Nutrition and Antisocial Behavior
What is the relationship between nutrition and antisocial behavior? Does not consuming adequate amounts of vitamins and minerals lead to an increased risk for antisocial behavior? If it does, then lower class people will have commit crimes at a higher rate, and part of the problem may indeed be dietary. Though, what kind of data is there that lends credence to the idea? It is well-known that malnutrition leads to antisocial behavior, but what kind of effect does it have on the populace as a whole?
About 85 percent of Americans lack essential vitamins and minerals. Though, when most people think of the word ‘malnutrition’ and the imagery it brings along with it, they assume that someone in a third-world country is being talked about, say a rail-thin kid somewhere in Africa who is extremely malnourished due to lack of kcal and vitamins and minerals. However, just because one lives in a first-world country and has access to kcal to where they’re “not hungry” doesn’t mean that vitamin and mineral deficiencies do not exist in these countries. This is known as “hidden hunger” when people can get enough kcal for their daily energy needs but what they are eating is lower-quality food, and thus, they become vitamin and nutrient deficient. What kind of effects does this have?
Infants are most at risk, more than half of American babies are at-risk for malnutrition; malnutrition in the postnatal years can lead to antisocial behavior and a lower ‘IQ’ (Galler and Ramsey, 1989; Liu et al, 2003; Galler et al, 2011, 2012a, 2012b; Gesch, 2013; Kuratko et al, 2013; Raine et al, 2015; Thompson et al, 2017). Clearly, not getting pertinent vitamins and minerals at critical times of development for infants leads to antisocial behavior in the future. These cases, though, can be prevented with a good diet. But the preventative measures that can prevent some of this behavior has been demonized for the past 50 or so years.
Poor nutrition leads to the development of childhood behavior problems. As seen in rat studies, for example, lack of dietary protein leads to aggressive behavior while rats who are protein-deficient in the womb show altered locomotor activity. The same is also seen with vitamins and minerals; monkeys and rats who were fed a diet low in tryptophan were reported to be more aggressive whereas those that were fed high amounts of tryptophan were calmer. Since tryptophan is one of the building blocks of serotonin and serotonin regulates mood, we can logically state that diets low in tryptophan may lead to higher levels of aggressive behavior. The role of omega 3 fatty acids are mixed, with omega 3 supplementation showing a difference for girls, but not boys (see Itomura et al, 2005). So, animal and human correlational studies and human intervention studies lend credence to the hypothesis that malnutrition in the womb and after birth leads to antisocial behavior (Liu and Raine, 2004).
We also have data from one randomized, placebo-controlled trial showing the effect of diet and nutrition on antisocial behavior (Gesch et al, 2002). They state that since there is evidence that offenders’ diets are lacking in pertinent vitamins and minerals, they should test whether or not the introduction of physiologically adequate vitamins, minerals and essential fatty acids (EFAs) would have an effect on the behavior of the inmates. They undertook an experimental, double-blind, placebo-controlled randomized trial on 231 adult prisoners and then compared their write-ups before and after nutritional intervention. The vitamin/mineral supplement contained 44 mg of DHA (omega 3 fatty acid docosahexaenoic acid; plays a key role in enhancing brain structure and function, stimulating neurite outgrowth), 80 mg of EPA (eicosapentaenoic acid; n3), and 1.26 g of ALA (alpha-linolenic acid), 1260mg of LA (linolic acid), and 160mg of GLA (gamma-Linolenic acid, n6) and a vegetable oil placebo. (Also see Hibbeln and Gow, 2015 for more information on n3 and nutrient deficits in childhood behavior disorders and neurodevelopment.)
Raine (2014: 218-219) writes:
We can also link micronutrients to specific brain structures involved in violence. The amygdala and hippocampus, which are impaired in offenders, are packed with zinc-containing neurons. Zinc deficiency in humans during pregnancy can in turn impair DNA, RNA, and protein synthesis during brain development—the building blocks of brain chemistry—and may result in very early brain abnormalities. Zinc also plays a role in building up fatty acids, which, as we have seen, are crucial for brain structure and function.
Gesch et al (2002) found pretty interesting results: those who were given the capsules with vitamins, minerals, and EFAs had 26.3 percent fewer offenses than those who got the placebo. Further, when compared with the baseline, when taking the supplement for two weeks, there was an average 35.1 percent reduction in offenses compared to the placebo group who showed little change. Gesch et al (2002) conclude:
Antisocial behaviour in prisons, including violence, are reduced by prisons, are reduced by vitamins, minerals and essential fatty acids with similar implications for those eating poor diets in the community.
