Adapting Minds, Evolutionary Psychology as Maladapted Psychology, and Getting Darwin Wrong—Books Against Evolutionary Psychology
Years ago I wanted to be an Evolutionary Psychologist. After I discovered the work of Lynn, Rushton, Jensen, Kanazawa et al, I was fascinated by the subject of Evolutionary Psychology (EP). Thankfully, I did not go down that route (I went into health sciences). I was enthralled by the work of those that claimed that our psychology reflects adaptations to the Pleistocene EEA (environment of evolutionary adaptedness; or OEE, original evolutionary environment). However, little did I know, these types of hypotheses were just-so stories—ad hoc explanations. They are ad hoc since they are made “for this” reason—i.e., noticing the existence of trait T.
Three books shaped my views on EP: Adapting Minds: Evolutionary Psychology and the Persistent Quest for Human Nature (Buller, 2006), Evolutionary Psychology as Maladapted Psychology (Richardson, 2007), and Getting Darwin Wrong: Why Evolutionary Psychology Won’t Work (Wallace, 2010). These three books are solid. Each one is different, but they all have the same theme: They are against the Santa Barbara School of EP, started by Tooby, Cosmides, and Barkow.
This is one of my favorite books by the philosopher of science David Buller. In the book, Buller distinguishes between “evolutionary psychology” and “Evolutionary Psychology”, the latter being the school of thought pushed by Pinker, Tooby and Cosmides, and Buss. On pages 3-4, Buller (2006) writes:
Initially, I was completely captivated by evolutionary psychology, and I was certain that it was providing a deep and accurate understanding of human mentality and behavior. But after six months’ research, it was unclear to me how everything that went by the name “evolutionary psychology” fit together, and I began having serious doubts about many of the confident claims made by evolutionary psychologists (such as Mooris’s claim that “research has proved” that the majority of sperm in an ejaculate function as sperm warriors). A year’s research later, it was clear to me that there were distinctly different lines of research being conducted under the “evolutionary psychology” label, and I became convinced that the line of research had garnered the most attention, both within academia and throughout the popular media, was wrong in almost every detail. This book emerged as my effort to sort the promising from the wrongheaded lines of research. Accordingly, I originally intended to write a book about the “strong” and the “weak” evolutionary psychology. As the project evolved, however, I found that there was too much to be said about the problems with the “weak” evolutionary psychology, and the project consequently became a critique of evolutionary psychology.
But at many junctures, I felt that I didn’t want to go public with a critique of evolutionary psychology. For, as my research progressed, I became disheartened over the scarcity of reasoned intellectual exchange regarding evolutionary psychology. I found that published criticism of evolutionary psychology typically contained more vitriol than serious analysis of the claims made by evolutionary psychologists, and I didn’t want to be associated with that.
I can see how he was captivated by EP. Initially, I was too, since I believed that it actually had something to say about the evolution of our psychology.
Buller then makes a solid point on page 6:
Accordingly, the rhetoric sets up the following dichotomy: Either you accept biology, in which case you must accept the claim of evolutionary psychologists, or you don’t. Critics have thus been portrayed as necessarily committed to scientifically empty theories from the social sciences, to some form of postmodernist relativism, or to creationism [which is ironic, since EP and creatonism are nothing but just-so stories]. No one who truly accepts evolution, the rhetoric goes, can seriosuly question any of the specific claims of evolutionary psychology.
Each chapter of the book focuses on specific programmes that EPists push: Chapter 1 is about Evolution; Chapter 2 is about Mind; Chapter 3 is about Adaptation; Chapter 4 is about Modularity; Chapter 5 is about Mating; Chapter 6 is about Marriage; Chapter 7 is about Parenthood; and Chapter 8 is about “Human Nature.”
I’m just now reading through the book again, and it’s damn good. It gives a nice critical eye to the claims made by Buss, Pinker, Tooby and Cosmides et al.. Of course, there are critics of EP who decry the claim that we are evolved animals, so that critique isn’t without (some) merit. However, EPists make similarly idiotic claims:
All too often I found evolutionary psychologists dismissing their critics as “antiscientific,” “politically correct postmodernists,” or closeted creationists. Any skepticism about the claims of evolutionary psychology was typically portrayed as a product of dogmatic indoctrination in the social sciences, and the attendant belief that all of human psychology is the product of “socialization,” or else as evidence of a commitment to the “superstitious” belief that humans somehow managed to “transcend” the evolutionary process. Indeed, many critics have been dismissed as simply not wanting to accept the implications of the fact that humans evolved just like beasts in the field. (Buller, 2006: 5)
These types of claims are, though, ridiculous. Critiquing an abortive research programme does not make one “antiscientific” in any way.
Buller’s book is solid and really attacks the EP orthodoxy along with popular accounts of EP. I highly recommend it to anyone who wants to read a well-reasoned critique of all of the popular concepts of EP, which EPists push as “the truth.”
Getting Darwin Wrong
Getting Darwin Wrong is written by psychologist Brendan Wallace. He explicitly states that the book is not about the nature-nurture debate; it is not about whether we should use Darwinian thinking to help understand the human mind; nor is it about other recent attempts—such as sociobiology—to apply Darwinian thinking to human psychology. Though, what the book is about, of course, is EP. It is, specifically, like Buller’s and Richardson’s books, about the books written by Pinker, Tooby and Cosmides et al..
So: why another book discussing EP? To begin with, it might well be thought wise to write a book after the initial storm [of controversy] has died down. Far too much of the initial discussion created mich heat but threw little light on the basic claims of EP, but led instead to a situation where various terms of abuse (‘relativist’, ‘determinist’, ‘reductionist’) were thrown about, without much thought being given to defining these terms, or deciding whether or not EP (or its opponents) were guilty of the myriad intellectual ‘sins’ of which they were accused. Moreover, there was a (to my mind) reprehensible tendency to inder political tendencies from the various scientific theories proposed. EP has political connotations of course: all scientific theories (including those of theoretical physics) have political implications. But it’s grossly unfair to argue that just because a theory might lead to ‘right wing’ (or ‘left wing’) conclusions that therefore it must be rejected. As an old philosophy lecturer once told us as fresh eyed undergraduates in our first years at University: if something has been proven to be true, you just have to accept it, whether you like its implications or not. ‘It makes me feel bad, therefore it is false’ is not an argument.
I, of course, agree with this. Though, funnily enough, people I have debated EP with have accused me of having political motivations for denying EP just-so stories. What is most funny about those accusations, though, is that if I DID have political motivations regarding EP, I WOULD accept EP just-so stories, as a lot of them line-up with political beliefs that I hold. It seems that people cannot fathom that one can be on the right and reject the storytelling of EPists.
Wallace attacks three views of EP: the “information processing”—“… the idea that human cognition consists mainly (or exlclusively) of the processing of information” (Wallace, 2010: 7), the theory of cognitivism—“… the belief that cognition is the manipulation of symbols by rules or algorithms” (Wallace, 2010: 7), and computationalism, “… the belief that the human brain is (or can be usefully compared to) a digital computer” (Wallace, 2010: 7).
So the argument of this book is (I think) novel and quite simple. It is this. Evolutionary Psychology is NOT (as it is normally taken to be) an unproblematic adaption of Darwinian theory to the science of psychology. Instead, EP is an adaption of a specific ‘school’ of psychology: that of cognitivism (or the ‘information processing view of human cognition’ or ‘computationalism’). Essentially EP is an attempt to reinterpret and restate the basic precepts of cognitivism within a Darwinian framework.
This seems like a controversial argument but actually, a careful reading of the seminal works of Cosmides, Tooby, Pinker and other associated with EP shows that they have always been fairly clear about what EP really is, and what they are trying to do. I will also attempt to show that Cosmides et al. were forced to adopt their cognitivist position because of certain assumptions they began with about what psychology is and should be, and that these assumptions themselves are by no means unproblematic. (Wallace, 2010: 8-9)
In one of the major themes of the book, Wallace attacks the massive modularity hypothesis (MMH) that EPists push. According to EP, the mind is made up of different modules which evolved for specific tasks in our OEE. However, as I have noted before, the arguments erected in favor of this view fail.
Getting Darwin Wrong is the most different of the three books discussed today, and I like it as a solid history into the underpinnings of EP and its assumptions.
Evolutionary Psychology as Maladapted Psychology
The final book I will discuss is Evolutionary Psychology as Maladapted Psychology by the philosopher of science Robert Richardson. It is most similar to Buller’s book, in that it specifically attacks EP theories, whereas Wallace’s book shows the history of EP and how and why the assumptions underpinning them are false. Richardson, like Buller, attacks the just-so stories of Pinker, Tooby and Cosmides, and Buss. He shows, for instance, that so-called “evolved fears” of snakes and spiders are baseless. (Indeed, there is good evidence that these are learned fears.)
Richardson discusses the aims of EP, reverse engineering, adaptation, massive modularity and Tooby and Cosmides’ integrated causal model (ICM) vs their version of what social ‘scientists’ believe—the standard social science model (SSSM). He notes how they have erected a false dichotomy between an untenable view and their own, so that others would accept their own view.
The structure of his book is as follows (Richardson, 2007: 51):
The heart of this book is organized around three different approaches toward empirically evaluating evolutionary explanations. These include what is called “reverse engineering” (chap. 2); another alternative is to infer the effect from the relevant causes, an approach that reflects the dynamic perspective of much of evolutionary biology (chap. 3); finally I will turn to analyses designed to disentangle history from structurem which depends on disentangling historical ancestry (chap. 4). I believe that the later analyses are the most powerful.
