2500 words

As is the case with the other lines of evidence that intend to provide sociobiological evidence in support of the genetic basis of human behavior and development (relating to homology, heritability, and adaptation), Rushton’s work reduces to no evidence at all. (Lerner, 2018)

Introduction

From 1985 until his death in 2012, J. P. Rushton attempted to marshal all of the data and support he could for a theory called r-K selection theory or Differential K theory (Rushton, 1985). The theory posited that while humans were the most K species of all, some human races were more K than others, so it then followed that some human races were more r than others. Rushton then collated mass amounts of data and wrote what would become his magnum opus, Race, Evolution and Behavior (Rushton, 1997). So in the r/K theory first proposed by MacArthur and Wilson, unstable, unpredictable environments favored an r strategy whereas a stable, predictable environments favored a K strategy. (See here for my response to Rushton’s r/K.)

So knowing this, one of the suite of traits Rushton put on his r/K matrix was twinning rates. Rushton (1997: 6) stated:

the rate of dizygotic twinning, a direct index of egg production, is less than 4 per 1,000 births among Mongoloids, 8 per 1,000 among Caucasoids, and 16 or greater per 1,000 among Negroids.

I won’t contest the claim that the rate in DZ twinning is higher by race—because it’s pretty well-established with recent data that blacks are more likely to have twins than whites (that is, blacks have a slightly higher chance of having twins than whites, who have a slightly higher chance of having twins than Asians) (Santana, Surita, and Cecatti, 2018; Wang, Dongarwar, and Salihu, 2020; Monden, Pison, and Smits, 2021)—I’m merely going to contest the causes of DZ twinning. Because it’s clear that Rushton was presuming this to be a deeply evolutionary trait since a highs rate of twins—in an evolutionary context—would mean that there would be a higher chance for children of a particular family to survive and therefore spread their genes and thusly would, in his eyes, lend credence to his claim that Africans were more r compared to whites who were more r compared to Asians.

But to the best of my knowledge, Rushton didn’t explain why, biologically, blacks would have more twins than whites—he merely said “This race has more twins than this race, so this lends credence to my theory.” That is, he didn’t posit a biological mechanism that would instantiate a higher rate of twinning in blacks compared to whites and Asians and then explain how environmental effects wouldn’t have any say in the rate of twinning between the races. However, I am privy to environmental factors that would lead to higher rates of twinning and I am also privy to the mechanisms of action that allow twinning to occur (eg phytoestrogens, FSH, LH, and IGF). And while these are of course biological factors, I will show that there are considerable effects of environmental interactions like diet on the levels of these hormones which are associated with twinning. I will also explain how these hormones are related to twinning.

While the claim that there is a difference in rate of DZ twinning by race seems to be true, I don’t think it’s a biological trait, nevermind an evolutionary one as Rushton proposed (because even if Rushton’s r/K were valid, “Negroids” would be K and “Mongoloids” would be r, Anderson, 1991). Nonetheless, Rushton’s r/K theory is long-refuted, though he did call attention to some interesting observations (which other researchers never ignored, they just didn’t attempt some grand theory of racial differences).

Follicle stimulating hormone, leutinizing hormone, and insulin-like growth factor

We know that older women are more likely to have twins while younger women are less likely (Oleszczuk et al, 2001), so maternal age is a factor. As women age, a hormone called follicle stimulating hormone (FSH) increases due to a decline in estrogen, and it is one of the earliest signs of female reproductive aging (McTavish et al, 2007), being one of the main biomarkers of ovarian reserve tested on day 3 of the menstrual cycle (Roudebush, Kivens, and Mattke, 2008). It is well established that twinning is different in different geographic locations, that the rate of MZ twins is constant at around 3.5 to 4 per 1,000 births (so what is driving the differences is the birth of DZ twins), and that it increases due to an increase in FSH (Santana, Surita, and Cecatti, 2018). We also know that pre-menopausal women who have given birth to DZ twins have higher levels of FSH on the third day of their menstrual cycle (Lambalk et al, 1998).

