Genetic determinism is the belief that behavior/mental abilities are ‘controlled by’ genes. Gerick et al (2017) note that “Genetic determinism can be described as the attribution of the formation of traits to genes, where genes are ascribed more causal power than what scientific consensus suggests“, which is similar to Oyama (1985) who writes “Just as traditional though placed biological forms in the mind of God, so modern thought finds ways of endowing genes with ultimate formative power.” Moore (2014: 15) notes that genetic determinism is “the idea that genes can determine the nature of our characteristics” or “the old idea that biology controls the development of characteristics like intelligence, height, and personality” (pg 39). (See my article DNA is not a Blueprint for more information.)
On the other hand, epigenetic determinism is “the belief that epigenetic mechanisms determine the expression of human traits and behaviors” (Wagoner and Uller, 2016). Both views are, of course, espoused in the scientific literature as well as usual social discourse. Both views, as well, are false. Moore (2014: 245) notes that epigenetic determinism is “the idea that an organism’s epigenetic state invariably leads to a particular phenotype.”
The concept of genetic determinism was first proposed by Weismann in 1893 with a theory of germplasm. This, in contemporary times, is contrasted with “blank slatism” (Pinker, 2002), or the Standard Social Science Model (SSSM; Tooby and Cosmides, 1992; see Richardson, 2008 for a response). Genes, genetic determinists hold, determine the ontogeny of traits, being a sort of “director.” But this betrays modern thinking on genes, what they are, and what they “do.” Genes do nothing on their own without input from the physiological system—that is, from the environment (Noble, 2011). Thus, gene-environment interaction is the rule.
This lead to either-or thinking in regard to the origin of traits and their development—what we now call “the nature-nurture debate.” Nature (genes/biology) or nurture (experience, how one is raised), gene determinists hold, are the cause of certain traits, like, for example, IQ.
Plomin (2018) asserts that nature has won the battle over nurture—while also stating that they interact. So, which one is it? It’s obvious that they interact—if there were no genes there would still be an environment but if there were no environment there would be no genes. (See here and here for critiques of his book Blueprint.)
This belief that genes determine traits goes back to Galton—one of the first hereditarians. Indeed, Galton was the one to coin the phrase “nature vs nurture”, while being a proponent of ‘nature over nurture.’ Do genes or environment influence/cause human behavior? The obvious answer to the question is both do—and they are intertwined: they interact.
Griffiths (2002) notes that:
Genetic determinism is the idea that many significant human characteristics are rendered inevitable by the presence of certain genes; that it is futile to attempt to modify criminal behavior or obesity or alcoholism by any means other than genetic manipulation.
Griffiths then argues that genes are very unlikely to be deterministic causes of behavior. Genes are thought to have a kind of “information” in them which then determines how the organism will develop. This is what the “blueprint metaphor” for genes attempts to show. Genes contain this information for trait development. The implicit assumption here is that genes are context-independent—that the (environmental) context the organism is in does not matter. But genes are context-dependent—“the very concept of a gene requires the environment” (Schneider, 2007). This speaks to the context-dependency of genes. There is no “information”—genes are not like blueprints or recipes. So genetic determinism is false.
The claim that genes determine phenotypes can be shown in the following figure from Kampourakis (2017: 187):
Figure 9.6 (a) The common representation of gene function: a single gene determines a single phenotype. It should be clear by what has been present in the book so far that is not accurate. (b) A more accurate representation of gene function that takes development and environment into account. In this case, a phenotype is produced in a particular environment by developmental processes in which genes are implicated. In a different environment the same genes might contribute to the development of a different phenotype. Note the “black box” of development.
Richardson (2017: 133) notes that “There is no direct command line between environments and genes or between genes and phenotypes.” The fact of the matter is, genes do not determine an organism’s characters, they are merely implicated in the development of the character—being passive, not active templates (Noble, 2011).
Moore (2014: 199) tells us how genetic determinism fails since genes do not work in a vaccuum:
There is just one problem with the neo-Darwinian assumption that “hard” inheritance is the only good explanation for the transgenerational transmission of phenotypes: It is hopelessly simplistic. Genetic determinism is a faulty idea, because genes do not operate in a vacuum; phenotypes develop when genes interact with nongenetic factors in their local environments, factors that are affected by the broader environment.