One of the strengths of his book is the forcefulness of his analyses of EP claims. For example, his discussion of so-called evolved fears of snakes and spiders is particularly strong:
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. (Richardson, 2007: 28)
It is important to note that, for example in chimps, fear of snakes is learned (socially), since captive chimps show no fear to snakes (Anderson, 2018). See also Ehrlich (2003: 89) who notes that this fear of snakes is not found in New Guinea natives, where one would assume that it would be found if the claims from Pinker hold.
Richardson attacks the false dichotomy pushed by Tooby and Cosmides (1992), writing:
Tooby and Cosmides’ portrayal [of the SSSM] is very effective. It is also a piece of sophistry, offering a false dichotomy between a manifestly untenable view and their own. The alternative is one that sees no differences between individuals and no biological contribution to individual or social development. I think no serious figure embraces that view, since, perhaps, John Watson in the early twentieth century.
Tooby and Cosmides also say that “There is no small irony in the fact that [the] Standard Social Science MOdel’s hostility to adaptationist approaches is often justified through the accusation that adaptationist approaches purportedly attribute important differences between individuals, races and classes to genetic differences. In actuality, adaptationist approaches offer the explanation for why the psychic unity of humankind is genuine and not just an ideological fiction” (1992, 79).
Of course, if one puts for an untenable view with their own, theirs will then be accepted.
Lastly, Richardson (2007: 73) attacks one of Buss’s hypotheses:
We begin by assessing differences between men and women in terms of their sexual attitudes. Let’s suppose, contrary to fact, that we actually have reasonable gauges of these differences. Buss uses the evidence to conclude that there are sexual differences, notes the consistency of this with some evolutionary models, and infers that our ancestors not only actually behaved in a way that reflects the differences in our attitudes, but that there were selective pressures to behave. These differences in attitude are supposed to reflect some deeper underlying differences in mating strategies. The mating strategies are taken in turn to reflect some fundamental biological imperative. This argument is put forth without citing evidence concerning, say, group structure, which would certainly be relevant. It is put forth without so much as information concerning group size. It is put forth without information concerning similarities between ancestral and current group structures, mating structures, or group sizes. It is, of course, put forth without evidence concerning actual mating behavior, or the differences supposed to exist in ancestral groups. From all this, and less, we infer that there is an evolutionary and adaptive explanation of the differences between the sexes. That conclusion, in turn, allows Buss to interpret the evidence in a way that he thinks somehow makes evolutionary sense. If this is the way the argument works, then it is a case of reverse engineering. But it is not a very compelling case of reverse engineering.
EP, since its inception in the early 90s, has been the subject of numerous debates. I, personally, reject EP on the grounds that no EP hypothesis can be independently verified. However, contrary to my views, Richardson, Buller, and Wallace are hopeful in the EP paradigm, though they strongly criticize it. For example, Richardson (2007: 25) writes that he “views evolutionary psychology as more speculation than science” and that “It does not warrant our acceptance“, so “Evolutionary psychology as currently practiced is often speculation disguised as results. We should regard it as such.” I agree with this—speculation is not science. Just-so stories are not science.
In any case, all three of these books, if read with an open mind, will have one become extremely skeptical of EP, and, hopefully, reject the abortive research programme since it cannot do what it purports to.
(Ir)RationalWiki (IW) is a Wikipedia-style website, where anyone can edit or create an article on whatever they’d like. They are a left-leaning website, so they, of course, don’t like what they consider to be “right-wingers.” Many “HBDers” have IW articles on them, notable hbdchick, JayMan (though it seems like his article was deleted), Emil Kirkegaard, Anatoly Karlin, and even a new one on the philosopher of biology Nathan Cofnas (see his response here). When I discovered my own article on IW, I laughed, since it grouped me in with “Frogs and Swastikas, AltRight.” Well, I think that the “Pepe the frog” meme is idiotic and childish, and I’m not a Nazi (National Socialist).
In any case, I recently looked at the page and discovered that they finally edited it to reflect my new views. My views changed around April/May 2017 due to two books: DNA is not Destiny: The Remarkable, Completely Misunderstood Relationship Between You and Your Genes (Heine, 2017) and Genes, Brains, and Human Potential: The Science and Ideology of Intelligence (Richardson, 2017). I would say that before reading these two books that I was a “genetic determinist.” However, Richardson’s work lead me to the work of Denis Noble, Jablonka and Lamb, Susan Oyama, and David Moore and the philosophy of developmental systems theory (DST). My deterministic views (and outdated views on genes and the physiological system) were then cured.
In any case, here is what the new edit says about me now:
RaceRealist started out as a supporter of hereditarianism racist theories about IQ and a fanboy of Richard Lynn and Arthur Jensen, but later to his credit rejected these views. Instead however of giving up all his racialist beliefs, he still defends racialism, albeit minus the IQ pseudoscience. The latter has led to him to be criticised as still being a racist but using a deceptive motte and bailey strategy of trying to present himself as a more moderate non-hereditarian “race realist” when he still retains the old racist IQ beliefs about inferior black people in private. Furthermore, despite claiming to have changed his views on the latter – all his old pro-hereditarianism posts on his blog are still up alongside background photos of white supremacists.
The first sentence is true; I did start out as supporter of hereditarianism. When I discovered the work of people like Rushton, Lynn, Kanazawa, and Jensen I thought “Wow, this all makes so much sense and explains why our societies are stratified the way they are.” Though, as mentioned above, I did change my views.
Yes, I do “still defend racialism”, but a softer, non-hereditarian view of human races (Spencer, 2014, Hardimon 2017). These types of arguments about race are non-hereditarian, non-hierarchical. I do agree that “IQ science” is psuedoscience, but the claim that “I still retain [my] old racist IQ beliefs about inferior black people in private” are completely unfounded. How does whoever wrote this know what views I hold in private? Further, they claimed that I “rejected [those] views” in reference to hereditarianism (Jensenism) but then they say that “I still retain [my] old racist IQ beliefs about inferior black people in private”? How does that make any sense?
Further, I have explicitly stated that the terms “superior” and “inferior” are strictly anatomic terms and, outside of that context, make no sense. The head is superior to the feet; the feet is inferior to the head. It seems that the author of this did not read my article Blumenbachian Partitions and Minimalist Races where I explicitly state:
Biological racial realism (the fact that race exists as a biological reality) is true, however, just like with Hardimon’s minimalist races, they do not denote “superiority”, “inferiority” for one race over another. Most importantly, Blumenbachian populations do not denote those terms because the genetic evidence that is used to support the Blumenbachian partition use noncoding DNA. (It should also be noted that the terms “superior” and “inferior” are nonsensical, when used outside of their anatomic contexts. The head is the most superior part of the human body, the feet are the most inferior part of the human body. This is the only time these terms make sense, thus, using the terms outside of this context makes no sense.)
Yes I have changed my “views on the latter [hereditarianism]”, and no, I will not remove my “old pro-hereditarianism posts” on my blog. I leave them up to show the evolution of my views over time. My blog is almost four years old, and half of the time I was a staunch hereditarian/genetic determinist and the other half I discarded those views and embraced the philosophy of DST.
In any case, the race debate is a philosophical, not biological, one; genetic variation exists between human populations which no one denies. The question “What is race?” is strictly a philosophical question and so, after that question is answered, it follows that the argument about the existence of race is then philosophical. Holding views on racial realism (the claim that our racial categories pick out real kinds in nature; Smith, 2015; 43). Therefore, the views that I hold on race are not scientific, but philosophical.
Re my views on immigration: yes I did write that non-western people are abnormal to our societies (fun fact: I wrote that as a paper for an Abnormal Psychology course, and I got an A). I do still hold that immigration should be restricted/completely halted, though it should not be based on IQ testing, as I once argued in the past. I agree that these views that I once held are idiotic. Looking back at what I wrote and used to believe in the past, I believed a lot of bullshit and pseudoscience. I openly admit that my former prejudices drove my old beliefs. However, as noted earlier (and in the past), I rejected those kinds of genetic determinist “racist” views after discovering the philosophy of DST and reading Richardson and Heine.
A final note on my politics: I support closed borders, I support capitalism and I am a nationalist. I don’t care about what people do in private, just don’t bring it out on the streets. I would say that I am somewhat of a libertarian, and while I do hold some “AltRight” views, I would not self-identify as an alt-righter.
In sum, (Ir)RationalWiki is a joke of a website with how they attack individuals who do use their real names. I’m just some anon guy with a blog and Twitter account. They libel people with mined quotes and don’t reflect their views correctly. In any case, yes my views have changed, and no, it’s not some “cover” for my old views. I do not still hold those same beliefs “in private” (how would whoever wrote this know what views I hold in private? It’s idiotic). I’m not “AltRight”, nor have I ever been.
I’ve written on steroid use between blacks and whites last year, but it was a smaller part of an article concerning the misconceptions people have on steroids and what they do (responding to the hysteria that the media and the like discuss with their claims of “roid rage”). I cited some studies showing that blacks use more drugs than whites; that blacks are more likely to lie about drug-use than whites; and that blacks are more likely to use steroids than whites (indeed, minorities were twice as likely to use steroids compared to whites in one study). (It is also worth noting that “roid rage” is a myth; AAS use is associated with other drug use, which explains the relationship. See Lundholm et al, 2015. For further information on this matter, see the documentary Bigger, Stronger, Faster.)