So if FSH levels stay too high for too long then multiple eggs are released, which could lead to an increase in DZ twinning. FSH stimulates the maturation and growth of ovarian follicles, each of which contains an immature egg called an oocyte. FSH acts on the ovaries to promote the development of multiple ovarian follicles during pregnancy, a process which is called recruitment. In a normal menstrual cycle, only one follicle is stimulated to release one egg; but when FSH levels are elevated, this results in the development and maturation of more than one follicle which is known as polyovulation. Polyovulation then increases the chance of the release of multiple eggs during ovulation. Thus, if more than one egg is released during a menstrual cycle, and they both are fertilized, it can then lead to the development of DZ twins.

Along with FSH, we also have luetenizing hormone (LH). So FSH and LH act synergistically (Raju et al, 2013). LH, like FSH, isn’t directly responsible for the increase in twinning, but the process that it allows (playing a role in ovulation) is a crucial factor in twinning. So LH is responsible for triggering ovulation, which is the release of a mature egg from the ovarian follicle. (Ovulation occurs typically 24 to 36 hours after LH increases.) In a typical menstrual cycle, only one follicle is stimulated to release one egg, which is triggered by the surge in LH. But if there are multiple mature follies in the ovaries (which could be influenced by FSH), then a surge in LH can lead to the release of more than one egg. So the interaction of LH with other hormone like FSH, along with the presence of multiple mature follicles, can be associated with having a higher chance of having DZ twins. FSH therapies are also used in assisted reproduction (eg Munoz et al, 1995 in mice; Ferraretti et al, 2004; Pang, 2005; Pouwer, Farquhar, and Kremer, 2015; Fatemi et al, 2021).

So when it comes to FSH, we know that malnutrition may play a role in twinning, and also that wild yams—a staple food in Nigeria—increases phytoestrogens which increase FSH in the body of women (Bartolus, et al, 1999). Wild yams have been used to increase estrogen in women’s bodies (due to the phytoestrogens they contain), and it enhances estradiol through the mechanism of binding to estrogen receptor sites (Hywood, 2008). And since Nigeria has the highest rate of twinning in the world (Santana, Surita, and Cecatti, 2018), and their diet is wild yam-heavy (Bartolus, et al, 1999), it seems that this fact would go a long way in explaining why they have higher rates of twinning. Mount Sinai says that “Although it does not seem to act like a hormone in the body, there is a slight risk that wild yam could produce similar effects to estrogen.” It acts as a weak phytoestrogen (Park et al, 2009). (But see Beckham, 2002.) But when phytoestrogens are consumed, they can then bind to estrogen receptors in the body and trigger estrogenic effects which could then lead to the potential stimulation and release of multiple eggs which would increase the chance of DZ twinning.

One study showed that black women, in comparison to white women, had “lower follicular phase LH:FSH ratios” (Reuttman et al, 2002; cf Marsh et al, 2011), while Randolph et al (2004) showed that black women had higher FSH than Asian and white women. So the lower LH:FSH ratio could affect the timing and regulation of ovulation, and a lower LH:FSH level could reduce the chances of premature ovulation and could affect the release of multiple eggs.

Lastly, when it comes to insulin-like growth factor (IGF), this could be influenced by a high protein diet or a high carb diet. Diets high in high glycemic carbs can lead to increase insulin production which would then lead to increased IGF levels. Just like with FSH and LH, increased levels of IGF could also in concert with the other two hormones influence the maturation and release of multiple eggs during a menstrual cycle which would then increase the chance of twinning (Yoshimura, 1998). IGF can also stimulate the growth and development of multiple follicles (Stubbs et al, 2013) and have them mature early if IGF levels are high enough (Mazerbourgh and Monget, 2018). This could then also lead to polyovulation, triggering the release of more than one egg during ovulation. IGF can also influence the sensitivity of the ovaries to hormonal signals, like those from the pituitary gland, which then leads to enhanced ovarian sensitivity to hormones like FSH and LH which then, of course, would act synergistically increasing the rate of dizygotic twinning. (See Mazerbourgh and Monget, 2018 for a review of this.)

So we know that black women have higher levels of IGF-1 and free IGF-1—but lower IGF-2 and IGFBP-3—than white women (Berrigan et al, 2010; Fowke et al, 2011). The higher IGF-1 levels in black women could lead to increase ovarian sensitivity to FSH and LH, and thus enhanced ovarian sensitivity could lead to the promotion and release of multiple eggs during ovulation. The lower IGF-2 levels could contribute to the balance of IGF-1 and IGF-2, which would then further influence the ovarian sensitivity to other hormones. IGFBP-3 is a binding protein which regulated the bioavailability of IGF-1, so lower levels of IGFBP-3 could lead to higher concentrations of free IGF-1, which would then further stimulate the ovarian follicles and could lead to polyovulation, leading to increased twinning. Though there is some evidence that this difference does have a “genetic basis” (Higgins et al, 2005), we know that dietary factors do have an effect on IGF levels (Heald et al, 2003).