On the other hand, epigenetic determinism, the belief that epigenetic mechanisms determine the behavior of the organism, is false but in the other direction. Epigenetic determinists decry genetic determinism, but I don’t think they realize that they are just as deterministic as they are.
Dupras et al (2018) note how “overly deterministic readings of epigenetic marks could promote discriminatory attitudes, discourses and practices based on the predictive nature of epigenetic information.” While epigenetics—specifically behavioral epigenetics—refutes notions of genetic determinism, we can then fall into a similar trap, but determinism all the same. This means, though, that since genes don’t determine, epigenetics does not either, so we cannot epigenetically manipulate pre- or perinatally since what we would attempt to manipulate—‘intelligence’, contentment, happiness—all develop over the lifespan. Moore (2014: 248) continues:
Even in situations where we know that certain perinatal experiences can have very long-term effects, determinism is still an inappropriate framework for thinking about human development. For example, no one doubts that drinking alcohol during pregnancy is bad for the fetus, but in the hundreds of years before scientists established this relationship, innumerable fetuses exposed to some alcohol nonetheless grew up to be healthy, normal adults. This does not mean that pregnant women should drink alcohol freely, of course, but it does mean that developmental outcomes are not as easy to predict as we sometimes think. Therefore, it is probably always a bad idea to apply a deterministic worldview to a human being. Like DNA segments, epigenetic marks should not be considered destiny. How a given child will develop after trauma, for example, depends on a lot more than simply the experience of the trauma itself.
In an interview with The Psych Report Moore tells us that people not know enough about epigenetics for there to be epigenetic determinists (though many journalists and some scientists talk like they are :
I don’t think people know enough about epigenetics yet to be epigenetic determinists, but I foresee that as a problem. As soon as people start hearing about these kinds of data that suggest that your early experiences can have long-term effects, there’s a natural assumption we all make that those experiences are determinative. That is, we tend to assume that if you have this experience in poverty, you are going to be permanently scarred by it.
The data seem to suggest that it may work that way, but it also seems to be the case that the experiences we have later in life also have epigenetic effects. And there’s every reason to think that those later experiences can ameliorate some of the effects that happened early on. So, I don’t think we need to be overly concerned that the things that happen to us early in life necessarily fate us to certain kinds of outcomes.
While epigenetics refutes genetic determinism, we can run into the problem of epigenetic determinism, which Moore predicts. But journalists note how genes can be turned on or off by the environment, thereby dictating disease states, for example. Though, biological determinism—of any kind, epigenetic or genetic—is nonsensical as “the development of phenotypes depends on the contexts in which epigenetic marks (and other developmentally relevant factors, of course, are embedded” (Moore, 2014: 246).
What really happens?
What really happens regarding development if genetic and epigenetic determinism are false? It’s simple: causal parity (Oyama, 1985; Noble, 2012): the thesis that genes/DNA play an important role in development, but so do other variables, so there is no reason to privilege genes/DNA above other developmental variables. Genes are not special developmental resources and so, nor are they more important than other developmental resources. So the thesis is that genes and other developmental resources are developmentally ‘on par’. ALL traits develop through an interaction between genes and environment—nature and nurture. Contra ignorant pontifications (e.g., Plomin), neither has “won out”—they need each other to produce phenotypes.
So, genetic and epigenetic determinism are incoherent concepts: nature and nurture interact to produce the phenotypes we see around us today. Developmental systems theory, which integrates all factors of development, including epigenetics, is the superior framework to work with, but we should not, of course, be deterministic about organismal development.
A not uncommon reaction to DST is, ‘‘That’s completely crazy, and besides, I already knew it.” — Oyama, 2000, 195, Evolution’s Eye
The existence of race is important for the hereditarian paradigm. Since it is so important, there must be some theories of race that hereditarians use to ground their theories of race and IQ, right? Well, looking at the main hereditarians’ writings, they just assume the existence of race, and, along with the assumption, the existence of three races—Caucasoid, Negroid, and Mongoloid, to use Rushton’s (1997) terminology.
But just assuming race exists without a definition of what race is is troubling for the hereditarian position. Why just assume that race exists?
A race is one of a number of statistically distinguishable groups in which individual membership is not mutually exclusive by any single criterion, and individuals in a given group differ only statistically from one another and from the group’s central tendency on each of the many imperfectly correlated genetic characteristics that distinguish between groups as such.