Steroids are synthetic hormones—lab-made hormones that mimic the so-called “male hormone” testosterone. Though the term “steroid” is misleading; what is being discussed are androgenic anabolic steroids (AAS), since, for example, estrogen is a steroid and does not have the muscle-building and recovery properties of AAS. The term “anabolic” refers to muscle-building whereas the term “androgenic” refers to the increase in male sexual characters. AAS abuse is associated with tendon ruptures, a lower incidence of prostate hypertrophy, anxiety, depression, and a decreased libido (Bagge et al, 2017). Furthermore, the negative effects of AAS (ab)use cause cardiovascular problems, dyslipedemia—which may impact vascular functioning, ventricular arrhythmias while training, hypertension, etc. (Goldman and Basaria, 2018). Further negative effects include raised cholesterol, hair thinning, sterility, and decreased hormone levels. Croaker (2017) notes that AAS use is prevalent throughout high school and collegiate sports, though “When the desired outcome is achieved, the results are always short lived.”
Individuals use steroids for myriad reasons—despite the well-known adverse effects. A few considered are: (1) to become better at sports; (2) to increase muscle mass (which then relates to increased recovery time so the individual can train more); and (3) they are administered a script by their primary care doctor because their testosterone levels are low for their age range. In any case, in this article, I will discuss (1) and (2).
Whichever way the racial differences in AAS use go, we can all agree on one thing: in young men, they most likely want to become better athletes. AAS use is associated with shorter recovery times (
How can you tell if any individual is using steroids? It’s very simple. An increase in upper-body mass, most notably the shoulders and traps. The reason for this is that there are more androgen receptors in the shoulders and so they respond better to the flood of synthetic hormone.
AAS (ab)use is pretty prevalent throughout America. For example, Blashill et al (2017) write that “Black, Hispanic, and White sexual minority boys reported misuse at approximately 25%, 20%, and 9%, respectively.” “Sexual minorities” refers to sexual identity and the sex of the sexual partner. “Whites” were those who said they were not “Hispanic” and were white; “blacks” were those who said that they were not “Hispanic” and were black; while “Hispanics” were those who identified as a “Hispanic” ethnicity while marking down another race. (Note that “white” and “black” are socialraces.)
The (ab)use of AAS particularly affects homosexual minorities. Blashill et al (2017) write:
Sexual orientation health disparities in anabolic steroid misuse disproportionally affect Black and Hispanic sexual minority adolescent boys …
Blashill et al (2017) conclude from the results of their study that the (ab)use of AAS by sexual minorities may be due to “muscularity-oriented body image concerns.” I have heard (albeit, anecdotally) that a lot of homosexuals use AAS in order to look good so they would fall under (2).
The Child Trends Data Bank writes that “There are no significant differences in use of steroids in the past 12 months when comparing whites, blacks, and Hispanics.”
Hua and Braddock (2008: 29) write that “White males reported higher prevalence of steroid use than Black males, and sport participation served as a protective factor, but only for Black males.” They conclude that:
Specifically, our results show that sport participation served as a protective factor, but only for Black males. Sports active black male adolescents reported lower rates of steroid use than Black males who were not involved in sports.
So, it seems that sport participation is protective for blacks in regard to steroid use. However, black males lie about drug use more than white males, and so, I don’t see why we should accept the conclusions of this study. I also find it hard to believe that sport participation would be protective against AAS use. Intuitively, you would expect it to cause more AAS use.
The Journal of Ethics states that AAS (ab)use was higher in white (6.2%) and “Hispanic” students (7.2%) than black students (3.6%).
Irving et al (2002) state that 2.1% of white males 7.6 percent of black males, 6.1% of “Hispanic” males, 14.8% of Hmong males, 7.9% of “other Asian”, 3.1% of Native Americans, and 11.3% of mixed race males reported AAS use. Whereas 0.5% of white females, 4.3% of black girls, 0.9% of “Hispanic” girls, 8.9% of Hmong girls, 3% of “other Asian” girls, 4.7% of Native American girls, and 4.1% of mixed race girls used steroids. Here is table 1 from Irving et al (2002):
Low SES individuals were more likely to (ab)use AAS than high SES individuals in both sexes. Middle schoolers were more likely than high schoolers. (Where are they getting the AAS? Their parents? Older siblings?)
Irving et al noted that the male AAS users were least satisfied with their shoulders (we can’t all be so lucky). Fortunately for them, as noted above, the shoulders have the most androgen receptors in the body and so their shoulders will grow. However, other than not being satisfied with their shoulders, body image was not associated with AAS use in males. Female AAS users, more so than non-AAS users, were more likely to report that they used AAS to for “weight and shape.” Further, sport players were more likely than non-sport players to use AAS—as expected. In a nutshell, AAS use is associated with poor markers of physical health—most importantly because many individuals wanted to lose weight (most likely fat mass). It should be noted that those who were dissatisfied with their bodies were less knowledgable about nutrition, so to amleiorate some of this, nutrition should be taught earlier in schools.
I can’t think of any reasons why, however, Hmong males and females would be using AAS more than other ethnies. However, Irving et al (2002: 251) write:
One finding regarding the demographic characteristics of steroid users in our sample is worth noting. Steroid use was more common in non-Caucasian respondents (both male and female), with particularly high rates among Hmong participants. Initially, we were puzzled by this result and questioned its validity. However, in consultation with community informants from social service agencies that work with southeast Asian youth in the Minneapolis/St. Paul area, we were told by some informants that the “word on the street” was the Hmong youth were attempting to “bulk up” physically, by working out and using steroids. One possible explanation for this finding is that, as fairly recent immigrants (most Hmong immigrated to the U.S. in the past 20 years), Hmong youth may be “bulking up” to gain status in a culture that emphasizes physical appearance, including weight, shape, and physical strength. This interpretation is supported by anthropological research wherein exposure to western ideals of beauty and eating habits is followed by increases in weight and shape preoccupation and disordered eating practices among individuals from non-western cultures. On the other hand, it is possible that Hmong youth may have misinterpreted the question.
So if the Hmong did not misunderstand the question, it is possible, for example, that they were getting bullied (due to being new immigrants) and decided to take AAS in order to get bigger to stop the bullying.
Stilger et al (1999) note that (my emphasis):
Of the 873 high school football players participating in the study, 54 (6.3%) reported having used or currently using AAS. Caucasians represented 85% of all subjects in the survey. Nine percent were African-American while the remainder (6%) consisted of Hispanics, Asian, and other. Of the AAS users, 74% were Caucasian, 13% African American, 7% Hispanic, and 3% Asian, x2 (4,854 4) 4.203, p 4 .38. The study also indicated that minorities are twice as likely to use AAS as opposed to Caucasians. Cross tabulated results indicate that 11.2% of all minorities use/used AAS as opposed to 6.5% of all Caucasians (data not displayed).
Lastly, Green et al (2001) note that whites and blacks used AAS at the same rate, though the n = 10,850 Caucasians while for African Americans the n = 1,883.
However, unless a study notes that the participants’ blood was assayed, why should we believe the results when it’s been noted that blacks underreport and lie about drug use more than whites (Bauman and Ennett (1994); Ledgerwood et al, 2008; Lu et al, 2001)?
In sum, many studies report different results. I would say that the difference is due to cultural/social differences based on where the studies were carried out. The mixed results of these studies points to one thing: AAS use is prevalent throughout school life, and since it starts so young with many people, older siblings seem to be getting it for them. Sexual minorities are more likely to use than whites and this seems to come down to body image; Hmong seem more likely to use than non-Hmong; and the racial differences seem to hold with females as well.
Steve Stewart-Williams wrote an article for Nautilus yesterday titled Nurture Alone Can’t Explain Male Aggression. He begins the article by describing a bank robber who shoots and kills a bank teller and then takes police on a high-speed chase where he finally gets killed. Then it is revealed that the bank robber had an extensive criminal history. Oh, it was a male. “you weren’t being sexist“, he writes, “you were playing the odds.” Most men aren’t violent, but most violent individuals are men. Stewart-Williams then discusses a recent article published by The New York Times titled It’s Dangerous to Be a Boy, with the headline (emphasis mine) “They smoke more, fight more and are far more likely to die young than girls. But their tendency to violence isn’t innate.” I will discuss the use of the term “innate” further down.
Stewart-Williams then states, going off the headline quoted above, that the statement means that “sex differences in aggression come entirely from the environment: from culture rather than biology, nurture rather than nature.” Nevermind the false dichotomy here, let’s finish up discussing the gist of the article before getting onto what’s wrong with it. He then states that biology matters as well, and that the claim that male violence isn’t “innate” is the “Nurture Only” position, while we know that “Biology matters as well.” This seems to be the strawman that all evolutionary psychologists battle with: Anyone who disagrees with EP claim C is a “blank slatist” (this phrase taken care of by Robert Richardson in Evolutionary Psychology as Maladapted Psychology); but due to the interaction of nature and nurture, genes and environment, you can’t partition them into percentages—as is done with heritability estimates (see Moore and Shenk, 2016).
So these sex differences in aggression are noticed in all cultures. What could explain this? Stewart-Williams then discusses the Eagly and Woods’ (2016) social role theory of sex differences. They agree—of course—that there are sex differences in aggression and crime found throughout all cultures on earth, but the cause of domination is due to the effect of evolved differences in body size—men being bigger, stronger, and faster than women while women are smaller, weaker, and slower than men. So this proposed hypothesis states that the psychological differences found throughout all cultures is due to physical sex differences.
