1550 words

The etiology of the increase in lung cancer over the course of the 20th century has been a large area of debate. Was it smoking that caused cancer? Or was some other, unknown, factor the cause? Causation is multifactorial and multi-level—that is, causes of anything are numerous and these causes all interact with each other. But when it comes to smoking, it was erroneously argued that genotypic differences between individuals were the cause of both smoking and cancer. We know now that smoking is directly related to the incidence of lung cancer, but in the 20th century, there were researchers who were influenced and bribed to bring about favorable conclusions for the tobacco companies.

Psychologist Hans Eysenck (1916-1997) was a controversial psychologist researching many things, perhaps most controversially, racial differences in intelligence. It came out recently, though, that he published fraudulent papers with bad data (Smith, 2019). He, among other weird things, believed that smoking was not causal in regard to cancer. Now, why might Eysenck think that? Well, he was funded by many tobacco companies (Rose, 2010; Smith, 2019). He accepted money from tobacco companies to attempt to disprove the strong correlation between smoking and cancer. Between the 1977-1989, Eysenck accepted about 800,000 pounds from tobacco companies. He is not alone in holding erroneous beliefs such as this, however.

Biostatistician Ronald Fisher (1890-1962) (a pipe smoker himself), the inventor of many statistical techniques still used today, also held the erroneous belief that smoking was not causal in regard to cancer (Parascandola, 2004). Fisher (1957) argued in a letter to the British Medical Journal that while there was a correlation between smoking and the acquisition of lung cancer, “both [are] influenced by a common cause, in this case the individual genotype.” He went on to add that “Differentiation of genotype is not in itself an unreasonable possibility“, since it has been shown that genotypic differences in mice precede differences “in the frequency, age-incidence and type of the various kinds of cancer.”

So, if we look at the chain it goes like this: people smoke; people smoking is related to incidences in cancer; but it does not follow that since people smoke that the smoking is the cause of cancer, since an unknown third factor could cause both the smoking and cancer. So now we have four hypotheses: (1) Smoking causes lung cancer; (2) Lung cancer causes smoking; (3) Both smoking and lung cancer are caused by an unknown third factor. In the case of (3), this “unknown third factor” would be the individual genotype; and (4) the relationship is spurious . Fisher was of the belief that “although lung cancer occurred in cigarette smokers it did not necessarily follow that the cancer was caused by cigarettes because there might have been something in the genetic make up of people destined to have lung cancer that made them addicted to cigarettes” (Cowen, 1999). Arguments of this type were popular in the 19th and 20th century—what I would term ‘genetic determinists’ arguments, in that genes dispose people to certain behaviors. In this case, genes disposed people to lung cancer which made them addicted to cigarettes.

Now, the argument is as follows: Smoking, while correlated to cancer is not causal in regard to cancer. Those who choose to smoke would have acquired cancer anyway, as they were predisposed to both smoke and acquire cancer at X age. We now know, of course, that such claims are ridiculous—no matter which “scientific authorities” they come from. Fisher’s idea was that differences in genotype caused differences in cancer acquisition and so along with it, caused people to either acquire the behavior of smoking or not. While at the time such an argument could have been seen as plausible, the mounting evidence against the argument did nothing to sway Fisher’s belief that smoking did not outright cause lung cancer.

The fact that smoking caused lung cancer was initially resisted by the mainstream press in America (Cowen, 1999). Cowen (1999) notes that Eysenck stated that, just because smoking and lung cancer were statistically associated, it did not follow that smoking caused lung cancer. Of course, when thinking about what causes, for example, an observed disease, we must look at similar habits they have. And if they have similar habits and it is likely that those with similar habits have the hypothesized outcome (smokers having a higher incidence of lung cancer, in this case), then it would not be erroneous to conclude that the habit in question was a driving factor behind the hypothesized disease.

It just so happens that we now have good sociological research on the foundations of smoking. Cockerham (2013: 13) cites Hughes’ (2003) Learning to Smoke: Tobacco Use in the West where he describes the five stages that smokers go through: “(1) becoming a smoker, (2) continued smoking, (3) regular smoking, (4) addicted smoking, and, for some, (5) stopping smoking.” Most people report their first few times smoking cigarettes as unpleasant, but power through it to become a part of the group. Smoking becomes somewhat of a social ritual for kids in high-school—with kids being taught how to light a cigarette and how to inhale properly. For many, starting smoking is a social thing that they do with their friends—it can be said to be similar to being social drinkers, they were social smokers. There is good evidence that, for many, their journey as smokers starts and is fully dependent on their social environment than actual physical addiction (Johnson et al, 2003; Haines, et al, 2009).

