushing this nonsense. He added a “5th law” proposed by Emil Kirkegaard, which states that “All phenotypic relationships are to some degree genetically mediated or confounded.”
But what is a “law” and are these “laws of behavioral genetics” laws in the actual sense? First I will describe what a “law” is and if there even are biological laws. Then I will address each “law” in turn. I will then conclude that the LoBG aren’t real “laws”, they are derived from faulty thinking about the relationship between genes, traits, environment and the system and how the “laws” were derived rest on false assumptions.
What is a law? Are there biological laws?
Laws are “true generalizations that are “purely quantitative” … They have counterfactual force” (Sober, 1993: 458). Philosopher of mind Donald Davidson argued that laws are strict and exceptionless (Davidson, 1970; David-Hillel, 2003). That is, there must be no exceptions for that law. Sober (1993) discusses Rosenberg’s and Beatty’s arguments against laws of biology—where Rosenberg states that the only law in biology is “natural selection.” (See Fodor, 2008 and Fodor and Piattelli-Palmarini, 2009, 2010 for the argument against that claim and for arguments against the existence of laws of selection that can distinguish between causes and correlates of causes.) It has even been remarked that there are “so few” laws in biology (Dhar and Giuliani, 2010; also see Ruse, 1970).
Biology isn’t reducible to chemistry or physics (Marshal, 2021), since there are certain things about biology that neither chemistry or physics have. If there are laws of biology, then they will be found at the level of the organism or its ecology (Rull, 2022). In fact, it seems that although three laws of biology have been proposed (Trevors and Sailer Jr., 2008), they appear to be mere regularities, including McShea and Brandon’s (2010) first law of biology; all “laws of biology” seem to be mere laws of physics (Wayne, 2020). The “special sciences”, it seems, “are not fit for laws” (Kim, 2010). There seem to be, though, no uncontroversial laws or regularities in biology (Hamilton, 2007).
Now that I have described what laws are and have argued that there probably aren’t any biological laws, what does that mean for the LoBG? I will take each “law” in turn.
“Laws” of behavioral genetics
(1) All human behavioral traits are heritable.
JayMan gives derivations for the “laws”, and (1) and (2) have their bases in twin studies. We know that the equal environments assumption is false (Charney, 2012; Joseph, 2014; Joseph et al, 2015), and so if the EEA is false then we must reject genetic claims from twin study proponents. Nevertheless, the claim that these “laws” have any meaning gets pushed around a lot.
When it comes to the first law, the claim is that “ALL human behavioral traits are heritable”—note the emphasis on “ALL.” So this means that if we find only ONE behavioral trait that isn’t heritable, then the first law is false.
Reimann, Schilke, and cook (2017) used a sample of MZ and DZ twins and asked questions related to trust and distrust. They, of course, claim that “MZ and DZ twins share comparable environments in their upbringing“—which is false since MZ twins have more comparable environments. Nevertheless, they conclude that while trust has a heritability or 30%, “ACE analyses revealed that the estimated heritability [for] distrust is 0%.” This,therefore, means, that the “1st law” is false.
This “first law”, the basis of which is twin, family, and adoption studies, is why we have poured countless dollars into this research, and of course people have their careers (in what is clear pseudoscience) to worry about, so they won’t stop these clearly futile attempts in their search for “genes for” behavior.
(2) The effect of being raised in the same family is smaller than genes.
This claim is clearly nonsense, and one reason why is that the first “law” is false. In any case, there is one huge effect on, children’s outcomes due to birth order and how, then, parental attitudes–particularly mothers—affect child outcomes (Lehmann, Nuevo-Chiquero, and Vidal-Fernandez, 2018).
Why would birth order have an effect? Quite simply, the first-born child will get more care and attention than children who are born after, and so variations in parental behavior due to birth order can explain differences in education and life outcomes. They conclude that “broad shifts in parental behavior appear to set later-born children on a lower path for cognitive development and academic achievement, with lasting impact on adult outcomes.” Thus, Murray’s (2002) claim that birth order doesn’t matter and JayMan’s claim that “that the family/rearing environment has no effect on eventual outcomes” is clearly false. Thus, along with this and the falsity of the “1st law”, the “2nd law” is false, too.
(3) A substantial portion of the variation in complex human behavioral traits is not accounted for by the effects of genes or families.
This “law” covers the rest of the variance not covered in the first two “laws.” It was coined due to the fact that the first two “laws” had variance left that wasn’t “explained” by them. So this is basically unique experience. This is what behavioral genetics call “non-shared environment.” Of course, unique experiences (that is, subjective experiences) would definitely “shape who we are”, and part of our unique experiences are cultural. We know that cultural differences can have an impact on psychological traits (Prinz, 2014: 67). So the overall culture would explain why these differences aren’t “accounted for” in the first two “laws.”
Yet, we didn’t need the LoBG for us to know that individual differences are difference-makers for differences in behavior and psychology. So this means that what we choose to do can affect our propensities and then, of course, our behavior. Non-shared environmental effects are specific to the individual, and can include differing life events. That is, they are random. Non-shared environment, then, is parts of the environment that aren’t shared. Going back to Lehmann, Nuevo-Chiquero, and Vidal-Fernandez (2018) above, although children to grow up in the same family under the same household, they are different ages and so they also experience different life events. They also experience the same things differently, due to the subjectivity of experience.