“Why wouldn’t natural selection create psychological sex differences as well as physical ones?“, Stewart-Williams writes. Well the answer to this question is that there are no psychophysical laws so psychological traits/mental abilities can’t be selected. Then there is the fact that natural selection is not an explanatory mechanism since it cannot explain trait fixation because there are no laws of selection for trait fixation (Fodor, 2008; Fodor and Piatteli-Palmarini, 2010).
Stewart-Williams writes “Some argue that, even if culture doesn’t create the aggression sex difference out of nothing, it does still amplify a relatively trivial inborn difference.” This is ridiculous: “culture doesn’t create the sex difference out of nothing”, however, small differences between males and females can be magnified by culture (Eliot, 2009). Note that this is a developmental perspective, and that developmental systems theory (DST) is completely at-ends with Evolutionary Psychology.
Is it just a coincidence that this alleged surge in socialization comes at the same time as the massive surge in circulating testosterone that accompanies puberty in males?
I see he is implying that circulating testosterone levels explain differences in aggression between males and females and that this also explains aggression as well. Though, as I have documented, the claim is false.
Stewart-Williams than writes:
The socialization hypothesis offers no particular reason to expect this. But the decline in violence coincides almost perfectly with the decline in testosterone found in men throughout the adult years, and mirrors the decline found in males of other species. Once again, this is much easier to explain in evolutionary than in sociocultural terms.
How interesting to bring this up. I’m sure most have heard the claim that testosterone levels begin to decrease at around age 25-30 (a decrease in total T of 1-2 percent per year after age 30). Though, note that age-range. What major life events occur during that time for most men? Marriage, children (some bouts of depression). Smoking, too, explains some of it. Shi et al (2013) write:
The annual decline in T (−0.8% per year) is similar to that reported from longitudinal cohort studies in the United States (17), Denmark (36), and Australia (16). The current study strongly suggests that the decline in T is not an inevitable part of aging, which is consistent with a recent cross-sectional study of 325 men 40 years and older self-reporting very good or excellent health (37). Our data show that variability in the change in T is largely explained by smoking behavior and intercurrent changes in health status, particularly obesity, depression, the overall burden of chronic disease, and marital status.
Though, predominantly, the biggest culprit to decreasing testosterone is obesity. Further, smokers have higher levels of testosterone than non-smokers (Wang et al, 2013). This is because smoking cessation causes fat mass to accumulate, and higher fat mass is associated with lower testosterone levels.
In any case, Stewart-Williams continues to talk about the “Nurture Only” (“blank slate”) position. He discusses how human males commit around 95 percent of crime while being 79 percent of homicide victims. He then states that male chimpanzees commit 92 percent of “chimpicides” while male chimps are 72 percent of those who are killed. So if he will use chimps as an example for an “innate” tendency, then I’ll use something on chimps to prove the point that it’s not testosterone that causes aggression, as Stewart-Williams is implying.
In The Trouble with Testosterone, Sapolsky (1997) discusses five chimpanzees. The chimpanzees were then allowed to form a hierarchy, 1-5. Number 3 pushed his weight around on numbers 4 and 5 but was subservient to numbers 1 and 2. Number three was taken and then injected with testosterone. He then began engaging in more aggressive behavior, which would confirm the hypothesis that testosterone causes aggression, right? Wrong. Sapolsky (1997) writes:
So even though small fluctuations in the levels of the hormone don’t seem to matter much, testosterone still causes aggression. But that would be wrong. Check out number 3 more closely. Is he now raining aggression and terror on any and all in the group, frothing in an androgenic glaze of indiscriminate violence. Not at all. He’s still judiciously kowtowing to numbers 1 and 2 but has simply become a total bastard to number 4 and 5. This is critical: testosterone isn’t causing aggression, it’s exaggerating the aggression that’s already there.
Now let’s get to the problem with the term “innate”: It’s an empty term. It’s a term that people use when they don’t want to think about the development of the trait in question. For example, the term “innate” is thought by numerous researchers today to be driven “by” genes. It is assumed that “innate traits” are “non-malleable.” Maybe the assumption is that only genes are needed for the culmination of trait X. Or maybe the assumption is that a trait is “innate” iff it is fully genetically influenced. Though, there is a problem there, too. What does it mean for something to be “genetically influenced”? What a priori justification exists to privilege genes over any other developmental variables? There is none. Noble’s (2012; 2017) argument rears its head whenever the discussion of “genetic traits” comes up: it’s nonsensical to talk about, since, in a multi-level complex biological system, pinpointing one level is useless since they all interact.
However, Bateson and Mameli (2007) dispense with the term “innate”. They write that “Over-used metaphors from engineering such as ‘‘hardwiring’’ and ‘‘pre-programming’’ applied globally to the outcome of development fail to capture the character of the processes and once again invite the mistaken view that they can be contrasted with their opposites. We believe that a thorough investigation of developmental processes has been hindered by indiscriminate use of the labels ‘‘innate’’ and ‘‘acquired.’’”
So the next time you see a marvelous and complex behavior—such as a border collie herding sheep or birds flying south for the winter—try to resist the temptation to label it as instinctive, hardwired, genetic, or innate. By foregoing a label and digging deeper, you will open yourself to consideration of the myriad of factors that shape who we are and why we behave the way we do.
In sum, Stewart-Williams does not understand endocrinology (positing evolutionary explanations for T decreases at around the mid-20s in comparison to socio-cultural ones); he does not understand that socialization in male and female babies makes small gaps wider (Eliot, 2009); he does not understand (though he only implied this and did not outright claim it) that testosterone does not cause violence/aggression/crime. Evolutionary Psychologists really need to get a clue. Positing evolutionary explanations (i.e., just-so stories when they cannot be independently verified of the data they purport to explain) does not lend itself to any kind of explanation for why a certain trait persists in the modern world. Lastly (though he did not make the claim here), the terms “innate” and “genetic” are baseless and empty and do not give us any new information about the trait in question.
Blacks are better sprinters and whites are better swimmers. Why is this? A whole slew of factors influence this—social, physiological, anatomic. However, there is a stereotype about blacks that has been repeated since I was a child: that blacks can’t swim. How true is this? If it is true, what explains it? It is my opinion that it is true, and that social, cultural, and anatomic and physiologic factors account for this. The same for whites and running. Black children drown at a rate of about 3 times higher than white children. About 70 percent of black children cannot swim, compared to 60 percent of “Hispanic” children and 40 percent of white children. Why is that? Well, one of the most telling answers why is anatomic. Irwin et al (2011) note in their study that blacks are more likely to be “aquaphobes”—having a fear of water—compared to whites.
Almost three years ago, I wrote White Men Can’t Jump? That’s OK, Black Men Can’t Swim. In the article, I explain how and why blacks have a harder time swimming than whites. One anatomic reason is their chest cavity. Compared to whites, blacks have a narrower chest cavity. They have denser, shallower chests. This is a burden while swimming, since those who have a wider chest can take longer strides with their arms while swimming. Blacks have denser bones than whites (Ettinger et al, 1997), Swimmers have lower bone density than non-swimmers (Gomez-Bruton et al, 2013), and so, high bone density is not conducive to swimming success, either.
The first black man to make the swim team for America in the Olympics was Anthony Ervin in 2000. (Funny story. In a class I took a few years ago, racial differences in sports came up. I brought up race differences in swimming. A black guy behind me said “My grandfather was the first to qualify for the Olympics.” I said “Yea? Your grandfather is Anthony Ervin?” He didn’t say anything, it seemed like he got mad at me for calling him out.) That it took this long for a black man to qualify for the US in swimming is telling, and anatomy and physiology, in my opinion, are how we can explain the observed disparity,
So, blacks have lower body fat (on average), and narrower chest cavities. These two things play a role in why blacks are not good swimmers. Yet another role-player, could be, the fact that black women don’t want their hair to get wet and so never taught their children how to swim, parental encouragement, to “swimming is something that white people do” (Wiltse, 2014). Who knows? Maybe in the coming years, blacks could match whites at swimming. Though, with what we know about anatomy and physiology of elite swimmers, this is highly unlikely. It’s like saying “Who knows? Maybe in the coming years, whites could match blacks at running.” Our knowledge of anatomy and physiology throws a wrench in claims like that.
The phenomenon of fast black sprinters and fast white swimmers is predictable through physics (Bejan, Jones, and Charles, 2010). The finalists of running competitions are continuously black, whereas in the swimming competitions they are continuously white. What accounts for this? Well, other than the factors discussed above, there is one more: center of mass.
It is well-known that different races have different anatomic measurements. Blacks have longer limbs than whites (Gerace et al, 1994; Wagner and Heyward, 2000) and longer legs and smaller muscle circumferences (e.g., calves, arms), then they have a higher center of mass than an individual of the same height. So since Asians and whites have long torsos (i.e., since they are endomorphic), they have a lower centers of mass. Asians have the tallest sitting heights, matched with people of the same height, and so we would expect them to be exceptional swimmers. However, since they are not as tall as whites, they do not set records. Blacks, on the other hand, have a lower sitting height when matched with someone of the same height—3 cm shorter. Whites’ sitting height was lower than Asians, but whites are taller so whites dominate swimming compared to Asians because of their average center of mass. See Table 3 from Bejan, Jones, and Charles (2010).