One individual interviewed in Johnson et al (2003: 1484) stated that “the social setting
of it all [smoking] is something that is somewhat addictive itself.” So, not only is the nicotine the addictive substance on the mind of the youth, so too is the social situation for the youth in which the smoking occurs. The need to fit in with their peers is one important driver for the beginning—and continuance—of the behavior of smoking. So we now have a causal chain in regard to smoking, the social, and disease: youths are influenced/pressured to smoke by their social group which then leads to addiction and then, eventually, health problems such as lung cancer.

The fact that the etiology of smoking is social leads us to a necessary conclusion: change the social network, change the behavior. Just as people begin smoking in social groups, so too, do people quit smoking in social groups (Christakis and Fowler, 2008). We can then state that, on the basis of the cited research, that the social is ultimately causal in the etiology of lung cancer—the vehicle of cancer-causation being the cigarettes pushed bu the social group.

Eysenck and Fisher, two pioneers of statistics and different methods in psychology, were blinded by self-interest. It is very clear with both Eysenck and Fisher, that their beliefs were driven by Big Tobacco and the money they acquired from them. Philosopher Donald Davidson famously stated that reasons are causes for actions (Davidson, 1963). Eysenck’s and Fisher’s “pro-belief” (in this case, the non-causation of smoking to lung cancer) would be their “pro-attitude” and their beliefs lead to their actions (taking money from Big Tobacco in an attempt to show that cigarettes do not cause cancer).

The etiology of lung cancer as brought on by smoking is multifactorial, multilevel, and complex. We do have ample research showing that the beginnings of smoking for a large majority of smokers are social in nature. They begin smoking in social groups, and their identity as a smoker is then refined by others in their social group who see them as “a smoker.” Since individuals both begin smoking in groups and quitting in groups, it then follows that the acquisition of lung cancer can be looked at as a social phenomenon as well, since most people start smoking in a peer group.

The lung cancer-smoking debate is one of the best examples of the dictum post hoc, ergo propter hoc—or, correlation does not equal causation (indeed, this is where the dictum first originated). While Fisher and Eysenck did hold to that view in regard to the etiology of lung cancer (they did not believe that since smokers were more likely to acquire lung cancer that smoking caused lung cancer), it does speak to the biases the two men had in their personal and professional lives. These beliefs were disproven by showing a dose-dependent relationship in regard to smoking and lung cancer: heavier smokers had more serious cancer incidences, which tapered down the less an individual smoked. Fisher’s belief, though, that differences in genotype caused both behavior that led to smoking and the lung cancer itself, while plausible at the time, was nothing more than a usual genetic determinist argument. We now know that genes are not causes on their own; they do not cause traits irrespective of their uses for the physiological system (Noble, 2012).

Everyone is biased—everyone. Now, this does not mean that objective science cannot be done. But what it does show is that “… scientific ideas did not develop in a vacuum but rather reflected underlying political or economic trends” (Hilliard, 2012: 85). This, and many more examples, speak to the biases of scientists. For reasons like this, though, is why science is about the reproduction of evidence. And, for that, the ideas of Eysenck and Fisher will be left in the dustbin of history.

Last time I’ve posted on this subject, it was dissecting the association between magical thinking and technological progress among Africans proposed by Rinderman. In general, I found it wanting of an up-to-date understanding of African anthropology, either in material culture or belief systems. This time, however, the central subject can’t be dismissed on the matter of ignorance. In fact, in a rather awkward way, his dismissal in on the grounds of how much he knows in bot his field and his own writings.

Henry Harpending, deceased, has been listed by the SPLC as a “white nationalist”, though it is the specific content of his quotes in regards to Africans, in light of his admittedly impressive contributions to SW African anthropology, is the major focus than classifying the nature of his bias. The claims in question are

1. He has never meet an African who has a hobby, that is, one with the inclination to work.
2.  Hunter Gatherers are impulsive, lazy, and violent.
3. Africans are more interested in breeding than raising children.
4. Africans, Baltimore Aframs, and PNG natives all share the same behavior in regard to points 2 and 3.
5. Superstitions are pan-african and the only Herero he’s met that was an atheist had a ethnic German Father.

