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The Bajau spleen size and better-living-through-evolution story is also a reminder that since the dawn of the theory of evolution, humans have been incredibly creative in coming up with evolutionary and hence genetic narratives and explanations for just about every human trait that can be measured. This effort recycles from time to time and is again reaching a peak in an era when it is possible to quickly and cheaply “genotype” human populations. (Joyner, Boros, and Fink, 2018: 524-525)

Yesterday on Twitter Matt Yglesias—Vox blogger—tweeted out a 2018 paper in which the authors argue that ‘natural selection’ explained the bigger spleens of the Bajau and, consequently, how they could hold their breaths for such a long time (Ilardo et al, 2018). The main claim of the paper is that ‘natural selection’ ‘selected-for’ larger spleens which then increases how much oxygen can be stored. The point of the study was to find out if their exceptional diving abilities had a ‘genetic basis.’ Thankfully, though, a group of physiologists looked into the claims of Ilardo et al (2018) and found their main claims wanting (Joyner, Boros, and Fink, 2018). That’s how easy it is for selectionists: Notice a trait; then work backward and attempt to formulate the best story you can (see Smith, 2016).

These diving capabilities are similar to high-altitude hypoxia—indeed the authors assume that there was an adaptation for breath-hold diving. They compared some Bajau people (n=59) and close neighbors who did not—the Saluan (n=34)—really interact with the water environment. So, using a portable ultrasound machine, they photographed the spleens of the two groups and noted a “clear visual difference” between Bajau spleens and Saluan spleens. The Bajau had spleens about 40-50 cc bigger than the Saluan.

These results suggest a physiological difference between the Bajau and the Saluan that is not solely attributable to a plastic response of the spleen to diving activity. While other unknown environmental factors could potentially explain the observed difference between the groups, genetic factors remain a possibility.

So big spleens mean big breath-diving ability. And big spleens were an object of selection. So breath-diving was therefore selected for—so the just-so story goes. But, “a slightly larger spleen is almost certainly not the most important [part of diving] from a physiological perspective” (Joyner, Boros, and Fink, 2018: 524). They then found ‘genes for’ big spleens and they then formulated their just-so story. Accompanying evidence was the fact that deep-diving animals have bigger spleens, so since the Bajau have bigger spleens, this then would mean that the bigger spleens then allows for better breath-diving. Joyner, Boros, and Fink (2018: 525) write:

The general idea is that, like blood doping in cyclists, bigger spleens that contract would give the Bajau divers a boost of oxygen-carrying red cells that would make them more successful at underwater-based hunting and gathering. Thus, spleen size was selected for via evolution over the last 1,000 years or so. A few simple back-of-the-envelope calculations about oxygen stores are instructive. A 40 cc bigger spleen that was all red cells and contracted completely with diving might give the Bajau 20 milliliters of extra oxygen. That is about 1% or less of the oxygen stored in the body and lungs of healthy humans.

Joyner and colleagues then go on to note other ethnies who perform similar breath-dives, while also noting that the Bajau routinely perform dives at 5-10 meters for 30 seconds, which while impressive, is something that fit people can do if they train their lung capacity.

Of note, in the famous Japanese and Korean breath-hold divers who have been studied for decades, repeated descents of this depth and duration don’t cause oxygen levels in the blood to fall much (Schagatay, Lodin-Sundstrom, and Abrahamsson 2011; Stanek et al. 1993). Second, repeated dives of this duration with brief periods of rest only cause whole-body oxygen consumption to rise to the level seen during a brisk walk or slow jog (Craig and Medd 1968). This is hardly the sort of maximum efforts made by deep-diving seals, competitive breath-hold divers, and blood-doping cyclists. The extra oxygen from a slightly larger spleen could easily be generated by a slightly larger breath prior to starting the dive.

It is incredibly easy to think up just-so stories for anything you notice (e.g., my just-so story on Mesoamerican human sacrifices). The Bajau learn to do breath-dive like that—it is an acquired ability. ALL human traits are experience-dependent and plastic, but obviously not to the same degrees.

The spleen is a blood filter. Being a blood filter, if it can filter MORE blood by being bigger, then it will give the individual whose spleen it is an advantage at certain tasks. It sits upper-left part of the abdomen and is protected by the rib cage while also being a place for blood cell storage (Pernar and Tavakkoli, 2019). The spleen acts as a reservoir of oxygen storing “‘thick blood’ rich in cells” so that when the diving animal the oxygen levels are stressed, the body has the reservoir of extra oxygen (Milton, 2004). Esperson et al (2002) also note how the spleen acts as a reservoir of red blood cells, while the contraction of the spleen causes extra hemoglobin production after exposure to diving events.