In any case, the dichotomy between shared and non-shared environment is a dichotomy that upholds the behavioral geneticists main tool—the heritability estimate—from which these “laws” derive (from studies of twins, adoptees, and families). So, due to how the law was formulated (since there were still portions “unaccounted for” by the first two “laws”), it doesn’t really matter and since it rests on the first two false “laws”, therefore the third “law” is also false.
(4) Human behavioral traits are associated with many genes of small effect which contribute to a small amount of behavioral variability.
This “law” was formulated by Chabris et al (2015) due to the failure of molecular genetic studies which hoped to find genes with large effects to explain behavior. This “law” also “explains why the results of “candidate-gene” studies, which focus on a handful of genetic variants, usually fail to replicate in independent samples.” What this means to me is simple—it’s an ad-hoc account, meaning it was formulated to save the gene-searching by behavioral geneticists since the candidate gene era was a clear failure, as Jay Joseph noted in his discussion of the” 4th law.”
So here is the time line:
(1) Twin studies show above-0 heritabilities for behavioral traits.
(2) Since twin studies show high heritabilities for behavioral traits, then there must be genes that will be found upon analyzing the genome using more sophisticated methods.
(3) Once we started to peer into the genome after the completion of the human genome project, we then came to find candidate genes associated with behavior. Candidate gene studies “look at the genetic variation associated with disease within a limited number of pre-specified genes“, they refer to genes “believed to be” associated with a trait in question. Kwon and Goat (2000) wrote that “The candidate gene approach is useful for quickly determining the association of a genetic variant with a disorder and for identifying genes of modest effect.” But Sullivan (2020) noted that “Historical candidate gene studies didn’t work, and can’t work.” Charney (2022) noted that the candidate gene era was a “failure” and is now a “cautionary tale.”
Quite clearly, they were wrong then, and the failure of the candidate gene era led to the ad-hoc “4th law.” This has then followed us to the GWAS and PGS era, where it is claimed that we aren’t finding all of the heritability that twin studies say we should find with GWAS, since the traits under review are due to many genes of small effect. It’s literally just a shell game—when one claim is shown to be false, just make a reason why what you thought would be found wasn’t found, and then you can continue to search for genes “for” behavior. But genetic interactions create a “phantom heritability” (Zuk et al, 2011), while behavioral geneticists assume that the interactions are additive. They simply outright ignore interactions, although they pay it lip service.
So why, then, should we believe behavioral geneticists today in 2023 that we need larger and larger samples to find these mythical genes “for” behavior using GWAS? We shouldn’t. They will abandon GWAS and PGS in a few years when the new kid on the block shows up that they can they champion and claim that the mythical genes “for” behavior will finally be found.
(5) All phenotypic relationships are to some degree genetically mediated or confounded.
This claim is something that comes up a lot—the claim of genetic confounding (and mediation). A confound is a third variable that influences both the dependent and independent variable. The concept of genetic confounding was introduced during the era where it was debated whether or not smoking caused lung cancer (Pingault et al, 2021). (Do note that Ronald Fisher (1957), who was a part of this debate, claimed that smoking and lung cancer were both “influenced by a common cause, in this case individual genotype.“
However, in order for the genetic confounding claim to work, they need to articulate a mechanism that explains the so-called genetic confounding. They need to articulate a genetic mechanism which causally explains X and Y, explains X independent of Y and explains Y independent of X. So for the cop-out genetic confounding claim to hold any water: G confounds X and Y iff there is a genetic mechanism which causally explains X and Y, causally explains X independent of Y and Y independent of X.
The “laws of behavioral genetics” uphold the false dichotomy of genes and environment, nature and nurture. Though, developmental systems theorists have rightly argued that it is a false dichotomy (Homans, 1979; Moore, 2002; Oyama, 2002; Moczek, 2012) and that it is just not biologically plausible (Lewkowicz, 2012). In fact, the h2 statistics assumes that G and E are independent, non-interacting factors, so if the claim is false then—for one of many reasons—we shouldn’t accept their conclusions. The fact that G and E interact means that, of course, we should reject h2 estimates, and along with it, the entire field of behavioral genetics.
Since the EEA is false, h2 equals c2. Furthermore, h2 equals 0. So Polderman’s (2015) meta analysis doesn’t show that for all traits in the analysis that h2 equals 49%. (See Jay Joseph’s critique.) Turkheimer (2000: 160) claimed that the nature-nurture debate is over, since everything is heritable. However, the debate is over because developmental systems approach has upended the false dichotomy of nature vs nurture, since all developmental resources interact and are therefore irreducible to development.
However, for the field to continue to exist, they need to promulgate the false dichotomy, since their heritability estimates depend on it. They also need to hold onto the claim that twin, family and adoption studies can show the “genetic influence” on traits to justify the continued search for genes “for” behavior. Zuk and Spencer (2020) called the nature-nurture “debate” “a zombie idea, one that, no matter how many times we think we have disposed of it, springs back to life.” This is just like Oyama (2000) who compared arguing against gene determinism like battling the undead (Griffiths, 2006).
Jay Joseph proposed a 5th “law” in 2015 where he stated:
Behavior genetic Laws 1-4 should be ignored because they are based on many false assumptions, concepts, and models, on negative gene finding attempts, and on decades of unsubstantiated gene discovery claims.