Rushton’s misinterpretations

Rushton got a ton wrong, but he was right about some things too (which is to be expected if you’re looking to create some grand theory of racial differences). I’m not too worried about that. But what I AM worried about, is Rushton’s outright refusal to address his most serious critics in the literature, most importantly Anderson (1991) and Graves (2002 a, b). If you check his book (Rushton, 1997: 246-248), his responses are hardly sufficient to address the devestating critiques of his theory. (Note how Rushton never responded to Graves, 2002—ever.) Gorey and Cryns (1995) showed how Rushton cherry-picked what he liked for his theory while stating that “any behavioral differences which do exist between blacks, whites and Asian Americans for example, can be explained in toto by environmental differences which exist between them” while Ember, Ember, and Peregrine (2003) concluded similarly. (Rushton did respond to Gorey and Cryns, but not Ember, Ember, and Peregrine.) Cernovsky and Littman (2019) also showed how Rushton cherry-picked his INTERPOL crime data.

Now that I have set the stage for Rushton’s “great” scholarship, let’s talk about the response he got to his twinning theory.

Allen et al (1992) have a masterful critique of Rushton’s twinning theory. They review twinning stats in other countries across different time periods and come to conclude that “With such a wide overlap between races, and such great variation within races, twinning rate is probably no better than intelligence as an index of genetic status for racial groups.” They also showed that the twinning mechanism didn’t seem to be a relevant factor in survival, until the modern day with the advancement of our medical technologies, that is. So since twinning increases the risk for death in the mother (Steer, 2007; Santana et al, 2018). Rushton also misinterpreted numerous traits associated with twinning:

individual twin proneness and its correlates do not provide Rushton’s desired picture of a many-faceted r- strategy (even if such individual variation could have evolutionary meaning). With the exception of shorter menstrual cycles found in one study, the traits Rushton cites as r-selected in association with twinning are either statistical artifacts of no reproductive value or figments of misinterpretation.

Conclusion

I have discussed a few biological variables that lead to higher rates of twinning and I have cited some research which shows that black women have higher rates of some of the hormones that are related to higher rates of twinning. But I have also shown that it’s not so simple to jump to a genetic conclusion, since these hormones are of course mediated by environmental factors like diet.

Rushton quite clearly takes these twinning rate differences to be “genetic” in nature, but we are in the 2020s now, not the 1980s, and we now know that genes are necessary, but passive players in the formation of phenotypes (Noble, 2011, 2012, 2016; Richardson, 2017, 2021; Baverstock, 2021; McKenna, Gawne, and Nijhout, 2022). These new ways of looking at genes—as passive, not active causes, and as not special from any other developmental resources—shows how the reductionist thinking of Rushton and his contemporaries were straight out false. Nonetheless, while Rushton did get it right that there is a racial difference in twinning, the difference, I think, isn’t a genetic difference and I certainly don’t think they it lends credence to his Differential K theory, since Anderson showed that if we were to accept Rushton’s premises, then African would be K and Asians would be r. So while there also are differences in menarche between blacks and whites, this too also seems to be environmentally driven.

Rushton’s twinning thesis was his “best bet” at attempting to show that his r/K theory was “right” about racial differences. But the numerous devestating critiques of not only Rushton’s thesis on twinning but his r/K Differential K theory itself shows that Rushton was merely a motivated reasoner (David Duke also consulted with Rushton when Duke wrote his book My Awakening, where Duke describes how psychologists led to his “racial awakening”), so “The claim that Rushton was acting only as a scientist is not credible given this context” (Winston, 2020). Even the usefulness of psychometric life history theory has been recently questioned (this derives from Rushton’s Differential K, Sear, 2020).

But it is now generally accepted that Rushton’s r/K and the current psychometric life history theory that rose from the ashes of Rushton’s theory just isn’t a good way to conceptualize how humans live in the numerous biomes we live in.