So the difference between blacks’ and whites’ center of mass is 3 percent. This 3 percent difference can account for why the two races excel in running and swimming. When it comes to the runners (blacks), the 3 percent increase in center of mass translates to a 1.5 percent increase in winning speed for the 100 m dash, and a 1.5 percent decrease in winning time, from 10 s to 9.85 s, for example. So the 3 percent difference in running is a huge advantage for blacks.
When it comes to whites, the same holds, except for swimming. So the 3 percent increase in correct length for whites translates over to a 1.5 increase in winning speed and a 1.5 decrease in winning time.
So for taller athletes, mass that falls from a higher altitude falls faster, down and forward; speed increases with larger physiques. So since blacks have larger physiques than whites, then, at the extremes of elite sports (running), their mass allows them to fall down forward, faster and since they have larger physiques, they are faster. So world records are set by athletes with different centers of mass: black athletes in running and white athletes in swimming.
Shifting away from physics, we will now discuss the cultural/social component. The fact that many blacks do not know how to swim became apparent after the Red River drownings of 2010 (Wiltse, 2014). Wiltse (2014) notes three reasons why blacks may be bad swimmers compared to whites: (1) white swimmers denied blacks access to pools; (2) cities provided few pools to black communities and the pools they did provide were small; and (3) the cities closed many public pools after desegregation occurred. White parents taught their children how to swim, but black parents hardly ever did. As this occurred as swimming became popular in American culture, this could be one reason why blacks aren’t as represented in swimming when compared to whites.
Wiltse’s (2014) argument is that past discrimination to blacks from whites when it came to swimming explains the drowning disparity between the races. Whites passed down their swimming knowledge, whereas blacks had little to no chance to pass theirs down—if they even knew how to swim, that is. This type of cultural transmission could explain most—if not all—of the disparity in drowning between the races. It is simple: to address the disparity, the claim that swimming is “what white people do” needs to be addressed. I would assume that this claim grew from the 60s and desegregation from when blacks were barred from swimming pools, as Wiltse (2014) notes. While the swimming and drowning gap can be closed, the elite sports (running and swimming) gap cannot be—as most of what drives the relationship between race and those sports are anatomic and physiologic in nature, combined with numerous other irreducible variables.
However, pointing to these types of cultural/social causes can be reversed. We can say that since white parents don’t teach their children how to sprint and thus they have not taught their children how to sprint for successive generations, then if white parents did just that then whites would begin to close the gap when it comes to sprinting. While I do not deny that we would have more black swimmers had these types of discriminatory acts had not occurred, it is ridiculous to claim that the two races can and will become equal if this were to occur. It’d be like saying that if we train this person from birth to become an elite sprinter then they would be. Though the right analogy would be that since there are fewer whites than blacks in elite running sports, then what explains the disparity is that they are not trained that way from pretty much conception. However this betrays the systems view of athleticism, and while there are necessary factors in regard to running success, the whole system must be looked at when assessing what makes an elite athlete.
In conclusion, there are many anatomic and physiologic reasons why blacks and whites differ in running and swimming sports. Anatomic differences, such as center of mass, explain the disparities in swimming and running. Blacks’ morphology—long limbs and short torso—is conducive to running success. They can take longer strides and take fewer strides a race compared to someone of the same size that does not have the same limb length. When it comes to white swimmers, where the altitude is set by the body rising out of the water, whites hold a 1.5 percent speed advantage in swimming.
Though there are these anatomic differences that lend themselves to differences in elite sporting competitions, these differences do not lend themselves do the swimming and drowning gap in regard to blacks and whites. What explains those gaps is generational access to swimming pools; blacks were barred access to swimming pools just as they started to become popular in America, after the 60s when the country was desegregated. This led to swimming being looked at as “something that white people do”, and so, fewer and fewer black parents taught their children how to swim. Further cultural and social factors explain this, too. While I would assume that some of these aforementioned factors would then play a role in the black-white swimming/drowning gaps, I doubt that it would count for a super-majority of it. Thus, the gap can be closed by ridding the stigma that swimming is “something that white people do”.
The elite sporting gap in running and swimming, however, cannot be closed.
Usain Bolt is one of—if not the—fastest men who has ever lived. At age 12 he was already the fastest boy in his school (Irving, 2010: 54). At the 2009 Berlin Olympics, he set the world record for 100 m race (Bolt also holds the world record for the 200 m dash, at 19.19s), clocking in at 9.58 seconds. His average speed was 27.8 mph with an average speed of 23.5 mph. Why is Bolt so fast? Of course, there are multiple interacting factors that contribute to Bolt’s world record times. Bolt’s somatotype, muscle fibers, will to win, intense training, mind, etc all contribute to his world record—along with the type of athlete he is. In this article I will discuss what Bolt does, his anatomy and physiology, what lead up to his record-breaking time, and a possible challenge to his record.
Usain Bolt is tall, as far as sprinters go, with a height of 6’5”. Since he is so tall, compared to other sprinters, his average stride length is at the extreme upper-limit of modern sprinters. So what makes Bolt unique as a sprinter is his stride length (Shinabarger, Hellrich, and Baker, 2010). So Bolt has to take fewer strides than other sprinters, which, in part, explains his success.
During Bolt’s record-setting 9.69 s dash in 2008, during the last 2 seconds—when 20 meters were left to run—Bolt looked to the side and started celebrating (Eriksen et al, 2009). Bolt’s coach claimed that he would have shattered even his future record-setting performance of 9.58 s running 9.52 s or better. The runner-up of this race was Richard Thompson. By 4 s, Bolt and Thompson were neck-and-neck, so Bolt’s medal was won between 4 and 8 s. After 8 s, Bolt considerably decelerated while Thompson equalizes and surpasses Bolt. Thompson could not match Bolt’s speed, though, and slows down after 8.5 s. Then, to answer the question “How fast would Bolt have run had he not celebrated the last 2 s?”, Eriksen et al (2009: 226) make two assumptions:
Assumption 1: Bolt matches Thompson’s speed at up to 8 s.
Assumption 2: Bolt maintains a 0.5 m/s2 higher acceleration than Thompson at 8.5 s.
Of course the justification for A1 is obvious: Bolt outran Thompson between 4 and 8 s. But in regard to A2, it is difficult to quantify exactly how much stronger Bolt was than Thompson, since Bolt is a 200m specialist, they take the 0.5 m/s2. So, in two scenarios that Eriksen et al (2009) put forth, the world record would either be 9.61 s or 9.55 s. Eriksen et al (2009: 228) conclude “that a new world record of less than 9.5 s is within reach by Usain Bolt in the near future.” And what do you know: a year later, Bolt ran the 100 m at 9.59 s.
Bolt has a slow reaction to the gun—that is, he has more moving to do to get to the sprinting start since he is so tall. His reaction time at the Beijing Olympic Final was 0.165 s. So if he could reduce his reaction to the gun by .3 s then he would have beaten his world record of 9.58 s to 9.56 s. If he could get it down to 0.12 s then he would be looking at a 9.55 s time, and if he could get it down to as fast as the rules allow—at 0.10 s—then his time would have been 9.53 seconds, almost right there by his coach’s prediction had he not celebrated during his record-setting run (Darrow, 2012).
Since Bolt is so tall—taller than his competitors—he can take fewer steps per 100 m. For instance, he set his record time in 2009 taking 41 steps to win, whereas his competitors took 45 steps (Beneke and Taylor, 2010). The average sprinter has a higher proportion of type II fibers compares to type I fibers (Zierath and Hawley, 2004). So one thing that separates Bolt from his contemporaries is superior biomechanical efficiency along with relative power generated per-step (Beneke and Taylor, 2010; Coh et al, 2018). So Bolt’s record-setting performances comes down to anthropometric characters, coordinated motor abilities, his ability to generate power, and an effective running technique. Sprint performance on the force generated during ground contact.
Bolt has an ectomorphic-dominant somatotype. Since he is ecto-dominant, this gives him certain advantages over more endo- and meso-dominant competitors. Furthermore, along with his body type, Bolt is Jamaican. Most of the ancestry found in Jamaicans is derived from West Africa. Jamaicans are more likely to have the RR ACTN3 genotype (Scott et al, 2010), while the RR genotype—along with type II fibers (with a greater cross-section area) contributes to whole muscle performance during high-velocity contractions (Broos et al, 2016). I am not aware of any analyses of Bolt’s genotype, but I would bet what’s in my bank account that he has the RR genotype—that he has two copies of ACTN3.
Tyson Gay then emerged as a challenger to Bolt (in 2013, Gay gave a dirty urine for PEDs, performance-enhancing drugs, and Bolt said that Gay should be “kicked out of the sport“). Varlet et al (2015) state that Bolt and Gay influenced how fast the other ran in Berlin, 2009. Both Bolt’s and Gay’s steps were pretty much synchronized with each other. Though since Gay was slightly behind Bolt in the race, he had the better chance to synchronize his movement with Bolt’s. However, Blikslager and de Poel (2017) argue against this: they state that there is no sufficient evidence for the claim that Bolt and Gay had synchronized movements.
The center of mass in blacks is around 3 percent higher in blacks than it is in whites. This 3 percent difference in center of mass between whites and blacks leads to them doing better in one sport over another: sprinting for blacks and swimming for whites (this is one reason why blacks are worse swimmers than whites). Further, for runners, the 3 percent increase in center of height translates over to a 1.5 percent increase in running speed, translating to a difference of 10 s compared to 9.85 s (Bejan, Jones, and Charles, 2010). So the change is 0.15 s for runners. This is yet another reason why Bolt excels: he is exceptionally tall.