The “laws” should quite obviously be ignored. Since the whole field of behavioral genetics is based on them, why not abandon the search for “genes for behavior”? At the end of the day, it seems like there are no “laws” of behavioral genetics, since laws are strict and exceptionless. So why do they keep up with their claims that their “laws” tell us anything about human behavior? Clearly, it’s due to the ideology of those who hold that the all-important gene causes traits and behavior, so they will do whatever it takes to “find” them. But in 2023, we know that this claim is straight up false.
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.
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.
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)
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.
Science is concerned with studying physical processes and phenomena. So anything that isn’t physical (like the mind/consciousness) can’t studied by science. I have made many sound arguments for this conclusion. However, we can go deeper. Here is the argument:
(1) Mind is first-personal and subjective.
(2) But science is third-personal and objective.
So (3) it follows that science (a third-personal objective endeavor) can’t study mind (first-personal subjective states).
I will defend these both premises and the conclusion in this article.
Defending the premises
Premise (1) The existence of a first-person perspective (FPP) is necessary and sufficient for consciousness. It is this first-person perspective that we are experiencing, as I write this article and as you read it. A first-person view is subjective experience. Each human has their own special access to their own minds that is “private.” By “private”, I mean it is only accessible to them, the agent, and not accessible to anyone else. If it’s not accessible to anyone else, and another observer would be a third-person observer, then it isn’t accessible by the methods of science. Further, the pronoun “I” denotes an FPP. When we refer to ourselves, we say “I.” “I did that.” “I will do that.” “I have done that.” All of these considerations point to one thing: Consciousness is a subjective state in which agents experience sensations and feelings, and the world around them.
The FPP is the first person perspective of “I”—and by that I mean the experience that we all have every day of our lives. It’s how we ourselves experience the world around us. By “subjective” I mean simply that which belongs to the thinking subject. Subjective states can be said to be intentional states. Intentional states are normative and so irreducible to the physical. So subjective knowledge is—private—knowledge of one’s first-personal states, their beliefs, goals, and desires.
Premise (2) When I say “Science is third-personal”, I mean that there is an observer—on the outside, deliberating on things, viewing things. They are using their first-personal subjective experience to do science, which is in the third person. The mind, apparently, is just the electro-chemistry of the brain—basically the mind is what the brain does. However, mind isn’t identical to brain. Yes, scientists can study the brain since it is made up of physical parts, and neurophysiologists can study the states of the brain. Of course we use our first-personal subjective states to scientifically study what is third-personal. But this need not license the conclusion that since we can study the brain using neuroscience then we can study the mind using neuroscience since M and P are not identical. M is subjective, while P is objective. Lavazza and Robinson (2014) explain this perfectly:
Another set of arguments that present an apparently unanswerable objection to a materialist view is grounded in the fact that every item in an entirely material world would admit of third-person description. Every item would be accessible to the third-person viewpoint and would be amenable to description based on what is revealed to that viewpoint. The problem for the materialist view is that any such description will fail to capture what is accessible only to a first-person viewpoint and thus necessarily will omit the very centre of a person’s world; more specifically, it will omit the self, understood as the subject of conscious states as well as much of the intentional content of those states. As David Lund maintains, third-person information about oneself (knowledge of oneself by description) seems indeed to be neither necessary nor sufficient for consciousness of oneself. It is not sufficient, for (in first-person terms) I would be unable to see that the third-person information is information about me unless I were already aware of myself in a first-person way. But in the materialist view, it would have to be sufficient.
Conclusion I have successfully defended both premises, and so the conclusion that science (third-personal) cannot study mind (first-personal) follows. Of course there is the field of neuroscience where we study the brain’s physiology. Neuroscience contains 2 assumptions—(1) that the mind is physical; and (2) that the brain (or some aspect of the CNS) is sufficient for the mind, that is, we are our brains. The goal, then, is to attempt to discover the sufficient conditions of consciousness; basically the brain produces the mind and there are parts of the mind which are reducible to or identical to parts of the brain. The physical enables conscious experience—that is, it is a dependency condition. But dependency conditions are not sufficient conditions. The ultimate claim, then, is that phenomenal experience is identical to, reducible to, or sufficient from neural activity. Neuroscience neither has the skills nor methods to study the mind—being a science and third-personal, it can only study the physical and so it studies the brain, and the CNS, not the mind. There are organs that have specific processes that we can study, like the stomach and digestion, or the lung and breathing, or the heart and blood circulation. So then it would follow that we study the brain for mind, as neuroscientists assume. But the claim clearly fails (Manzotti and Moderato, 2014).
Francis Crick—one of the discoverers of DNA along with James Watson and Rosalind Franklin— in his book The Astonishing Hypothesis said that humans are
“Just a bunch of neurons…You, your joys, and your sorrows, your memories and your ambitions, your sense of personal identity and free will, are in fact no more than the behaviour of a vast assembly of nerve cells and their associated molecules.”
Of course neurons and everything else that makes up the brain is necessary for the mind but necessariness isn’t sufficientness and it definitely isn’t identity, so Crick’s claim is false.
Richard Dawkins in 1976 argued that humans are mere gene-machines, that is, humans exist merely to propagate selfish genes. But selfishness is a property of organisms (so that’s a mereological fallacy), his idea isn’t even testable by Dawkins’ own admission and DNA can’t be regarded as separate from the cell (Noble, 2011, 2018).
The attempt from Crick to reduce human mental life to mere neurons and by Dawkins to reduce human social life to being for “selfish genes” clearly fail. The most important part, I think, is that they are reductive perspectives, and reductionism is false, so their claims are false. These two claims are attempts at using science to explain the mind and (what appear to be, for Dawkins) intentionality (from his selfish genes), and they obviously fail.