Fish (2002: 6) continues:
This is an example of the kind of ethnocentric operational definition described earlier. A fair translation is, “As an American, I know that blacks and whites are races, so even though I can’t find any way of making sense of the biological facts, I’ll assign people to my cultural categories, do my statistical tests, and explain the differences in biological terms.” In essence, the process involves a kind of reasoning by converse. Instead of arguing, “If races exist there are genetic differences between them,” the argument is “Genetic differences between groups exist, therefore the groups are races.”
Fish goes on to write that if we take a group of bowlers and a group of golfers then, by chance, there may be genetic differences between them but we wouldn’t call them “golfer races” or “bowler races.” If there were differences in IQ, income and other variables, he continues, we wouldn’t argue that the differences are due to biology, we would attempt argue that the differences are social. (Though I can see behavioral geneticists try to argue that the differences are due to differences in genes between the groups.)
So the reasoning that Jensen uses is clearly fallacious. Though, it is better than Levin’s (1997) and Rushton’s (1997) assumptions that race exists, it still fails since Jensen (1998) is attempting argue that genetic differences between groups make them races. Lynn (2006: 11) uses a similar argument to the one Jensen provides above. (Nevermind Lynn conflating social and biological races in chapter 2 of Race Differences in Intelligence.)
Hardimon has four concepts: the racialist race concept (what I take to be the hereditarian position), the minimalist/populationist race concept (they are two separate concepts, but the populationist race concept is the “scientization” of the minimalist race concept) and the socialrace concept. Specifically, Hardimon (2017: 99) defines ‘race’ as:
… a subdivision of Homo sapiens—a group of populations that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographic ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population.
Spencer (2014, 2019), on the other hand, grounds his racial ontology in the Census and the OMB—what Spencer calls “the OMB race theory”—or “Blumenbachian partitions.” Take Spencer’s most recent (2019) formulation of his concept:
In this chapter, I have defended a nuanced biological racial realism as an account of how ‘race’ is used in one US race talk. I will call the theory OMB race theory, and the theory makes the following three claims:
(3.7) The set of races in OMB race talk is one meaning of ‘race’ in US race talk.
(3.8) The set of races in OMB race talk is the set of human continental populations.
(3.9) The set of human continental populations is biologically real.
I argued for (3.7) in sections 3.2 and 3.3. Here, I argued that OMB race talk is not only an ordinary race talk in the current United States, but a race talk where the meaning of ‘race’ in the race talk is just the set of races used in the race talk. I argued for (3.8) (a.k.a. ‘the identity thesis’) in sections 3.3 and 3.4. Here, I argued that the thing being referred to in OMB race talk (a.k.a. the meaning of ‘race’ in OMB race talk) is a set of biological populations in humans (Africans, East Asians, Eurasians, Native Americans, and Oceanians), which I’ve dubbed the human continental populations. Finally, I argued for (3.9) in section 3.4. Here, I argued that the set of human continental populations is biologically real because it currently occupies the K = 5 level of human population structure according to contemporary population genetics.
Whether or not one accepts Hardimon’s and Spencer’s arguments for the existence of race is not the point here, however. The point here is that these two philosophers have grounded their belief in the existence of race in a sound philosophical grounding—we cannot, though, say the same things for the hereditarians.
It should also be noted that both Spencer and Hardimon discount hereditarian theory—indeed, Spencer (2014: 1036) writes:
Nothing in Blumenbachian race theory entails that socially important differences exist among US races. This means that the theory does not entail that there are aesthetic, intellectual, or moral differences among US races. Nor does it entail that US races differ in drug metabolizing enzymes or genetic disorders. This is not political correctness either. Rather, the genetic evidence that supports the theory comes from noncoding DNA sequences. Thus, if individuals wish to make claims about one race being superior to another in some respect, they will have to look elsewhere for that evidence.
So, as can be seen, hereditarian ‘reasoning’ on race is not grounded in anything—they just assume that races exist. This stands in stark contrast to theories of race put forth by philosophers of race. Nonhereditarian theories of race exist—and, as I’ve shown, hereditarians don’t define race, nor do they have an argument for the existence of races, they just assume their existence. But, for the hereditarian paradigm to be valid, they must be biologically real. Hardimon and Spencer argue that they are, but hereditarian theories do not have any bearing on their theories of race.