Bolt is really tall compared to his contemporaries; Bolt goes through insane training (as do his contemporaries). Of course, the explanation for Bolt’s running success is due to numerous factors, including (but not limited to) his height, leg length/stride length, running economy, Vo2 max, training, where he grew up, and a whole slew of other—irreducible—factors. The fact that Bolt could have set an even more unbelievable record had he not celebrated with 2 s—or 20 meters—left during his record-setting run is incredible. That he can even hit at or near to what his coach predicted that he would have gotten had he not celebrated, while getting his reaction time better is even more incredible. Bolt does not even need to improve his running skill to become better—just improve his reaction to the gun and he will, in my opinion—set records that no one wull ever break.
The Boston Marathon is one of the oldest continuous running marathons around. The 122nd just finished today, and—surprise surprise—a Kenyan man and Ethiopian woman took first place. For the men, Lawrence Chereno (time at 2:07: 57) barely edged out the second place winner Lelisa Desisa Benti (2:07:59; an Ethiopian) while for the women Worknesh Degefa (2:23:31) beat Edna Kiplagat (2:24:13; a Kenyan). For the men, all 5 of the top placers were East African, whereas for the women all 3 were East African. What explains Kenyan marathon success? Incredibly, from 1992 onward—with the exception of 2001 and 2018—East Africans have won the Boston Marathon. We know that athleticism is irreducible to biology, and while genes do play a part in morphology and other things that are conducive to running success, they do not—of course—tell the whole story. A whole slew of factors needs to come together to make an elite athlete, while one thing does not fully explain marathon success.
Back in September of 2017, I covered many factors that make both elite marathoners and sprinters. All of the factors that make an elite athlete combine, no one factor is more important than any other, but if one does not have the will to train and win, of course, they will not do well.
When it comes to Kenyans, a small tribe in Kenya explain the success of—the Kalenjin, most specifically, the Nandi sub-tribe and a complex interaction of genotype, phenotype, and socioeconomic factors explain their success (Tucker, Onywera, and Santos-Concejero, 2015). The Kalenjin account for a whopping 84% of Kenya’s Olympic and world championship medals, 79 percent of Kenya’ top 25 marathon performances, contributing to 34%. Kenyans have won 152 medals, compared with 145 with other African countries—42-61% being Ethiopian—while the rest of the world combined won 153 medals. The Nandi sub-tribe has won 72 medals, accounting for 47& of the total for Kenya. What accounts for the insane disparity between East African marathoners (specifically Kalenjin, and a more specific sub-tribe at that) and the rest?
In his book The Genius in All of Us, David Shenk (2010: 102) writes:
Take the running Kenyans. Relatively new to the international competitions, Kenyans have in recent years become overwhelmingly dominant in middle- and long-distance races. “It’s pointless for me to run on the pro-circuit,” complained American 10,000 meter champion Mike Mykytok to the New York Times in 1998. “With all of the Kenyans, I could set a personal best time, and still only place 12th and win $200.”
The Kenyan-born journalist John Manners describes a just-so story to explain how and why Kenyans dominate these competitions: The best young men who were the fastest and had more endurance acquired more cattle, and those who acquired more cattle could then get a bride and have more children, Shenk explains. “It is not hard to imagine that such a reproductive advantage might cause a significant shift in a group’s genetic makeup over the course of a few centuries” (John Manners, quoted in Shenk, 2010: 103).
However, no matter what the origin of Kenyan running success is, the Kalenjin have a passionate dedication to running. Kipchoge Keino was the one who put Kenya on the map regarding distance running. Shenk quotes Keino saying:
I used to run from the farm to school and back … we didn’t have a water tap in the house, so you run to the river, take your shower, run home, change [run] to school . . . Everything is running.
However, when Keino entered 1968 Olympics in Mexico, he came down with gallstones and his doctor told him not to race. However, he took a cab to Aztec Stadium, and when he get caught in traffic he ran the last mile to the stadium and barely got there before the race started. Even though Keino was sick, he destroyed the then-world record by 6 seconds.
Sports geographers don’t point to one variable that explains Kenyan running success—because they all interact. They train at high altitude—and while high altitude is not the only factor regarding long-distance running success, it is crucial. Because training at a high altitude and then running at a lower altitude can change running time by a large amount. One with a normal running economy who goes by the mantra “live high, train low” can shave off about 8 minutes of their time in a 26.2-mile marathon (Chapman and Levine, 2007). Further, socioeconomic variables also explain the success, with it being part of what drives them to succeed, along with favorable morphology, a strong running economy, high intensity training (living at and training at high altitude) and a slew of psychological factors related to social status and socioeconomic factors (Wilbur and Pitsiladis, 2012). This paper speaks perfectly to the slew of variables that need to come together to make an elite athlete.
Shenk (2010: 108) then reverses John Manner’s just-so story:
… it’s an entertaining theory that fits well with the popular gene-centric view of natural selection [it fits well because it’s selected to be so]. But developmental biologists would point out that you could take exactly the same story line and flip the conclusion on its head: the fastest man earns the most wives and has the most kids—but rather than passing on quickness genes, he passes on crucial ingredients. such as the knowledge and means to attain maximal nutrition, inspiring stories, the most propitious attitude and beliefs, access to the best trainers, the most leisure time to pursue training, and so on. This nongenetic aspect of inheritance is often overlooked by genetic determinists: culture, knowledge, attitudes, and environments are also passed on in many different ways.
Further, Shenk also cites sports scientist Tim Noakes who states that the best Kenyan runners cover 230 km (about 143 miles) a week at 6,000 feet in altitude—and this, of course, would be conducive to running success when the event is held at lower altitudes.
David Epstein wrote a solid book on athleticism in 2014—The Sports Gene. Chapters 12 and 13 are pivotal for this discussion. Chapter 12 titled Can Every Kalenjin Run? In this chapter, Epstein, too, cites John Manners, explaining the same thing that Shenk did, but adds this:
In the next breath of the very same chapter [after describing the just-so story about cattle-gathering and wife-acquisiton], though, Manners seems to doubt the suggestion as soon as he raises it. “The idea just occurred to me, so I just put it in.” (pg 184)
Manners came to see his just-so story as less powerful since, over the years as he interviewed Kalenjin runners because “other “hot spots” of endurance running talent have materialized in East Africa, and the athletes responsible are also from traditionally pastoralist cultures that once practiced cattle raiding” (Epstein, 2014: 184-185).
Epstein then discusses how 17 American men in history have run a marathon better than 2:10—or 4:58 per mile—while 32 Kalenjin men did it in October of 2011 alone. Five American high-schoolers have run a sub-4 minute mile, while one high-school in Kenya alone produced 4 sub-4 mile runners!
Kenyan runners have long legs for their height, along with “upper leg length, total leg length and total leg length to body height ratio were correlated with running performance” (Mooses et al, 2014)—which means that they can cover more distance than one with shorter legs. This is critical for running success—of any kind. Kenyans have a high number of type I muscle fibers, but, of course, this alone does not explain their running success. Elite Kenyan distance runners are characterized by low BMI, low fat mass and slim limbs (Kong and de Heer, 2008).
So now let’s discuss altitude adaptation. One objection to this variable—out of many others, of course—that are conducive to running success is why are Tibetans and Andeas not succeeding in these types of competitions as well as the Kalenjin? The answer is simple—because they do not have the long, ecto-dominant (Vernillo et al, 2013) body types. There is also another, perhaps more critical, component to altitude training—hemoglobin, since the amount of oxygen one has in their blood is dictated by two factors—how much hemoglobin one has in their blood and the amount of oxygen the hemoglobin carries. Altitude increases the number of red blood cells in the body, since it is a good way to get oxygen in an environment with less oxygen.
Epstein (2014: 208) writes:
Preferable to moving to altitude to rain is being born there. Altitude natives who are born and go through dilchood at elevation tend to have proportionally larger lungs than sea-level natives, and large lungs have large surface ares that permit more oxygen to pass from the lungs into the blood. This cannot be the result of altitude ancestry that has altered the genes over generations, because it occurs not only in natives of the Himalayas, but also among American children who do not have altitude ancestry but who grow up in the Rockies. Once childhood is gone, though, so too is the chance for this adaptation. It is not genetic, but neither is it alterable after adolescence.
Epstein (2014: 213) quotes the first man to run a sub-4 minute mile, Roger Bannister who says:
The human body is centuries in advance of the physiologist, and can perform an integration of heart, lungs, and muscles which is too complex for the sciencist to analyze.
This, of course, is a hard pill to swallow for some people, who may not believe this. I believe this is true—though we can point to certain factors, each individual’s trajectory into X is unique, and so, explaining Y for all will be close to impossible.
Finally, Epstein (2014: 214) cites Claudio Berardelli:
Berardelli believes that Kenyans are, in general, more likely to be gifted runners. But he also knows that no matter their talent or body type or childhood environment or country of origin, 2:05 marathon runners do not fall from the sky. Their gifts must be coupled with herculean will.
Although that, too, is not entirely seperable from innate [whatever that means] talent.
Hamilton (2000) concludes that:
It seems that the presumed causes of such domination are often recycled, out of date, and based on misinformation and myth.
This, however, betrays understanding of a systems view of running success. Just because North Africans are beginning to show up in these types of competitions it does not mean that the systems view of athleticism is false.