A similar argument is made by Lynne Rudder Baker, where she gives an argument she calls “the master argument”: (1) All phenomena can be explained by science. (2) All science is constructed exclusively from a third-personal view. So (3) All phenomena can be explained with a third-personal view. (Also see Baker, 2007.)
Obviously it’s valid, but is it sound? No, it isn’t, since the first premise is obviously false—mind cannot be explained by a third-personal perspective.
Scientific naturalism is clearly false, since it cannot explain all phenomena like the mind since the mind isn’t physically/ontologically reducible. So, again, as many other arguments have established and entailed, we are not fully physical and, due to this, science can’t explain all aspects of humans. Two substances exist, one first-personal, subjective and private, and the other objective and public. So we should accept that there is an irreducible aspect of human constitution that science simply cannot study, as hard as they try. Thus, the limits of science are clear—Science CANNOT explain everything.
Why Purely Physical Things Will Never Be Able to Think: The Irreducibility of Intentionality to Physical States
What do “normativity” and “intentionality” mean?
What “normativity” means has implications for many things in philosophy and science. Normativity has been distinguished between “semantic normativity” and “conceptual normativity” (Skorupski, 2007). On the semantic version, “any normative predicate is definitionally reducible to a reason predicate” and on the conceptual version “the sole normative ingredient in any normative concept is the concept of a reason” (Skorupski, 2007). Skorupski rejects the semantic version and holds to the conceptual version. The conceptual version does hold value, so I will be operating on this definition in this article. “Intentionality” is the power of mental states to be “about” things. My mental state right now is to write this article on the normativity of psychological traits, so I have a desire to perform this action, making it normative.
Regarding the mind-body problem, the meaning of normativity entails that what is normative is not reducible to (physical) dispositions. Human psychology is intentional. What is intentional is normative. Intentions are done “on purpose”, that is, they’re done “for a reason.” If something is done for a reason, then there is a goal that the agent desired by performing their action. When someone performs an action, we ask “Why?”, and the answer is they performed the action for a reason. “Why did I go to work?”, because I wanted to make money. “Why did I write down my thoughts?”, because I wanted a written record of what I was thinking at a certain moment in time. So how the normativity of intentionality comes into play here is this—if agents perform actions for reasons, and reasons are due to beliefs, goals, and desires to bring about some end by an agent, then what explains why an agent performed an action is their reason TO perform the action.
When one “does something for a reason”, they intend to “do something”, that is they perform an action “on purpose”, meaning they have a desired outcome that the action they carried out will hopefully, for the agent, manifest in reality. The best example I can think of is murder. Murder is the intentional killing of an individual. For whatever reason, the agent that committed the act of murder has a reason they want the person they killed dead. Contrast this with manslaughter, which is “the unlawful killing of a human being without malice.” There are two kinds of manslaughter, voluntary manslaughter which would happen in the heat of the moment, think a passion killing. The other kind being the unintentional killing of a human being. This distinction between murder and manslaughter is, basically, down to what an agent INTENDS TO DO. Thus, one is a murderer if they set out one night to kill an individual, that is if they plan it out (have a goal to murder); and one commits manslaughter if they did not intend to kill the other individual, let’s say two people have a fight and one punches the other and the hit person hits their head on the curb and dies.
Now that I have successfully stated what normativity means, and have distinguished between intentional and unintentional action (murder and manslaughter), I must discuss the distinction between intentions and dispositions.
The normativity of psychological states
The problem of action is how to distinguish what an agent does for reasons, goals, or desires, and what merely happens to them (Paul, 2021). I have argued before that reasons, goals, beliefs, and desires (what an agent does) make the distinction between antecedent conditions which then cause an agent’s movement but were not consciously done (what happens to them).
We know what intentions are, but what are dispositions? Behavior is dispositional, so Katz’s considerations have value here:
a disposition [is] a pattern of behavior exhibited frequently … in the absence of coercion … constituting a habit of mind under some conscious and voluntary control … intentional and oriented to broad goals” (1993b, 16).
There is a wealth of philosophical literature which argues that intentions are irreducible to dispositions (e.g. Kripke, 1980; Bilgrami, 2005, 2006; also see Weber, 2008). Intentional states are, then, irreducible to physical or functional explanations. It then follows that intentional states can’t be explained/studied by science. If intentional states can’t be explained/studied by science, then intentional states are special, indeed they are unique to agents (minded beings).