So Harpending seemingly has the edge given his background in Anthropology with specific experiences with Africans…this only makes the only more painful to articulate.

1.  This will set the theme for the nature of my responses…his own work contradicts these assertions. The Herero refugee descent from Botswana, the main strain of Bantu-Speaking Africans he had studied,  were described and calculated as prosperous in regards to cattle per capita and ownership of rural homesteads that stand apart from typical Botswana farming infrastructure.
   

   ---

   Today, they are perceived as one of the wealthiest ethnic groups inBotswana and Namibia. They are known for their large herds, for theirs kill at managing cattle, and for their endogamy and staunch ethnicity even while participating fully in the developing economy and educational system of Botswana.

   His research even noted how age five is when Herero begin herding. A similar phenomenon is noted among the Dinka which prompted Dutton to review the literature of their intelligence scores.

2.  Violence among the Khoi-San groups I’ll admit has been undermined. However, the Hadza, known for their discourage mean of conflict, express this through much lower rates of violent deaths compared to most others. The general consensus is that there is a mix, with the general trend towards higher rates but with cautious interpretation into the causes. On the charge of Laziness, however, is once again unfounded by his work on the lesser resources faced by mobile bands of foragers compared to sedentary ones on labor camps. The same link on the Hadza also pinpoints the hours spent in HG life working and accounts for the difficulty of those hours.
3.  Harpending actually made a model of cads versus dads that he actually attributed to non-genetic factors. Otherwise, we are left with his work on the oddity of “Herero Households”.
   

   If women cannot provision themselves and their offspring without
   assistance, then the “cad/breeder” corner of Fig. 2 is not feasible, and we are left with “dad/feeder.” Draper and Harpending argue that this is true of the Ju/’hoansi, and other mobile foragers in marginal habitats. Among swidden agriculturalists, on the other hand, female labor is more productive, and men can afford to do less work. The theory thus predicts that such populations will be more likely to fall into the “cad/breeder” equilibrium, as in fact they seem to do. Although this theory is couched in Darwinian terms, Harpending and Draper do not see genetic evolution as the engine that accounts for variation within and among societies. Instead, they suggest a facultative adaptation: humans have “evolved the ability to sense household structure in infancy” and to alter their developmental trajectories in response to what is learned during this early critical period (1980, p. 63).

   There does not seem to be any durable group of associated individuals that we could usefully characterize as a household among the Herero. If forced we would say that the Herero have two parallel types of households. The “male household” is the homestead, consisting of an adult male, his wives, sisters, and other relatives, and it is defined by the herd and the kraals that he maintains for the herd. The “female household” is a woman and the children for whom she has responsibility, localized in a hut or hut cluster within a larger homestead. These aregynofocal households, rather than matrifocal households, since matrifocal implies mother and offspring while the Herero unit is a woman and children under the care of that woman. These children may be her own, her grandchildren, children of relatives, or even children leased from other tribes to work on the cattle. Men do not appear prominently in daily domestic life. They are gone at first light pursuing their own interests and careers with cattle, with hunting parties, or with other stereotyped male activities. Similarly, women are not prominently present at male areas like the wells where the cattle are watered. There is, then, not a Herero household, but rather there is a Herero male household that includes cattle and female households, and these females may be wives, or sisters, or other female relatives. The female households are the loci of domestic production and consumption. 

   However, it does not follow that the lack of interpersonal interaction means the lack of acknowledgement in parenthood within households. One is by association.

   ---

   We interviewed 161 adult Herero (112 females, 49 males) intensively about the residence of themselves, their siblings with whom they share a mother or a father and about their legal children (children born in marriage or children in whom they had purchased parental rights). None of the men we interviewed whose fathers were still alive (n = 10) considered his residence to be in a homestead different from his father’s. Only two of the men had sons with residences elsewhere –one was a child who had been purchased but was living with the mother and the other was a child borne by a wife from whom he was now divorced. We also heard of very few men ascertained in several hundred shorter demographic interviews that were residing in a homestead other than their fathers’. Most of the men(24/39) with deceased fathers had their own homesteads. Brothers who had both the same mother and father were more likely to stay together, however, than brothers who had different mothers. 

   The other comes from Harpending’s own blog post regarding his Herero friend who claims the children of his new wife as being of his household despite not actually conceiving them. Note, he also describes the man as “prosperous”.