When a diver submerges their body in the water, two things happen: bradycardia—slower heart rate and vasoconstriction—the narrowing of arteries. The increase in water pressure further causes blood shift—an extension of vasoconstriction which allows us to dive deeply and the spleen effect—meaning that the spleen of divers shrinks which then releases the stored RBCs into the body, allowing for prolonged diving. So, if we look at this in regard to the Bajau, their large spleen shrinks and since their spleen is large due to the number of RBCs it has, it would then follow that as they deep-dive the spleen would shrink (known as splenic contraction) causing the release of the RBCs into the body, allowing for the deep-diving phenotype. Thus, without the blood shift and spleen effect, divers would not be able to dive to such deep depths. (See Gooden, 1994.) The mammalian dive response has, also, been hypothesized to be a reflex to preserve life (Panneton, 2013).

Bajau and, for example, Tibetan environments are similar in that the Bajau spend time in low-oxygen environments (the water) and so do the Tibetans (the mountains). But the Tibetans are constantly exposed to this effect; the Bajau need to be in the water for this effect to occur.

Lastly, the “HBDers” in the comments on Yglesias’ tweet said the same ol’ predictable things. Such as “human spleen growth is complex and due to what the stereotypes of a group’s spleen size are”; “of course it’s true!”; “variation in spleen size within groups is greater than variation in spleen size within groups”; “spleens are a social construct”; “evolution only happened in humans below the neck”; etc. These are the same ol’ sayings that come out from “HBDers” whenever a finding like this comes out. And, you can tell that they are ignorant to the anatomy/physiology of this stuff. They just jump on anything that they can say “HBD is real!!” as if anyone denies that humans are biologically diverse (like when the Rushton retraction came ‘it doesn’t mean that HBD isn’t true!). They move and weave different definitions of ‘HBD’ to fit their needs.

Such storytelling can be done for any trait, as noted by Smith (2016). One can think up selectionist stories and competing ideas for the evolution of traits, but without a way of ajudicating between two stories. One of the best definitions of just-so stories I am aware of is from Not in Our Genes (Lewontin, Rose, and Kamin, 1984: 258-262) cited in Smith (2016). Just-so stories:

predicate a genetically determined contrast in the past…unstated assumption that genes may arise with any arbitrarily complicated action needed by the theory…insulated from any possibility of being contradicted by fact…. If one is allowed to invent genes with arbitrary complicated effects on phenotype and then to invent adaptive stories about the unrecoverable past of human history, all phenomena, real and imaginary, can be explained.

So what happens when a physiologist looks into “HBD” claims? They are found very, very wanting.

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I’ve been writing on this blog since June 15th, 2015. Back then, I held staunch hereditarian beliefs. Rushton’s views on testosterone were enticing to me, especially his theoretical article with Templer (Rushton and Templer, 2012). When I first read it I thought “Oh, justification for my prior beliefs about blacks and crime.” Then, when I started studying anatomy and physiology, I reread the paper and thought “Wow who gave the OK to publish this mess?”

So in February of 2018 I published a critique of the article, Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals? A Response to Rushton and Templer (2012). I critiqued many of the claims in their article; its biggest weakness completely handwaving the warnings of Ducrest et al (2008) that human populations “are therefore not expected to consistently exhibit the associations between melaninbased coloration and the physiological and behavioural traits reported in our study.” Rushton and Templer dodged this by saying that we should compare African and European crime rates and that we do, indeed, see that Africans commit more crimes than whites and Africans have darker skin than whites so this is sort of “preliminary evidence” for the relationship in human races.

However, unfortunately for Rushton, Cernovsky and Litmann (2019) reanlyzed the INTERPOL crime data:

When all data from the same two Interpol Yearbooks are re-calculated, most of the statistically significant trends in the data are in the direction opposite to Rushton’s beliefs: Negroids had lower crime rates than Caucasoids with respect to sexual offenses, rapes, theft, and violent theft or robbery, with most correlation coefficients exceeding .60. While we do not place much credence in such Interpol statistics as they only reproduce information provided by government officials of different countries, our re-analysis indicated that Rushton excluded data that would discredit his theory.

So, if we accept the INTERPOL data—as Rushton did—then we would be justified in saying that the proposed relationships and causal pathways do not hold.

Then at the end of October the Twitter account @evopsychgoogle wrote a long thread with a strong, in-depth critique of the arguments and sources in Rushton and Templer (2012). He then published his critique as a letter to the editor of Personality and Individual Differences (PaID). In the letter, he exposes the shoddy logic of Rushton and Templer, while showing their misreadings of sources and misunderstanding of pleiotropy. Their main point in the paper is that LHT may explain why dark-skinned individuals are more violent, mature faster, etc while they also argue that the melanocortin system is a physiological coordinator of LH traits and skin color.

Testosterone production is a simple bodily process—to quote myself from November, 2017:

There are five simple steps to testosterone production: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone) (Saladin, 2010: 137). Testosterone is a steroid and so there are no ‘genes for’ testosterone.