In the conclusion to Self-Knowledge and Resentment, Akeel Bilgrami describes his pincer argument using a Fregean extension of Moore’s non-naturalism:
Via a discussion of an imaginary subject wholly lacking agency, it was shown how deeply the very notion of thought or intentionality turns on possessing the point of view of agency, of subjectivity, the point of view of the first, rather than third, person. And it was there shown via an argument owing to a Fregean extension of Moore’s anti-naturalism that such a picture of intentionality required ceasing to see intentional subjects in wholly dispositional terns and, indeed, requires seeing intentional states such as beliefs and desires as themselves normative states or commitments. When so viewed, intentional states are very different from how they appear to a range of philosophers who think of them along normative lines, such as [Donald] Davidson. When so viewed, they are not only irreducible to and non-identical with the physical and causal states of the subjects; they cannot even be clearly assessed to be dependent on such states in the specific ways that philosophers like to capture with such terms as ‘supervenience’. (There are of course all sorts of other dependencies that intentional states have on the states of the central nervous system, which do not amount to anything like the relations that go by the name of ‘supervenience’.) This is because when they are so viewed, they are essentially first-person phenomena, phenomena whose claims to supervenient dependence on third person states such as physical or causal properties are either stateable or deniable. (Therefore, not assesable.) (Bilgrami, 2006: 291-292)
Intentionality is a sufficient and necessary condition for mentality according to Brentano. And intentionality along with normativity are 2 out of 5 of the “marks of the mental” (Pernu, 2017). It can even be said to be the aboutedness of the mind to a thing other than itself. If I talk about something or state that I have a desire to do something, this is the aboutness of intentional states. So mental states that are directed at things are said to be intentional states. Intentionality requires goals, beliefs, and desires, so this designates the intentional stance as one of action, which is distinguished from behavior. Since the mental is normative (Zangwill, 2005), then, since we have the problem of normativity for physicalism, this is yet another reason to reject dualism and to accept some kind of dualism.
Goal-directedness is another mark of intentionality. When one acts intentionally, they act in order to bring about a goal they have in mind about something. Take the example of murder I gave above. Knowing that murder is the intentional killing of a human being, the murderer has the goal in mind to end the life of the other person. They act in accordance with their desired to bring about the goal they have in mind.
Since psychological states are intentional states, and intentional states are normative (Wedgewood, 2007; Kazemi, 2022), then psychological states are normative. Since mental states that have content are normative then we cannot reductively explain mind. Thus, Yoo’s (2004) discussion of the normativity of intentionality holds value:
Thus, the reason why thought and behavior cannot be explained in terms of non-intentional, physical, vocabulary comes down to a certain “normative element” constitutive of our interpretation and attributions of the propositional attitudes. Clearly this normative element plays a pivotal role. But in spite of its significance, it is highly obscure and insufficiently understood. Indeed, there have been no serious attempts to systematically examine what, exactly, the normative element amounts to.
As Davidson points out, the normative element ultimately has its roots in the object of the interpreter’s inquiry, which is another mind. Unlike black holes and quarks, which do not conform to norms, let alone the norms of rationality, a mind, by its very nature, has to conform to the norms of rationality. Otherwise, we are not dealing with a mind, should no or too few norms of rationality apply. Black holes and quarks certainly conform to laws – nomological principles – that support statements like “Light ought to bend in a black hole,” but such uses of “ought” have no normative implications (see Brandom 1994, ch. 1). The mental states that make up a mind, on the other hand, are such that they bear normative relations among each other, since their very contents are individuated by the norms of rationality (which is clearly stated in the third account). And the observer of a person’s mind must discern in the other’s bodily movements and vocal utterances a rational pattern that is itself a pattern to which the observer (attributor, appraiser) must subscribe. Hence, insofar as the norms of rationality are reflexive – they constrain both the mental states of the interpreted mind as well as the process of interpretation engaged by the interpreter herself – this aspect of the normative fully satisfies the third constraint.
Many arguments exist which conclude that the mental cannot be explained in terms of words that refer only to physical properties, and this is one of them. And since the mental is normative, this is yet another reason why there cannot—and indeed why their never will be—reductive explanations of the mental to the physical.
The irreducibility of intentionality
If physicalism is true, then intentionality would reduce, or be identical to, something physical. Then we should have an explanation of intentionality in physical terms. However, I would say this is not possible. (See Heikinheimo’s Rule-Following and the Irreducibility of Intentional States.) It’s not possible because physical systems can’t intend, that is they can’t act intentionally.
The argument is a simple one: Only beings with minds can intend. This is because mind allows a being to think. Since the mind isn’t physical, then it would follow that a physical system can’t intend to do something—since it wouldn’t have the capacity to think. Take an alarm system. The alarm system does not intend to sound alarms when the system is tripped. It’s merely doing what it was designed to do, it’s not intending to carry out the outcome. The alarm system is a physical thing made up of physical parts. So we can then liken this to, say, A.I.. A.I. is made up of physical parts. So A.I. (a computer, a machine) can’t think. However, individual physical parts are mindless and no collection of mindless things counts as a mind. Thus, a mind isn’t a collection of physical parts. Physical systems are ALWAYS a complicated system of parts but the mind isn’t. So it seems to follow that nothing physical can ever have a mind.
Physical parts of the natural world lack intentionality. That is, they aren’t “about” anything. It is impossible for an arrangement of physical particles to be “about” anything—meaning no arrangement of intentionality-less parts will ever count as having a mind. So a mind can’t be an arrangement of physical particles, since individual particles are mindless. Since mind is necessary for intentionality, it follows that whatever doesn’t have a mind cannot intend to do anything, like nonhuman animals. It is human psychology that is normative, and since the normative ingredient for any normative concept is the concept of reason, and only beings with minds can have reasons to act, then human psychology would thusly be irreducible to anything physical. Indeed, physicalism is incompatible with intentionality (Johns, 2020). The problem of intentionality is therefore yet another kill-shot for physicalism. It is therefore impossible for intentional states (i.e. cognition) to be reduced to, or explained by, physicalist theories/physical things.
This is similar to Lynn Baker’s (1981) argument in Why Computers Can’t Act (note how in her conclusion she talks about language—the same would therefore hold for nonhuman animals):
P1: In order to be an agent, an entity must be able to formulate intentions.