There is the hereditarian ‘reasoning’ on race: either assume its existence sans argument or argue that genetic differences between groups exist so the groups are races. Hereditarians need to posit something like Hardimon or Spencer.
Jewish IQ is one of the most-talked-about things in the hereditarian sphere. Jews have higher IQs, Cochran, Hardy, and Harpending (2006: 2) argue due to “the unique demography and sociology of Ashkenazim in medieval Europe selected for intelligence.” To IQ-ists, IQ is influenced/caused by genetic factors—while environment accounts for only a small portion.
“Fourth, other environmentalists such as Majoribanks (1972) have argued that the high intelligence of the Ashkenazi Jews is attributable to the typical “pushy Jewish mother”. In a study carried out in Canada he compared 100 Jewish boys aged 11 years with 100 Protestant white gentile boys and 100 white French Canadians and assessed their mothers for “Press for Achievement”, i.e. the extent to which mothers put pressure on their sons to achieve. He found that the Jewish mothers scored higher on “Press for Achievement” than Protestant mothers by 5 SD units and higher than French Canadian mothers by 8 SD units and argued that this explains the high IQ of the children. But this inference does not follow. There is no general acceptance of the thesis that pushy mothers can raise the IQs of their children. Indeed, the contemporary consensus is that family environmental factors have no long term effect on the intelligence of children (Rowe, 1994).
The inference is a modus ponens:
P1 If p, then q.
C Therefore q.
Let p be “Jewish mothers scored higher on “Press for Achievement” by X SDs” and let q be “then this explains the high IQ of the children.”
So now we have:
Premise 1: If “Jewish mothers scored higher on “Press for Achievement” by X SDs”, then “this explains the high IQ of the children.”
Premise 2: “Jewish mothers scores higher on “Press for Achievement” by X SDs.”
Conclusion: Therefore, “Jewish mothers scoring higher on “Press for Achievement” by X SDs” so “this explains the high IQ of the children.”
Vaughn (2008: 12) notes that an inference is “reasoning from a premise or premises to … conclusions based on those premises.” The conclusion follows from the two premises, so how does the inference not follow?
IQ tests are tests of specific knowledge and skills. It, therefore, follows that, for example, if a “mother is pushy” and being pushy leads to studying more then the IQ of the child can be raised.
Looking at Lynn’s claim that “family environmental factors have no long term effect on the intelligence of children” is puzzling. Rowe relies heavily on twin and adoption studies which have false assumptions underlying them, as noted by Richardson and Norgate (2005), Moore (2006), Joseph (2014), Fosse, Joseph, and Richardson (2015), Joseph et al (2015). The EEA is false so we, therefore, cannot accept the genetic conclusions from twin studies.
Lynn and Kanazawa (2008: 807) argue that their “results clearly support the high intelligence theory of Jewish achievement while at the same time provide no support for the cultural values theory as an explanation for Jewish success.” They are positing “intelligence” as an explanatory concept, though Howe (1988) notes that “intelligence” is “a descriptive measure, not an explanatory concept.” “Intelligence, says Howe (1997: ix) “is … an outcome … not a cause.” More specifically, it is an outcome of development from infancy all the way up to adulthood and being exposed to the items on the test. Lynn has claimed for decades that high intelligence explains Jewish achievement. But whence came intelligence? Intelligence develops throughout the life cycle—from infancy to adolescence to adulthood (Moore, 2014).
Ogbu and Simon (1998: 164) notes that Jews are “autonomous minorities”—groups with a small number. They note that “Although [Jews, the Amish, and Mormons] may suffer discrimination, they are not totally dominated and oppressed, and their school achievement is no different from the dominant group (Ogbu 1978)” (Ogbu and Simon, 1998: 164). Jews are voluntary minorities, and voluntary minorities, according to Ogbu (2002: 250-251; in Race and Intelligence: Separating Science from Myth) suggests five reasons for good test performance from these types of minorities:
- Their preimmigration experience: Some do well since they were exposed to the items and structure of the tests in their native countries.
- They are cognitively acculturated: They acquired the cognitive skills of the white middle-class when they began to participate in their culture, schools, and economy.