Of course one could argue that these results would not transfer over to the general population, but to a critique like this, the observed effect of behavior is physiological; so by supplementing the prisoners’ diets giving them pertinent vitamins, minerals and EFAs, violence and antisocial behavior decreased, which shows some level of causation between nutrition/nutrient/fatty acid deprivation and antisocial behavior and violent activity.
Gesch et al (2002) found that some prisoners did not know how to construct a healthy diet nor did they know what vitamins were. So, naturally, since some prisoners didn’t know how to construct diets with an adequate amount of EFAs, vitamins and minerals, they were malnourished, though they consumed an adequate amount of calories. The intervention showed that EFA, vitamin and mineral deficiency has a causal effect on decreasing antisocial and violent behavior in those deficient. So giving them physiological doses lowered antisocial behavior, and since it was an RCT, social and ethnic factors on behavior were avoided.
Of course (and this shouldn’t need to be said), I am not making the claim that differences in nutrition explain all variance in antisocial and violent behavior. The fact of the matter is, this is causal evidence that lack of vitamin, mineral and EFA consumption has some causal effect on antisocial behavior and violent tendencies.
Schoenthaler et al (1996) also showed how correcting low values of vitamins and minerals in those deficient led to a reduction in violence among juvenile delinquents. Though it has a small n, the results are promising. (Also see Zaalberg et al, 2010.) These simple studies show how easy it is to lower antisocial and violent behavior: those deficient in nutrients just need to take some vitamins and eat higher-quality food and there should be a reduction in antisocial and violent behavior.
Liu, Zhao, and Reyes (2015) propose “a conceptual framework whereby epigenetic modifications (e.g., DNA methylation) mediate the link between micro- and macro-nutrient deficiency early in life and brain dysfunction (e.g., structural aberration, neurotransmitter perturbation), which has been linked to development of behavior problems later on in life.” Their model is as follows: macro- and micro-nutrient deficiencies are risk-factors for psychopathologies since they can lead to changes in the epigenetic regulation of the genome (along with other environmental variables such as lead consumption, which causes abnormal behavior and also epigenetic changes which can be passed through the generations; Senut et al, 2012; Sen et al, 2015) which then leads to impaired brain development, which then leads to externalizing behavior, internalizing behavior and autism and schizophrenia (two disorders which are also affected by the microbiome; Strati et al, 2017; Dickerson, 2017).
Clearly, since the food we eat gives us access to certain fatty acids that cannot be produced de novo in the brain or body, good nutrition is needed for a developing brain and if certain pertinent vitamins, minerals or fatty acids are missing, negative outcomes could occur for said individual in the future due to lack of brain development from being nutrient, vitamin, and mineral deficient in childhood. Further, interactions between nutrient deficiencies and exposure to toxic chemicals may be a cause of a large amount of antisocial behavior (Walsh et al, 1997; Hubbs-Tait et al, 2005; Firth et al, 2017).
Looking for a cause for this interaction between metal consumption and nutrient deficiencies, Liu, Zhao, and Reyes (2015) state that since protein and fatty acids are essential to brain growth, lack of consumption of pertinent micro- and macro-nutrients along with consumption of high amounts of protein both in and out of the womb contribute to lack of brain growth and, at adulthood, explains part of the difference in antisocial behavior. What you can further see from the above studies is that metals consumed by an individual can interact with the nutrient deficiencies in said individual and cause more deleterious outcomes, since, for example, lead is a nutrient antagonist—that is, it inhibits the physiologic actions of whatever bioavailable nutrients are available to the body for us.
Good nutrition is, of course, imperative since it gives our bodies what it needs to grow and develop as we grow in the womb, as adolescents and even into old age. So, therefore, developing people who are nutrient deficient will have worse behavioral outcomes. Further, lower class people are more likely to be nutrient deficient and consume lower quality diets than higher, more affluent classes, though it’s hard to discover which way the causation goes (Darmon and Drewnowski, 2008). Of course, the logical conclusion is that being deficient in vitamins, minerals and EFAs causes changes to the epigenome and retards brain development, therefore this has a partly causal effect on future antisocial, violent and criminal behavior. So, some of the crime difference between classes can be attributed to differences in nutrition/toxic metal exposure that induces epigenetic changes that change the structure of the brain and doesn’t allow full brain development due to lack of vitamins, minerals, and EFAs.