P2: In order to formulate intentions, an entity must have an irreducible first-person perspective.
P3: Machines lack an irreducible first-person perspective.
C: Therefore, machines are not agents.
So machines cannot engage in intentional behavior of any kind. For example, they cannot tell lies, since lying involves the intent to deceive; they cannot try to avoid mistakes, since trying to avoid mistakes entails intending to conform to some normative rule. They cannot be malevolent, since having no intentions at all, they can hardly have wicked intentions. And, most significantly, computers cannot use language to make assertions, ask questions, or make promises, etc., since speech acts are but a species of intentional action. Thus, we may conclude that a computer can never have a will of its own.
So PP’s “depression” about ChatGPT “scoring” 11 points on his little (non-construct valid) test is irrelevant. It’s a machine and, as successfully argued, machines will NEVER have the capacity to think/act/intend.
What does this mean for a scientific explanation of human psychology?
The arguments made here point to one conclusion—since intentions don’t reduce to the physical and functional states of humans (like neurophysiology; Rose, 2005), then it is impossible for science to explain intentions, since what is normative isn’t reducible to, or identical with, physical properties. This is another arrow in the quiver of the anti-physicalist/dualist to show that there is something more than the physical—there is an irreducible SELF or MIND and we humans are the only minded beings. Science can’t explain the human mind and, along with it, the intentions that arrive from a deliberating mind. This is also an argument against Benjamin Libet’s experiments in which he concludes that the subjects’ brain activity preceded their actions, that is, it is the brain that initiates action. This view, however, is false, since the (minded) agent is what initiates action. Libet is therefore guilty of the mereological fallacy. Freely-willed processes are therefore not initiated by the brain (Radder and Meynen, 2012).
Elon Musk and Sam Harris have warned of a “robot rebellion” like what occurred in The Terminator. Though, since what I’ve argued here is true—that purely physical things lack minds, that is they can’t intend or think—then such worries should rightly stay in the realm of sci-fi. The implication is clear—since purely physical things cannot intend, and humans can intend, then there is an irreducible SELF or MIND which allows us to intend. The claim, then, that the human brain is a computer is clearly false. It then follows that humans aren’t purely physical; there is a mental and physical aspect to humans—that is, there are two substances that make us up, the mental and the physical, and it is clear that M (the mental) is irreducible to P (the physical). Sentient machines are, luckily, a myth. It’s just not possible for scientists to imbue a machine with a mind since machines are purely physical and minds aren’t. John Searle’ s Chinese Room Argument, too, is an argument against strong A.I.. Machines will never become conscious since consciousness isn’t physical.
This is yet another argument against the scientific study of the mind/self and, of course, against psychology and hereditarianism. This is then added to the articles that argue against the overall hereditarian program in psychology, and psychology more broadly: Conceptual Arguments Against Hereditarianism; Reductionism, Natural Selection, and Hereditarianism; and Why a Science of the Mind is Impossible. For if the main aspect of IQ test-taking is thinking, thinking is cognition, cognition is intentional and therefore psychological, it follows that since there can be no explanations of intentional states in terms of physical vocabulary, and if cognition—being a psychological trait—is normative, then the conclusion is, again, that hereditarianism and psychology fail their main goal. It is impossible.
It has been commonly stated in hereditarian circles that by increasing aid to Africa, then we would be merely helping their demographic explosion. In 2020, the average adolescent fertility in Sub-Saharan Africa (SSA) rate was 98 births per 1000 girls. Birthrates in most African countries are very high, and to some, the claim is that if we give aid to these countries then they will continue to have more children as they have the means to do so. Though high birthrates in SSA are “concentrated among vulnerable groups where progress is often poorest” (Neal et al, 2020). This worry however, has no basis in reality. In this article, I will provide a few studies looking at the relationship between economic aid and decreasing birthrates. This, then, refutes the (racist) worries of people like Steve Sailer who warn that by increasing aid to Africa we are then helping their population explosion. However, what is borne out by data in countries where this has occurred, if there are sufficient family planning methods, the birthrate will decrease—not increase—with monetary aid to poor African countries.
What is hunger?
Hunger is a feeling of discomfort or weakness; having a desire or craving for food or having pain that is caused by lack of food. There is malnutrition (a condition caused by a diet that has insufficient nutrients for normal functioning), undernourishment (where the food one does eat does not give enough kcal for normal functioning), and starvation (a state of the body caused by long-term lack of food or nutrients). Hunger is a self-reported notion, and so, we would then need to indirectly measure physical variables that are associated with being well-fed or not. Like measuring one’s blood for the lack of certain nutrients, measuring the foods they do eat and ascertaining the macro-nutrient content of what they eat, measuring their height and weight and comparing it to a representative sample, checking to see if there are micro-nutrient deficiencies (Conway, 2012).
But what causes hunger? Inequality/inequities and poverty cause hunger. Indeed, we have enough food to feed 10 billion people—the world produces enough food to feed 1.5 times the world population, but people making $2 a day cannot afford the food (Holt-Giminez et al, 2012) while 828 million people per day go hungry. About 14 million children suffer from acute malnutrition, 45 percent of child deaths around the world are due to hunger and it’s causes, and 700 children die per day due to dirty water, unhygienic water sources, and hunger. So we DO have the food to feed these people, what they DON’T have is the money to feed themselves and their families due to the pittance wages they receive. The year 2022 has been called “a year of unprecedented hunger” by the World Food Programme.