Cells in the testes need to take cholesterol and then convert it into testosterone with the luteinizing hormone. According to Rushton and Templer, the result of this bodily process is part of the reason why blacks are more violent than whites—they have higher levels of testosterone and testosterone causes aggression/violence. Surely, Rushton and Templer were aware of Rohrmann et al (2007) who showed no difference in testosterone between blacks and whites. Surely Rushton and Templer were aware of all of the research that I cited in what I would call my ‘master article’ on race, testosterone, prostate cancer, and aggression. Rushton and Templer, quite obviously on a review of the literature, are misleading their readers.

Thankfully this paper has only been cited 15 times in the past 8 years since it was published. Evolution, presumably, accounts for the differences in death, AIDS rate, testosterone, lower life expectancy, etc. One recent citation can be found in the textbook Race and Crime (Gabiddon and Greene, 2018, 5th edition) in a discussion about Rushton’s r/K selection theory and causes for Rushton’s proposed relationship. They write (pg 122-123):

As with all theories, there have been several criticisms of the r/K selection theory. First, Rushton generally underemphasizes sociological factors. Most of his cross-national comparisons point strictly to numbers, without taking into account variables such as socioeconomic status, and other important sociological variables (Whihte, 2018). Second, in the 21st century, there are few “pure” races, especially in the United States, as noted in Chapter 1. White sexual aggression against Black females during the slave era produces countless mixed-race offspring. Therefore, the rigorous adherence to the Black-White-Asian split is problematic. Finally, if Rushton;s theory were true, what would explain White aggression as early colonizers and their current involvement in wars and violence across the globe? In contrast to Rushton’s theory, Bradley (1978) argued that, as a result of migration to colder regions, since the beginning of humanity, Whites have been the global aggressors.

So, testosterone does not cause aggression and it does not cause crime; the melanocortin system does not work in such a way that works for Rushton and Templer’s theory (Cone, 2006).

Hilliard (2012: 73) stated that “No evidence shows that racism motivated Rushton” while Dutton (2018) stated the same, interviewing Rushton’s ex-wife (whom he had an illegitimate black son with). But, knowing what we know about testosterone and Rushton’s views on blacks and whites, knowing about his (false) views on testosterone and race (while citing old, flawed studies like Ross et al) we can call into question the claim that Rushton had no racial animus. @evopsychgoogle also brought up the fact that COIs and funding sources were not brought up (this being Rushton’s final paper before his death and the fact that he was the head of the Pioneer Fund at the time means we don’t have to ask where the funding came from). Rushton and Templer should have never been published in the first place.

Lastly, Clark et al (2020) argued that ‘intelligence’ as ‘measured‘ by ‘IQ tests’ modulates the relationship between religiosity and crime at a country-wide level. They, of course, used Lynn’s global ‘IQ’ data. Though, there were many critiques of the paper and the data used in it (see here, here, and here) and Clark et al decided to finally retract their paper due to the problems of Lynn’s dataset. So, if they retracted due to the problems with Lynn’s dataset, does that mean that other papers that relied on Lynn’s shoddy work (e.g., Richardson, 2004; Morse, 2008) should be retracted too? Ebbeson (2020) notes the flawed ‘IQ estimates’ used in Clark (2020), noting the small, unrepresentative child samples used, along with showing that their dataset leads to “notions” which “are incompatible with psychological science” so “all conclusions drawn from these data are invalid.”

Clark et al “lost confidence in their findings” since “the homicide data have limitations that call [their] findings into question” while “The IQ data … have much more serious issues.” “Serious” is an understatement. To quote Ebbeson (2020)

For example, in the ‘NIQ_QNWSAS’ dataset, several African, South Asian and Central American countries have an average IQ below 50, such as Nepal (national IQ: 43.0), Sierra Leone (national IQ: 45.1), Guatemala (national IQ: 47.7) and Gambia (national IQ: 49.8) These estimates would seem to suggest that a majority of the population in these countries are moderately, severely, or profoundly cognitively impaired. (cf. Table 1). This notion is incompatible with psychological science and there is no doubt that these estimates are wrong.

All in all, this is not a good week for “HBD”—Rushton is being exposed for the know-nothing about physiology that he is, and Lynn’s ‘national IQ’ numbers are getting the scrutiny they finally deserve. So, I hold, if Clark et al was retracted for those reasons, we need to retract ALL papers that relied on Lynn’s ‘national IQ data.’ People may cry ‘censorship! HBD is dead!’, but ‘HBD’ (what I would term psychological hereditarianism) has been long dead. Rushton and Templer’s paper should have never been published but it’s better late than never that it is finally getting retracted. If you’re saying that Rushton and Templer got retracted for “political reasons” then it’s clear that you did not read either of the two existing critiques of the paper.