There seems to be a causal effect on criminal, violent and antisocial behavior regarding nutrient deficiencies in both juveniles and adults (which starts in the womb and continues into adolescence and adulthood). However, it has been shown in a few randomized controlled trials that nutritional interventions decrease some antisocial behavior, with the effect being strongest for those individuals who showed worse nutrient deficiencies.
If the relationship between nutrition/interaction between nutrient deficiencies and toxins can be replicated successfully then this leads us to one major question: Are we, as a society, in part, causing some of the differences in crime due to how our society is regarding nutrition and the types of food that are advertised to our youth? Are people’s diets which lead to nutrient deficiencies a driving factor in causing crime? The evidence so far on nutrition and its effects on the epigenome and its effects on the growth of the brain in the womb and adolescence requires us to take a serious look at this relationship. That lower class people are exposed to more neurotoxins such as lead (Bellinger, 2008) and are more likely to be nutrient deficient (Darmon and Drewnowski, 2008; Hackman, Farrah, and Meaney, 2011) then if they were educated on which foods to eat to avoid nutrient deficiencies along with avoiding neurotoxins such as lead (which exacerbate nutrient deficiencies and cause crime), then a reduction in crime should occur.
Nutrition is important for all living beings; and as can be seen, those who are deficient in certain nutrients and have less access to good, whole, nutritious food (who also have an increased risk for exposure to neurotoxins) can lead to negative outcomes. These things can be prevented, it seems, with a few vitamins/minerals/EFA consumption. The effects of sleep, poor diet (which also lead to metabolic syndromes) can also exacerbate this relationship, between individuals and ethnicities. The relationship between violence and antisocial behavior and nutrient deficiencies/the interaction with nutrient deficiencies and neurotoxins is a great avenue for future research to reduce violent crime in our society. Lower class people, of course, should be the targets of such interventions since there seems to be a causal effect—-however small or large—on behavior, both violent and nonviolent—and so nutrition interventions should close some of the crime gaps between classes.
The logic is very simple: nutrition affects mood (Rao et al, 2008; Jacka, 2017) which is, in part, driven by the microbiome’s intimate relationship with the brain (Clapp et al, 2017; Singh et al, 2017); nutrition also affects the epigenome and the growth and structure of the brain if vitamin and mineral needs are not met by the growing body. This then leads to differences in gene expression due to the foods consumed, the microbiome (which also influences the epigenome) further leads to differences in gene expression and behavior since the two are intimately linked as well. Thus, the aetiology of certain behaviors may come down to nutrient deficiencies and complex interactions between the environment, neurotoxins, nutrient deficiencies and genetic factors. Clearly, we can prevent this with preventative nutritional education, and since lower class people are more likely to suffer the most from these problems, the measures targeted to them, if followed through, will lower incidences of crime and antisocial/violent behavior.
A Simple Argument for the Existence of Race
Race deniers say that there is too small of a genetic distance between races to call the so-called races “races”. They latch on to Lewontin’s 1974 analysis, trumpeting that genetic distance is too small for there to be true “races”. There is, however, a simple way to bypass the useless discussions that would ensue if one cites genetic evidence for the existence of race: just use this simple argument:
P1) There are differences in patterns of visible physical features which correspond to geographic ancestry
P2) These patterns are exhibited between real groups, existing groups (i.e., individuals who share common ancestry)
P3) These real, existing groups that exhibit these physical patterns by geographic ancestry satisfy conditions of minimalist race
C) Therefore race exists and is a biological reality
This argument is simple; anyone who denies this needs to provide a good enough counter-argument, and I’m not aware of any that exist to counter the argument.
P1 shows that there are patterns of visible physical features which correspond to geographic ancestry. This is due to the climates said race evolved in over evolutionary history. Since these phenotypes are not randomly distributed across the globe, but show distinct patterning based on geographic ancestry, we can say that P1 is true; different populations show patterns of different physical features which are not randomly distributed across the globe. Further, since P1 establishes that races are populations that look different from each other, it guarantees that groups like the Amish, social classes etc are not counted as races. P1 further allows a member of a given race to not show the normative physical characters that are characteristic of that race. It further allows for the possibility that individuals from two different races may not differ in their physical characters. These visible physical characters that differ by populations we then call races also need to be heritable to be biological. “Because the visible physical features of race are heritable, the skin color, hair type, and eye shape of children of Rs tend to resemble the skin color, hair type, and eye shape of their parents” (Hardimon, 2017: 35). P1 is true.