In The State of Food Security and Nutrition in the world 2021 published in mid-2021 it was reported by the UN that an:
estimated that between 720 and 811 million people went hungry in 2020. High costs and low affordability also mean billions cannot eat healthily or nutritiously. Considering the middle of the projected range (768 million), 118 million more people were facing hunger in 2020 than in 2019 – or as many as 161 million, considering the upper bound of the range.
In 1974, the Food and Agriculture Organization of the United Nations (FAO) began reporting on the number of people that faced hunger issues. They define hunger as:
an uncomfortable or painful physical sensation caused by insufficient consumption of dietary energy. It becomes chronic when the person does not consume a sufficient amount of calories (dietary energy) on a regular basis to lead a normal, active and healthy life. For decades, FAO has used the Prevalence of Undernourishment indicator to estimate the extent of hunger in the world, thus “hunger” may also be referred to as undernourishment.
Hunger is related to food insecurity, where food insecurity is when one is unable to procure items for nourishment due either to availability or lack of monies to procure foodstuffs that would lead to normal development. The FAO also has a measure of food insecurity prevalence of undernourishment (PoU) along with the prevalence of moderate or severe food insecurity in a population based on the food insecurity experience scale (FIES) which estimates how prevalent food insecurity is in a population down to the household or individual level which is ascertained through interviews with the populace.
Now that I have defined hunger, how we indirectly measure hunger (with its physical correlates) and the troubling future we have with hunger across the world, we can now turn to the claim that aid to poor countries will increase their birthrates. This claim has been made a lot by many different groups, and it certainly is a logical claim to make, but what does the data say in countries where such an intervention did occur? Did their population increase even after aid was given to them? Or did their population decrease as they got aid? The answer to this question will be the answer to the question in Africa as we continue to reach the fabled year of 2050 when their population is expected to reach 5 times its present size by the year 2050 in one 1988 estimate (Yanagishita, 1988) to 4 projections based on different assumptions (Haub, 1997), to certain African countries increasing even past 2100 (Ezeh, Kissling, and Singer, 2020). Africa is quickly urbanizing (Veary et al, 2019), and since urbanization decreases fertility rates (Yi and Vaupel, 1989; White et al, 2008; Martine, Alves, and Cavenaghi, 2013; Lerch, 2019), I would hedge my bet that the population growth in Africa—if ample aid is provided since aid to developing countries decreases, not increases, a country’s population—will be far lower than predicted, nevermind the fact that the assumption would be that the population would increase linearly.
Food security and population growth
In his 2010 book One Billion Hungry: Can We Feed the World?, Gordon Conway (2010) writes about the claim that aid to Africa will increase the African population. He cites a study stating that giving developing populations more food is a self-defeating policy since it will cause their population to increase. He writes:
Nevertheless, the fertility rate decline has not been universal. In many Sub-Saharan countries fertility rate declines have stalled at rates over 5.0 after gradually decreasing for several years.25 The reasons are complex, but a common feature appears to be the decreased funding for family planning programs. According to data from thirty-one countries, on average 30 percent of women in Sub-Saharan Africa have an unmet need for modern family planning methods, a proportion that has not declined in the last decade.26 In nineteen of these countries, it is as high as nearly 50 percent. If fertility were to remain constant at current levels, the population of less-developed regions would increase to 9.8 billion in 2050 instead of the projected 7.9 billion.27
A popular misconception is that providing the developing countries with more food will serve to increase populations; in other words, it is a self-defeating policy.28 The more food women have, the more children they will have and the greater will be their children’s survival, leading to population growth, so goes the argument. However, the experience of the demographic transition described above suggests the opposite. As people become more prosperous, which includes being better fed and having lower child mortality, the fewer children women want. Providing they then have access to family planning methods, the fertility rates will drop and the population will cease to grow.29
Let’s take a look at these references in turn:
25 – Ezeh, A., Mberu, B., and Emina, J. 2009. Stall in fertility decline in Eastern African countries: regional analysis of patterns, determinants and implications. Philosophical Transactions of the Royal Society B 364:2991–3007.
In Kenya and Tanzania, fertility has declined for the most educated women and in certain other regions. In Uganda, while fertility levels remain at the pre-transition state, there is a decrease in fertility for specific demographics of women—the most educated and urbanized, along with those in the raster region of the country. In Zimbabwe, though fertility rates continue to fall, it isn’t falling for women with less than a secondary education and in certain regions. This is yet more data that speaks to the claim that as locals urbanize and get more educated, the fertility levels begin to decrease.
26 – Prata, N. 2009. Making family planning accessible in resource-poor settings. Philosophical Transactions of the Royal Society B 364:3093–3099.
Since 30 percent of women in SSA have an unmet need for family planning, by educating them on the need for family planning along with readily accessible contraceptives, ensuring that contraceptives become a permanent part of family planning, and taking action to remove barriers that hinder family planning, we can then help those 30 percent of women plan for families and therefore birth rates will decrease. It is therefore imperative that we roll out programs that would teach people how to plan for families and that would mean educating them on contraceptive use and, as I will explain below, give aid to them, since when people become more prosperous, the birth rate will decrease since they have more children since their death rates are so high.
28 – Hopfenberg, R. and Pimental, D. 2001. Human population numbers as a function of food supply. Environment, Development and Sustainability. 3:1–15.