4. I sadly lack data on Bantu rates of violence, swearing I once found data showing it to be low compared to that of the Khoi-san. If anybody has quantified data like in the link regarding the Hadza then that would be appreciated. In regards to parenting however it doesn’t reflect that by comparing non-resident fathers. Regarding Africans, here’s a perspective from a female perspective.
5. This point once again warrants the mention of superstitions still being quite common in non Western societies like China in regards to evil spirits and luck. Likewise, traditions are known to be modified or dropped among Herero in major urban centers. The Herero Harpending encountered that he labeled “employees” nonetheless grew up near the study areas.

Before I end this, I want to cover some further discrepancies by another author who refers to his work, Steve Sailer.

The small, yellow-brown Bushmen, hunters who mated more or less for life and put much effort into feeding their nuclear families, reminded Henry of his upstate New York neighbors. If fathers didn”€™t work, their children would go hungry.

In contrast, the Bantu Herero (distant relatives of American blacks) were full of surprises. In general, black African men seemed less concerned with bringing home the bacon to provision their children than did Bushmen dads.

This doesn’t deviate too far from what Harpending explains. That comes later.

In black African farming cultures, women do most of the work because agriculture involves light weeding with hoes rather than heavy plowing. Men are less expected to contribute functionally to their children’s upkeep, but are expected to be sexy.

So technically this is correct but only to a certain degree in regards to division of labor. It’s particular to farming schemes where root/tuber agriculture is done, and in those areas forest clearing is done by males.

One parallel is that Baumann views climatic and environmental factors as closely
associated with differences in the participation of the sexes in agriculture. He observes that the northern boundary of women’s predominance in agriculture is constrained by the limits of the tropical forest region, and that the boundary of female agriculture also tends to coincide with that between root crops and cereal grains. Baumann’s view of the economies of labor is also similar to our own. He emphasizes that land clearing is more difficult in the forest than in the savannah, and that males often perform clearing in the forest zones in spite of the predominance of female labor, whereas soil preparation is more difficult in the savannah than in the forest. He notes the higher male participation in agriculture in the savannah region of the Sudan than in the West African and Congo forest regions, and more generally, that women are much more likely to participate in root cultivation than in cereal cultivation.

Not mention other activities such as crafts and trading. Baumann’s old scheme as it is is still simplistic. More research shows that labor between sexes shift depending on circumstances. See this on Igbo yam farming or West African Cocoa farming. This trend of shifting continues into the modern day.

In many places in Africa, traditionally there has been a
strict division of labor by gender in agriculture. This
division of labor may be based on crop or task, and both
types of division of labor by gender may occur
simultaneously. Women may mobilize male labor for some
tasks involved in their crops and men frequently mobilize
women’s labor for crops that they control. These divisions
are not static and may change in response to new
economic opportunities.

Likewise, male development in connection to their father is represented in this early anthropological text through inheritance of property and apprenticeship. Collective Fatherhood through the extended family is also recognized, with actual absence being highly due to migrant labor in Southern African countries.

The “Sexy” part is rather presumptuous and absent from the text, where it is in fact the woman that is scrutinized uphold standards in the chapter of Ibo courtship, which seems to be widespread. The simple and lazy role reversal is obvious, as it assumes that female labor undermined the general trend of patriarchy since they weren’t always dependent on the male.

So with all this said, what is there to make of it?: As far as direct connections to the Herero go, Harpending didn’t show any particular malice. Any such was more towards western phenomenon that he draws parallels with. As far as his conference comments, obvious bias is just that. His blog posts don’t even read as such, clearly contradicting it comments of industry among Africans according to his experience for one matter.

It may sadly suggest the type of filter scene through experience in this “field”.

1550 words

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.”

Genetic Determinism

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.

But even though genetic determinism is false, it still stays in the minds of our society/culture and scientists (Moore, 2008), while still being taught in schools (Jamieson and Radick, 2017).

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.

Epigenetic Determinism

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

1100 words

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?

Fish (2002: 6) in Race and Intelligence: Separating Science from Myth critiques the usual hereditarians on what race is and their assumptions that it exists. He cites Jensen (1998: 425) who writes:

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.)

Arguments exist for the existence of race that doesn’t, obviously, assume their existence. The two best ones I’m aware of are by Hardimon (2017) and Spencer (2014, 2019).

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.