P2 shows that these patterns of visible physical features are exhibited between real, existing groups. That is, the groups that exhibit these patterns exist in reality. No one denies this either. Differences in physical features that these real, existing groups exhibit can then be used as proxies for factors in P1. Though, like with which populations figure into this concept, the minimalist race concept doesn’t say—it only establishes the biological existence of races. “In recent years the concept of the continent has come under fire for not being well defined. 59 It is of interest that the formation of the concepts CONTINENT and RACE are roughly coeval. One wonders if the geneses of the two ideas are mutually entwined. Could it be that our idea of continent derives in part from the idea of the habitat of a racial group? Could it be that the idea of a racial group gets part of its content from the idea of a group whose aboriginal home is a distinctive continent? Perhaps the concepts should be thought of as having formed in tandem, each helping to fix the other’s reference” (Hardimon, 2017: 51). Since these real, existing populations that were geographically separated for thousands of years show these visible physical patterns, P2 is true.
P3 follows from the specification of the concept of minimalist race. If these populations that exhibit these distinct visible characters and if they are non-randomly distributed across the globe then this satisfied the argument for the concept of minimalist race. The specification of the minimalist concept of race states that groups satisfy the requisites for the concept by being distinguishable by patterns of visible physical features (P1) and that individuals who share a common ancestry peculiar to them which derive from a distinct geographic location (P2) exist as real groups. Since P1 and P2 are true, P3 follows logically from P1 and P2, which then leads us to the conclusion which is true and establishes the argument for the minimalist concept of race as a sound and valid argument.
C is then the logical conclusion of the three premises: race exists and is a biological reality since the patterns of visible physical features are non-randomly distributed across the globe and are exhibited by real, existing groups. Since all three premises are true and the conclusion is true, it is a valid argument; since the premises are true the argument is sound. No one can—logically—deny the existence of race when presented with this logical proof.
Though notice the argument doesn’t identify which populations are designated as “races” (that’s for another article), the argument just establishes that race exists and it exists as a biological reality. Notice also how this conception of race is sort of like the “racialist concept”, but it takes it down to its barest bones—only taking the normatively important, superficial biological physical features (these features establish minimalist races as biologically existing).
Notice, too, that I did not appeal to any genetic differences between the races, indeed, in my opinion, they are not needed when discussing race. All that is needed when discussing race and whether or not it is a biological reality is asking three simple questions:
1) Are there differences in patterns of visible physical features that correspond to geographic ancestry? Yes.
2) Are these patterns exhibited by real, existing groups? Yes.
3) Do these real, existing groups satisfy conditions of minimalist race? Yes
Therefore race exists.
These three simple questions (just take the premises and ask them as questions) will have one—knowingly or not—admit to the biological reality and existence of race.
Do note, though, nothing in this argument brings up anything about what we “can’t see”, meaning things like “intelligence” or mores of these races. This concept is distinct from the racialist concept in that it does not mention normatively important characters; it does not posit a relationship between visible physical characters and normatively important characters; and it does not “rank” populations on some type of scale. “Also, the conjoint fact that a group is characterized by a distinctive pattern of visible physical characteristics and consists of members who are linked by a common ancestry and originates from a distinctive geographic location is of no intrinsic normative significance. The status of being a minimalist race has no intrinsic normative significance“ (Hardimon, 2017: 32).
Clearly, one does not need to invoke genetic differences to show that race exists as a biological reality. That races differ in patterns of visible physical features which are inherited from the parents and are heritable establishes the biological reality of minimalist race. I really see no way that one could, logically, deny the existence of race given the argument provided in this article. Race exists and is a biological reality and the argument for the existence of minimalist race establishes this fact. Races differ in physiognomy and morphology; these physical differences are non-randomly distributed by geographic ancestry/at the continental level. These populations that show these physical differences share a peculiar ancestry. Knowing these facts, we can safely infer the existence of race. It is the only logical conclusion to come to. Note that the minimalist concept is deflationist—meaning that racialist races do not exist and that this concept enjoys what the racialist concept was supposed to, it is deflationary in the aspect that it takes the normative physical differences from the racialist concept. It is realist since it acknowledges the existence of minimalist race as genetically grounded and relatively superficial but still very significant biological reality of race.
Races can exist as minimalist races and socialraces—no contradiction exists. minimalist race, and its “scientific” companion populationist race (which I will cover in the future) show that there is a well-formulated argument for the existence of race (minimalist race concept) whereas the other concept shows how it is grounded in science and partitions populations to races (populationist concept; both are deflationary). (Read the descriptions of racialist race, minimalist race, populationist race, and socialrace.) You don’t need genes to delineate race; you only need a sound, valid argument based on biological principles. Minimalist races exist.