The authors claim in this paper that experimental and correlational data state that as food production increases, so too will the population that is receiving that food, as they will then be unfettered by the ravenous issues that affect their death rates. They would then be able to have as many children as they want, so the story goes. However, as I will go into below, this is not what we have seen when aid and family planning have been to countries that so sorely needed it.
29 – Foster, A., and Rosenzwieg, M. 2006. Does economic growth reduce fertility? Rural India 1971–1999. Delhi: NCAER India Policy Forum. (pg 179-205)
Foster and Rosenzwieg showed that although female literacy rose to 81 percent in India from 1981-1999, they found no evidence that the increase in female literacy had an effect on decreasing the birthrate in India. The Green Revolution in India led to increased growth and the ability to diversify their occupations. This, in turn, made child-rearing more expensive which then led to a subsequent decrease in the birthrate. Their results do show that the decrease in fertility was driven by an increase in wages for Indian women. They, furthermore, found evidence that health centers (like hospitals) were associated with a decrease in fertility. Foster and Rosenzwieg, thus, “have clearly demonstrated that economic incentives have mattered greatly for the decline in rural fertility in India” (Desai, 2006).
29 – Gertler, P., and Molyneaux, J. 1994. How economic development and family planning programs combine to reduce Indonesian fertility. Demography 31:33–63.
Gertler and Molyneux show that the dramatic decrease in fertility in Indonesia between 1982 to 1987 was due to the increased use in contraceptives along with the increased demand of contraceptives. They found that improvements in women’s education along with an increase in wages for both men and women were responsible for 45 to 60 percent of the decline, and this was driven by contraceptive use. Further, 75 percent of the decline was due to contraceptive use, while 87 percent of the use in contraceptives was due to increased wages and education. They therefore showed that increasing education and wages were responsible for 65 percent of the fertility decline.
29 – Poston, D. Jr, and Gu, B. 1987. Socioeconomic development, family planning and fertility in China. Demography 24:531–551.
Poston and Gu showed that structural development had strong negative effects on fertility, and that family planning has a negative effect on fertility. Basically, SES factors led to a decrease in the birthrate in China. In urban Chinese areas, family planning is higher than in rural areas where fertility is higher, which then licenses the conclusion that family planning decreases birthrates (Poston, 2008). Limieng, Shatalova, and Kalabikhina (2022) show that the higher the per capita GDP, the lower the fertility rate is.
The studies reviewed here show that as people become more well-off, given that they have access to family planning methods, their population will then begin to decrease. There is though, as is the case with China, a fine line to walk through where the population will get too old and not enough younger people will be around, as is the case in Asia already (Goh, 2005). SSA lies at one end of the spectrum—increased fertility due to lack of family planning, low education, low contraceptive use, and low income—while Asian countries like China represent the other side of the spectrum—decreased fertility, higher contraceptive use, and a higher GDP which then leads to a decrease in fertility. Very clearly, there is a middle-ground where a population can be well-off and sustain a population when they have the resources to do so.
In an article for The Conversation, Akinyemi, Dungumaro, and Salaam write:
Why are birthrates so high in five African countries?
The major factors driving population growth in these countries include low contraceptive use, high adolescent fertility rates and a prevalence of polygamous marriages. There’s also the low education status of women, low to poor investment in children’s education, and factors related to religion and ideas.
The use of modern contraceptives is generally low across sub-Saharan Africa. The overall prevalence is 22%. In the Democratic Republic of Congo, however, the uptake of short-acting contraceptives is at 8.1%. In Nigeria, it is at 10.5%. The uptake in Ethiopia is 25%, in Tanzania it’s 27.1% and in Egypt 43%.
For long-acting family planning methods, apart from Egypt with over 20% uptake, the other four countries driving population growth in the region recorded very poor uptake. This low uptake will logically lead to a population explosion.
Some of the factors associated with high contraceptive use in Africa are women’s education, exposure to news and mass media, good economic status and urban residency.
Investing in women’s health, furthermore, leads to “strong intergenerational spillover effects” which then encourages economic development, which would then further decrease the birthrate (Bloom, Kuhn, and Pretnner, 2018). This is borne out in Kenya, Zimbabwe, and Botswana where women had higher levels of education and subsequent decreases in child mortality (Ramirez, Tania and Stewart, 1997). There is also evidence that declining fertility explained a bit less than one-third of the decrease in poverty in rural India in the years 1987 and 1988 and 1993 and 1994 (Dupta and Dubey, 2003). Reducing infant and child mortality also decreases fertility and increases schooling (Kalemli-Ozcan, 2000).
When locales are food secure, then they will have a lower child mortality rate, ceteris paribus and malnutrition is a large driver of this relationship (Bain et al, 2019). Household food insecurity along with dietary diversity is associated with “stunting” (low height for one’s expected age) in SSA (Gassara et al, 2021). So the claim that aid—whether it’s monetary or foodstuffs—will increase the population exponentially is obviously false.
So for people like Steve Sailer who look at current demographic trends using the UN’s data, calling it “the world’s most important graph“, the literature shows that, as Africa urbanizes, becomes more educated, has access to family planning and contraceptives, that their population will decrease. So, by giving aid and education, the population in Africa won’t increase, it will actually DECREASE. We have the means to feed the world on the basis of the food we already produce, it is we just need to educate propel, provide aid to them in all shapes and forms, and then people will have fewer children when they are food secure and have access to contraceptives along with education about them.
Thus, the answer to the question “Will aid to Africa increase the African population?” is a big “No.”