- The history and incentive of motivation: They are motivated to score well on the tests as they have this “preimmigration expectation” in which high test scores are necessary to achieve their goals for why they emigrated along with a “positive frame of reference” in which becoming successful in America is better than becoming successful at home, and the “folk theory of getting ahead in the United States”, that their chance of success is better in the US and the key to success is a good education—which they then equate with high test scores.
So if ‘intelligence’ is a test of specific culturally-specific knowledge and skills, and if certain groups are exposed more to this knowledge, it then follows that certain groups of people are better-prepared for test-taking—specifically IQ tests.
The IQ-ists attempt to argue that differences in IQ are due, largely, to differences in ‘genes for’ IQ, and this explanation is supposed to explain Jewish IQ, and, along with it, Jewish achievement. (See also Gilman, 2008 and Ferguson, 2008 for responses to the just-so storytelling from Cochran, Hardy, and Harpending, 2006.) Lynn, purportedly, is invoking ‘genetic confounding’—he is presupposing that Jews have ‘high IQ genes’ and this is what explains the “pushiness” of Jewish mothers. The Jewish mothers then pass on their “genes for” high IQ—according to Lynn. But the evolutionary accounts (just-so stories) explaining Jewish IQ fail. Ferguson (2008) shows how “there is no good reason to believe that the argument of [Cochran, Hardy, and Harpending, 2006] is likely, or even reasonably possible.” The tall-tale explanations for Jewish IQ, too, fail.
Prinz (2014: 68) notes that Cochran et al have “a seductive story” (aren’t all just-so stories seductive since they are selected to comport with the observation? Smith, 2016), while continuing (pg 71):
The very fact that the Utah researchers use to argue for a genetic difference actually points to a cultural difference between Ashkenazim and other groups. Ashkenazi Jews may have encouraged their children to study maths because it was the only way to get ahead. The emphasis remains widespread today, and it may be the major source of performance on IQ tests. In arguing that Ashkenazim are genetically different, the Utah researchers identify a major cultural difference, and that cultural difference is sufficient to explain the pattern of academic achievement. There is no solid evidence for thinking that the Ashkenazim advantage in IQ tests is genetically, as opposed to culturally, caused.
Nisbett (2008: 146) notes other problems with the theory—most notably Sephardic over-achievement under Islam:
It is also important to the Cochran theory that Sephardic Jews not be terribly accomplished, since they did not pass through the genetic filter of occupations that demanded high intelligence. Contemporary Sephardic Jews in fact do not seem to haave unusally high IQs. But Sephardic Jews under Islam achieved at very high levels. Fifteen percent of all scientists in the period AD 1150-1300 were Jewish—far out of proportion to their presence in the world population, or even the population of the Islamic world—and these scientists were overwhelmingly Sephardic. Cochran and company are left with only a cultural explanation of this Sephardic efflorescence, and it is not congenial to their genetic theory of Jewish intelligence.
Finally, Berg and Belmont (1990: 106) note that “The purpose of the present study was to clarify a possible misinterpretation of the results of Lesser et al’s (1965) influential study that suggested that existence of a “Jewish” pattern of mental abilities. In establishing that Jewish children of different socio-cultural backgrounds display different patterns of mental abilities, which tend to cluster by socio-cultural group, this study confirms Lesser et al’s position that intellectual patterns are, in large part, culturally derived.” Cultural differences exist; cultural differences have an effect on psychological traits; if cultural differences exist and cultural differences have an effect on psychological traits (with culture influencing a population’s beliefs and values) and IQ tests are culturally-/class-specific knowledge tests, then it necessarily follows that IQ differences are cultural/social in nature, not ‘genetic.’
In sum, Lynn’s claim that the inference does not follow is ridiculous. The argument provided is a modus ponens, so the inference does follow. Similarly, Lynn’s claim that “pushy Jewish mothers” don’t explain the high IQs of Jews doesn’t follow. If IQ tests are tests of middle-class knowledge and skills and they are exposed to the structure and items on them, then it follows that being “pushy” with children—that is, getting them to study and whatnot—would explain higher IQs. Lynn’s and Kanazawa’s assertion that “high intelligence is the most promising explanation of Jewish achievement” also fails since intelligence is not an explanatory concept—a cause—it is a descriptive measure that develops across the lifespan.