Race exists and is a biological reality, even if it is ‘socially constructed’ (what isn’t?), our social constructs still correspond to differing breeding populations who share peculiar ancestry and show patterns of visible physical features establish the existence of race.
From Hardimon (2017: 177)
(I also came across a book review from philosopher Joshua Glasgow (Book Review Rethinking Race: The Case for Deflationary Realism, by Michael O. Hardimon. Harvard University Press, 2017. Pp. 240.), author of A Theory of Race (2009) who has some pretty good critiques against Hardimon’s theses in his book, but not good enough. I am going to cover a bit more about these concepts then discuss his article. I will also cover “Latinos” and mixed race people as regards these concepts as well.)
4/19/2018 edit: Two more simple arguments:
(Where P is population, C is continent and T is trait(s)
Population P that evolved in continent C have physical traits T which correspond to C.
Snakes, Spiders, and Just-so stories
Evolutionary psychology (EP) purports to explain how and why humans act the way they do today. It is a framework that assumes that certain mental/psychological traits were useful in the EEA (Environment of Evolutionary Adaptedness) and thusly were selected for over time. It assumes that traits are adaptations then “works backward” by reverse engineering. Reverse engineering is the process of figuring out the design of the mechanism based on its function. (Many problems exist there which will be covered in the future; see also Evolutionary Psychology: The Burdens of Proof by Lloyd, 1999). But let’s discuss snakes and other animals that we have fears of today; is there an evolutionary basis for said behavior and can we really know if there was?
Fear of snakes and spiders
Ohman (2009: 543) writes that “Snakes … have a history measured in many millions of years of shaping mammalian and primate evolution in important respects” and that “snakes … are promising tools for probing the emotional ramifications of deep evolutionary heritages and their interaction with the current environment.” Are they promising tools, though? Were there that many snakes in our EEA that made it possible for us to ‘evolve’ these types of ‘fear modules’ (Ohman and Mineka, 2001)? No, it is impossible for our responses to snakes—along with some other animals—to be an evolved response to what occurred in our EEA because the number of venomous, dangerous snakes to humans and our ancestors was, in reality, not all that high.
Ohman and Mineka (2003: 5-6) also write that “the human dislike of snakes and the common appearances of reptiles as the embodiment of evil in myths and art might reflect an evolutionary heritage” and “fear and respect for reptiles is a likely core mammalian heritage. From this perspective, snakes and other reptiles may continue to have a special psychological significance even for humans, and considerable evidence suggests this is indeed true. Furthermore, the pattern of findings appears consistent with the evolutionary premise.”
Even the APA says that an evolutionary predisposition to fear snakes—but not spiders—exists in primates (citing research from Kawai and Koda, 2016). Conclusions such as this—and there are many others—arise from the ‘fact’ that, in our EEA, these animals were harmful to us and, over time, we evolved to fear snakes (and spiders), but there are some pretty big problems with this view.
Jankowitsch (2009) writes that “Fear of snakes and spiders, which are both considered to be common threats to survival in early human history, are not thought to be innate characteristics in human and nonhuman primates, learned.” For this to be the case, however, there would need to be many spiders and snakes in our EEA.