Of course, the East African running advantage is more than ‘genetic’, it is also cultural—which, rightly, shows how every part of the system interacts to produce an elite athletic phenotype. As Louis (2014: 41) notes “The analysis and explanation of racial athleticism is therefore irreducible to biological or socio-cultural determinants and requires a ‘biocultural approach’ (Malina, 1988; Burfoot, 1999; Entine, 2000) or must account for environmental factors (Himes, 1988; Samson and Yerl`es, 1988).” Genetics alone cannot explain the running success of East Africans.
In sum, what explains the success of East African runners? A whole slew of factors that are irreducible, since the whole system interacts. Of course, I do not deny the role that physiological and anatomic factors have on running performance—they are crucial, but not the only, determinant for running success. Reducing a complex bio-system to X, Y, or Z does not make any sense, as every factor interacts to create the elite athlete. East African dominance in middle- and long-distance running will, of course, continue, since they have the right mix of factors that all interact with each other.
Wind back the tape of life to the origin of modern multicellular animals in the Cambrian explosion, let the tape play again from this identical starting point, and the replay will populate the earth (and generate a right tail of life) with a radically different set of creatures. The chance that this alternative set will contain anything remotely like a human being must be effectively nil, while the probability of any kind of creature endowed with self‐consciousness must also be extremely small. (Gould, 1996. Full House)
Wind back the tape of life to the early days of the Burgess Shale; let it play again from an identical starting point, and the chance becomes vanishingly small that anything like human intelligence would grace the replay. (Gould, 1987. Wonderful Life)
Wind back the clock to Cambrian times, half a billion years ago, when mammals first exploded into the fossil record, and let it play forwards again. Would that parallel be similar to our own? Perhaps the hills would be crawling with giant terrestrial octopuses. (Lane, 2015: 21. The Vital Question)
I first read Full House (Gould, 1996) about two years ago. I never was one to believe in evolutionary “progress”, though. As I read through the book, seeing how Gould weaved his love for baseball into an argument against evolutionary “progress” enthralled me. I love baseball, I love evolution, so this was the perfect book for me (indeed, one of my favorite books I have read in my life—and I have read a lot of them). The basic argument goes like this: There are more bacteria on earth than other animals deemed more “advanced”; if evolutionary “progress”—as popularly believed— were true, then there would be more “advanced” mammals than bacteria; there are more bacteria (“simpler: animals) than mammals (more “advanced” animals); therefore evolutionary “progress” is an illusion.
Evolutionary “progress” is entrenched in our society, as can be seen from popular accounts of human evolution (see picture below):
This is the type of “progress” that permeates the minds of the public at large.
Some may look at the diversity of life and conclude that there is a type of “progress” to evolution. However, Gould dispatches with this type of assertion with his drunkard argument. Imagine a drunkard leaving the bar. There is the bar wall (the left wall of complexity) and the gutter (the right wall of complexity). As the drunkard walks, he may stumble in between the left wall and the gutter, but he will always end up in the gutter every time.
Gould explains then explains his reasoning for using this type of argument:
I bring up this old example to illustrate but one salient point: In a system of linear motion structurally constrained by a wall at one end, random movement, with no preferred directionality whatever, will inevitably propel the average position away from a starting point at the wall. The drunkard falls into the gutter every time, but his motion includes no trend whatever toward this form of perdition. Similarly, some average or extreme measure of life might move in a particular direction even if no evolutionary advantage, and no inherent trend, favor that pathway (Gould, 1996: 151).
The claim that there is a type of “progress” to evolution is only due to the fact—in my opinion—that humans exist and are the most “advanced” species on earth.
It seems that JP Rushton did not read this critique of evolutionary “progress”, since not even a year after Gould published Full House, Rushton published anew edition of Race, Evolution, and Behavior (Rushton, 1997) where Rushton argues (on pages 292-294) that there is, indeed, “progress” to evolution. He cites Aristotle, Darwin (1859), Wilson (1975) Russell (1983, 1989; read my critique of Russel’s theory), and Bonner.
To be brief:
The Great Chain of Being (which Rushton’s r/K selection theory attempts to revive) is not valid; Wilson’s idea of “biological progression” is taken care of by Gould’s drunkard argument; Bonner asks why there has been evolution from simple to advanced, and this, too, is taken care of by Gould’s drunkard argument, and finally Dale Russel’s argument about the troodon (I will expand on this below).
Rushton claims that Russell, in his 1989 book Odysseys in Time: Dinosaurs of North America (which I bought specifically to get more info on Russel’s thoughts on the matter and to get more information for an article on it) that “if [dinosaurs] had not gone extinct, dinosaurs would have progressed to a large-brained, bipedal descendent” (Rushton, 1997: 294). Either Rushton only glanced at Russel’s writings or he’s being inherently dishonest: Russel claimed that had the dinosaurs not gone extinct, one dinosaur—the troodon—would have evolved into a bipedal, human-like being. Russel made these claims since the troodon had EQs about 6 times the size of the average dinosaur and they ran on two legs and had use of their ‘hands.’ So, due to this, Russel argues that had the dinosaurs not gone extinct, the troodons could possibly have been human-like. However, there are two huge problems for this hypothesis.
In the book Up From Dragons, Skoyles and Sagan (2002: 12) write:
But cold-bloodedness is a dead-end for the great story of this book—the evolution of intelligence. Certainly reptiles could evolve huge sizes, as they did over vast sweeps of Earth as dinosaurs. But they never could have evolved our quick-witted and smart brains. Being tied to the sun restricts their behavior: Instead of being free and active, searching and understanding the world, they spend too much time avoiding getting too hot or too cold.
So, since dinosaurs are cold-blooded and being tied to the sun restricts their behavior, if they would have survived the K-T extinction event, then it is highly implausible that they would have grown brains our size.
Furthermore, Hopson (1977: 444) writes:
I would argue, as does Feduccia (44), that the mammalian/avian levels of activity claimed by Bakker for dinosaurs should be correlated with a great increase in motor and sensory control and this should be reflected in increased brain size. Such an increase is not indicated by most dinosaur endocasts.
Gould even writes in Wonderful Life:
If mammals had arisen late and helped to drive dinosaurs to their doom, then we could legitimately propose a scenario of expected progress. But dinosaurs remained dominant and probably became extinct only as a quirky result of the most unpredictable of all events—a mass dying triggered by extraterrestrial impact. If dinosaurs had not died in this event, they would probably still dominate the large-bodied vertebrates, as they had for so long with such conspicuous success, and mammals would still be small creatures in the interstices of their world. This situation prevailed for one hundred million years, why not sixty million more? Since dinosaurs were not moving towards markedly larger brains, and since such a prospect may lay outside the capability of reptilian design (Jerison, 1973; Hopson, 1977), we must assume that consciousness would not have evolved on our planet if a cosmic catastrophe had not claimed the dinosaurs as victims. In an entirely literal sense, we owe our existence, as large reasoning mammals, to our lucky stars. (Gould, 1989: 318)
I really don’t think it’s possible that brains our size would have evolved had the dinosaurs not gone extinct, and the data we have about dinosaurs strongly points to that assertion.
Staying on the topic of progression and brain size, there is one more thing I want to note. Deacon (1990a) argues that fallacies exist in the assertion that brain size progressed throughout evolutionary history. One of Deacon’s fallacies is the “evolutionary progression fallacy.” The concept of “progress” finds refuge “implicit expression in the analysis of brain-size differences and presumed grade shifts in allometric brain/body size trends, in theories of comparative intelligence, in claims about the relative proportions of presumed advanced vs. primitive brain areas, in estimates of neural complexity, including the multiplication and differentiation of brain areas, and in the assessment of other species with respect to humans, as the presumed most advanced exemplar” (Deacon, 1990a: 195).
This, in my opinion, is the last refuge for progressionists: looking at the apparent rise of brain size in evolutionary history and saying “Aha! There it is—progress!” So, the so-called progress in brain size evolution is only due to allometric processes, there is no true “progress” in brain size, no unbiased allometric baseline exists, therefore these types of claims from progressionists fail. Lastly, Deacon (1990b) argues that so-called brain size progress vanishes when functional specialization is taken into account.
Therefore it is unlikely that dinosaurs would have evolved brains our size.
In sum, there are many ways that progressionists attempt to show that there is “progress” in evolution. However, they all fail since Gould’s argument is always waiting to rear its head. Yes, some organisms have evolved greater complexity—i.e., moved toward the right wall—though this is not evidence for “progress.” Many—if not all—accounts of “progress” fail. There is no “progress” in brain size evolution; there would not be human-like dinosaurs had the dinosaurs not gone extinct in the K-T extinction event. We live on a planet of bacteria, and since we live on a planet of bacteria—that is, since bacteria are the most numerous type of organism on earth, evolutionary progress cannot be true.
Complexity—getting to the right wall—is an inevitability, just as it is an inevitability that the drunkard would eventually stumble to the gutter. But this does not mean that there is “progress” to evolution.
The argument in Gould’s Full House can be simply stated like this:
P1 The claim that evolutionary “progress” is real and not illusory can only be justified iff organisms deemed more “advanced” outnumber “lesser” organisms.
P2 There are more “lesser” organisms (bacteria/insects) on earth than “advanced” organisms (mammals/species of mammals).
C Therefore evolutionary “progress” is illusory.