Philosopher of science Robert C. Richardson, in his book Evolutionary Psychology and Maladapted Psychology (Richardson, 2007) concludes that EP explanations are speculation disguised as results. He says that the stories that state that we evolved to evolved to fear snakes and spiders lack evidence. Most spiders aren’t venomous and pose no risk to humans. In the case of snakes, one quarter are poisonous to humans and we’d have to expect this ‘module’ to evolved on the basis of a minority of snakes that are poisonous to humans:
On this view, at least some human fears (but not all) are given explanations in evolutionary terms. So a fear of snakes or spiders, like our fear of strangers and heights, serves to protect us from dangers. Having observed that snakes and spiders are always scary, and not only to humans, but other primates, Steven Pinker (1997: 386) says “The common thread is obvious. These are the situations that put our evolutionary ancestors in danger. Spiders and snakes are often venomous, especially in Africa…. Fear is the emotion that motivated our ancestors to cope with the dangers they were likely to face” (cf. Nesse 1990). This is a curious view, actually. Spiders offer very little risk to humans, aside from annoyance. Most are not even venomous. There are perhaps eight species of black widow, one of the Sydney funnel web, six cases of brown recluses in North and South America, and one of the red banana spider in Latin America. These do present varying amounts of risk to humans. They are not ancestrally in Africa, our continent of origin. Given that there are over 37,000 known species of spiders, that’s a small percentage. The risk from spiders is exaggerated. The “fact” that they are “always scary” and the explanation of this fact in terms of the threat they posed to our ancestors is nonetheless one piece of lore of evolutionary psychology. Likeways, snakes have a reputation among evolutionary psychologists that is hardly deserved. In Africa, some are truly dangerous, but by no means most. About one quarter of species in Uganda pose a threat to humans, though there is geographic variability. It’s only in Australia—hardly our point of origin—that the majority of snakes are venomous. Any case for an evolved fear of snakes would need to be based on the threat from a minority. In this case too, the threat seems exaggerated. There is a good deal of mythology in the anecdotes we are offered. It is not altogether clear how the mythology gets established, but it is often repeated, with scant evidence. (pg. 28)
The important point to note here, of course, is the assumption that we have an evolved response to fear snakes (and spiders) based on a minority of actually dangerous species to humans.
The EP enterprise is built on what Gould (1978) termed “just-so stories”, borrowed from Rudyard Kipling’s (1902) book of stories called “Just So Stories” (which he told to his daughter) where he imagined ways that in which certain animals look the way they do today. These stories needed to be told “just so” or she would complain.
And the Camel said ‘Humph!’ again; but no sooner had he said it than he saw his back, that he was so proud of, puffing up and puffing up into a great big lolloping humph.
‘Do you see that?’ said the Djinn. ‘That’s your very own humph that you’ve brought upon your very own self by not working. To-day is Thursday, and you’ve done no work since Monday, when the work began. Now you are going to work.’
‘How can I,’ said the Camel, ‘with this humph on my back?’
‘That’s made a-purpose,’ said the Djinn, ‘all because you missed those three days. You will be able to work now for three days without eating, because you can live on your humph; and don’t you ever say I never did anything for you. Come out of the Desert and go to the Three, and behave. Humph yourself!’ (How the Camel got His Hump)
These stories “sound good” but is there any way to verify these nice-sounding stories? One can then make the same argument for EP hypotheses: can they be independently verified? The thing about functional verification is that we cannot possibly know the EEA of humans—or other animals—and thusly any explanation for the functionality of a certain trait are nothing but just-so stories.
Kaplan (2002: S302) argues that:
Evolutionary psychology has not yet developed the tools necessary to uncover our “shared human nature” (if such there is—see Dupre 1998) any more than physical anthropology has been able to uncover the specifics even of such clear human adaptations as our bipedalism. It is obvious that our brains were subject to selective pressures during our evolutionary history; it is not at all obvious what those pressures were.
I don’t deny that we are the products (partly, natural selection isn’t the only mode of evolution) of evolution; I do deny that these fantasy stories can tell us anything about how and why we evolved though. I don’t see how EP can develop such tools to uncover our “shared human nature”—or any other “nature” for that matter—unless time machines are developed and we can directly observe the evolution of trait X that is being discussed.
A simple argument to show that EP hypotheses are just-so stories:
P1) A just-so story is an ad-hoc hypothesis
P2) A hypothesis is ad-hoc if it’s not independently verified (verified independently of the data the hypothesis purports to explain)
P3) EP hypotheses cannot be independently verified
C) Therefore EP hypotheses are just-so stories
This simple argument shows that all EP hypotheses are just-so stories since they cannot be independently verified of the data they attempt to explain. Stories can “sound good”, they can “sound logical”, they can even be “parsimonious” and they can even be the “inference to the best explanation“, (how do you but just because these stories are “parsimonious”, “sound logical” and are the “inference to best explanation” doesn’t make the stories true. The above argument holds for one of HBD’s pet theories, too, the cold winter theory (CWT). It cannot be independently verified either, and it was formulated after national IQ differences were known; therefore CWT is a just-so story.
(I will cover this more in the future.)
Stories about snakes and spiders in our evolutionary history are likely wrong—especially if they derive from what supposedly occurred in our EEA, an environment we know almost nothing about. The fact of the matter is, regarding snakes and spiders, there is no evidence that our fear of them is an adaptive response to what occurred in our EEA. That is a just-so story. Just-so stories are ad-hoc hypotheses that cannot be independently verified, therefore EP hypotheses are just-so stories.