The Shroud of Turin is a long cloth that bears the negative image of a man that was purportedly crucified. The study of the Shroud even has its own name—sindonology. The Shroud, ever since its discovery, has been the source of rampant controversy. Does the Shroud show a crucified man? Is this man Christ after the crucifixion? Is the Shroud real or is it a hoax? For centuries these questions have caused long and drawn-out debate. Fortunately, recent analyses seem to have finally ended this centuries-old question: “Does the Shroud of Turin show Christ after the crucifixion?” In this review, I will discuss the history of the Shroud, the pro- and the con-side of the Shroud and what, if any, bearing it has any on the truth of Christianity. The Shroud has been marred in controversy ever since its appearance in the historical record, and for good reason. If it can be proven that the Shroud was Christ’s burial linen and if it can be proven that, somehow, Christ’s image, say, became imprinted when his spirit left his body, this would lend credence to claims from Christians and Catholics—but reality seems to bear different facts of the matter from these claims.
Various theories of the Shroud have been put forth to explain the image that appears when a negative picture is taken of the Shroud. From people hypothesizing that the great Italian artist da Vinci drew it on the cloth (Picknett and Prince, 2012), to it actually being the blood-soaked burial cloth of Christ himself, to its being just a modern-day forgery, we now have the tools in the modern-day to carry out analyses to answer these questions and put them to rest for good.
The history of the Shroud dates back to around the 1350s, as the Vatican historian Barbara Frale notes in her book The Templars and the Shroud of Christ: A Priceless Relic in the Dawn of the Christian Era and the Men Who Swore to Protect It (Frale, 2015). Meachem (1983) discusses how the Shroud has generated controversy ever since it was put on display in 1357 in France. That the Shroud first appeared in written records in the 1350s does not, however, mean that the Shroud is not Christ’s burial linen.
Some, even back when the Shroud was discovered, argued that it was just a painting on linen cloth. As McCrone (1997: 180) writes “The arrangement of pigment particles on the “Shroud” is […] completely consistent with painting with a brush using a water-color paint.” So this would lend credence to the claim that the Shroud is nothing but a painting—most likely a medieval one.
The Shroud itself is around 14’3” long (Crispino, 1979) and, believers claim, it dates back to two millennia ago and bears the imprint of Jesus Christ. It is currently housed at the Cathedral of Saint John the Baptist in Turin, Italy. The Shroud shows what appears to be a tall man, though Crispino (1979) shows that there have been many height estimates of the man on the Shroud, estimates ranging between 5’3.5” to 6’1.5”. With such wide-ranging height estimates, it is therefore unlikely that we will get an agreed-upon height measurement of the man on the Shroud. But Crispino (1979) does note that estimates of Palestinian males 2000 years ago were between 5’1” to 5’3”, and so, if this were Christ’s burial cloth, then it stands to reason that the man would be closer to the lower bound noted by Crispino (1979).
The Shroud shows a man who seems to bear the marks of the crucifixion. If the Shroud was really the burial cloth of a man who was crucified, then there would be blood on the linen. There are blood spots on the Shroud, and there have been recent tests on the cloth to see if it really is human blood.
A method called blood pattern analysis (BPA) is a very useful—ingenious—way to ascertain whether or not the veracity of the claim that the Shroud really was Christ’s burial cloth is true. BPA “refers to the collection, categorization and interpretation of the shape and distribution of bloodstains connected with a crime” (Peschel et al, 2010). By using a model and draping a cloth over them and using the same wounds that Christ was said to have, we can glean—with good accuracy—if the claim that the Shroud was Christ’s burial cloth is true.
A recent study using BPA was undertaken, to ascertain whether or not the blood stains on the Shroud are realistic, and not just art (Borrini and Garleschelli, 2018). They used a living subject to see if the blood patterns on the cloth are realistic. Their analysis showed that “blood visible on the frontal side of the chest (the lance wound) shows that the Shroud represents the bleeding in a realistic manner for a standing position” whereas the stains on the back were “totally unrealistic.”
Zugibe (1989) also puts forth a scientific hypothesis: the claim that Christ was washed prior to his being rolled in the linen cloth that is the Shroud we know of today. So, if Christ were washed before being placed in the linen, then it would lend veracity to the claim that the Shroud truly is Christ’s burial linen. Citing the apocryphal text The Lost Gospel According to Peter, Zugibe (1989) provides scriptural evidence for the claim that Christ was washed before death, which lends credence to the hypothesis that the Shroud truly is Christ’s burial linen. Zugibe (1989) clearly shows that, even after a body has been washed, it can still bleed profusely, which may have caused the blood stains on the Shroud.
Indeed, even Wilson (1998: 235) writes that “ancient blood specialist Dr Thomas Loy confirm[s] that blood many thousands of years old can remain bright red in certain cases of traumatic death.” This coheres well with Zugibe’s (1989) argument that in certain cases, even after a body has been washed and wrapped in linen, that there can still be apparent blood stains on the linen (and we know from Biblical accounts that Jesus did die a traumatic death).
To really see if the Shroud truly is the burial cloth of Christ, analyses of the linen can be undertaken to ascertain an average range of time for when the linen was made. There have been analyses of the linen, and the dates that we get are between the 1250s to 1350s. However, those who believe that the Shroud is truly the burial cloth of Christ state that the fibers that were tested were taken from medieval repairs of the cloth, since one of the locations the cloth was housed in burned down due to a fire in 1532 (Adler, 1996), causing damage to the cloth. For example, Rogers (2005) argues that the threads of linen tested were from medieval repairs, and that the true date of the Shroud is between 1300 and 3000 years old.
Barcaccia et al (2015) undertook an analysis of some dust particles on the back of the Shroud by vacuuming them. They found that there were multiple, non-native plant species on the Shroud, along with multiple mtDNA (mitochondrial DNA) haplogroups (H1-3, H13/H2a, L3C, H33, R0a, M56, and R7/R8). However, the fact that multiple mtDNA halpogroups were found on the Shroud is consistent with the fact that the Shroud took many journeys throughout its time, before ending up in Turin, Italy. It could also reflect the fact that numerous contemporary researchers’ DNA has contaminated the Shroud as well. In any case, Barcaccia et al (2015) show that there were numerous species of plants from all around the world along with many different kinds of mtDNA, and so, both believers and skeptics can use this study as evidence for their side. Barcaccia et al (2015) conclude that the Shroud may have been weaved in India, due to its original name Sindon, which is a fabric from India—which mtDNA analyses corroborate.
There is even evidence that the face on the Shroud is that of da Vinci himself. Artist Lillian Schwartz, using computer imaging, showed that the facial dimensions on the Shroud matched up to the facial dimensions of da Vinci (Jamieson, 2009). It is hypothesized that da Vinci used what is called a camera obscura to put his facial features onto the Shroud. Since we know that da Vinci made some ultra-realistic drawings of the human body since he had access to the morgue (Shaikh, 2015), then it is highly plausible that da Vinci himself was responsible for the image on the Shroud. Jamieson (2009) states that, in the documentary that explains how da Vinci created the Shroud: the most likely way for it to have been made was hanging the Shroud in a dark room with silver sulfate. So when the sun’s rays went through a lens on the wall, da Vinci’s face would have been burnt into it.
Further, there are some arguments that state that the man on the Shroud is not Christ, but is, in fact, the Jacque de Molay—the last Grand Master of the Knights Templar. If the claim turns out to be true, this could be why the Knights protected the Shroud so fervently. Although there is little historical evidence as to how Molay was tortured, we do know he was tortured. Though what is also interesting is that apparently Molay was put through the same exact process of crucifixion that Christ was said to have gone through. If this is the case, then that could explain the same marks in the hands and blood on the Shroud that would have been on the Shroud had Christ been the one crucified and wrapped in the linen that eventually became the Shroud. Though, those who were to kill Molay were “expressly forbidden to shed blood“, though we know he was tortured, it is not out of the realm of possibility that he did bleed after death. Molay was killed in 1317 C.E., and this lines up with the accounts from Frale (2015) and Meachem (1983) that the Shroud appeared around the 1350s. So the Knights protecting the Shroud as they did—even if it were not Christ—would have some backing.
The validity of the Shroud is quite obviously a hot-button topic for Catholics. No matter the outcome of any study on the matter, they can concoct an ad-hoc hypothesis to immunize their beliefs from falsification. No doubt, some of the critiques they bring up are valid (e.g., that they are taking fibers of linen from restored parts of the Shroud), though, after so many analyses one would have to reason that the hypothesis that the Shroud truly was Christ’s burial cloth is false. Furthermore, even if the Shroud is dated back to the 1st century, that would not be evidence that the Shroud was Christ’s burial shroud. The mtDNA analyses also seem to establish that the Shroud passed through many hands—as the hypothesis predicts. However, this also coheres with the explanation that it was made during medieval times, with numerous people touching the linen that eventually ended up becoming the Shroud. It is also, of course, not out of the realm of possibility that contemporary researchers have contaminated the Shroud with their own DNA, making objective genomic analyses of the Shroud hard to verify, while there would be no way to partition contaminated DNA from DNA that was originally on the Shroud.
In any case—irrespective of the claims of those who wish that this is Christ’s burial cloth and thus will concoct any ad-hoc hypothesis to immunize their beliefs from falsification—it seems to be the case that the Shroud was not Christ’s burial cloth. On the basis of mtDNA analyses, blood pattern analyses (which seem to point to the fact that it is an artistic representation of Christ’s burial), to the evidence that facial dimensions on the Shroud match up with da Vinci’s face, the apparent claims that the Shroud was the last Grand Master of the Knights Templar, along with the fact that the original name of the Shroud was Indian in origin, all point to the fact that the Shroud was, in fact, not Christ’s burial linen, no matter how fervent believers are about the veracity of the claim.