The Behavior Genetics of r and K selected Life History Strategy

I’ve been studying r and K selection in earnest, in greater depth than most of the manosphere wonks who toss the terms around.  I’ve made no secret of the fact that I consider the teaching of game little more than the reorientation of western men to r-selected mating strategy, nor have I concealed my opinion that high-K people are clearly happier.  I’m posting the end product of this research, with a few notes:

1.  The terms r and K actually refer to different forms of environmental pressure which selected for short and long term mating strategy in the ancestral environment.  There is no denying that high and low-K life history strategies exist within the human population.  There is controversy surrounding the assumption that, a.) this selection process was density-dependent, which it may not have been, and b.) that high and low-K mating strategy were produced by natural selection at all, which I have generally sided against at the end of the day.  For this reason, I advocate the manosphere start using the terms High and Low-K instead of r-selected and K-selected, because these terms tie it to established suites of life history traits instead of a 50 year old theory in evolutionary biology that most academics reject — without sacrificing what you’re really trying to say.

2.  I think there is some correlation between race and life history strategy, but that was not the focus of the paper so I avoided the topic.

3.  There’s a strong argument for passive, evocative, and active gene-environment interactions which ultimately produce an individual’s life history strategy, but I did not go into detail.

The Behavior Genetics of Life History Strategy

Humans, like all organisms, pursue mating with an eye towards maximizing their reproductive success – passing their genes on in the manner which affords them the greatest likelihood of survival.  To that end, individuals unconsciously pursue a wide variety of reproductive strategies, wherein differences in mate preference and sexual behavior produce significant variation in the qualities of their offspring.  One woman may pursue the long-term commitment of a man with qualities that suggest protectiveness or an ability to provide, while another seeks only the genes of one with good fitness indicators like masculinity, attractiveness, and muscularity (Buss & Shackleford, 2008.)  Each of these reflects a preference for long or short-term mating and each can be understood as a selective adaptation to the environment into which their children will be born.  The question this raises, however, is why individuals tend to pursue the strategies they do across different stages of the fertile periods of their lives.  Beyond the immediate context of mating decisions themselves, what accounts for the seemingly consistent mating preferences of individuals?

A number of researchers have proposed both genetic and environmental explanations.  None are more notorious than J. Philippe Rushton, who has appropriated E.O. Wilson’s r/K selection theory of life history as a means of understanding biological predilection in terms of ancestral evolutionary adaptation.  By this theory, individual differences in strategy are subordinate to between-group variations, which developed over thousands of years in response to widely varying ancestral environments.  That the various approaches to reproduction evoked by these environments live on in the genotypes of their descendants is the basis of Rushton’s work.  Much of this revolves around the capacity of the evolutionary r/K approach to explain population-level differences in life history strategy along racial lines, and for this reason he may be better known for the bitter controversy surrounding his publication than the actual strengths or weaknesses of his writing.  Suffice it to say, both strengths and weaknesses are present and each seems to be conveniently obscured by the biases of those writing in support or in violent disagreement.

Criticisms of Rushton’s theory tend to take three forms: first, that the categories of race examined by Rushton are functionally non-existent and offer no real value as a means of studying the genetics of life history strategy; second, that the r/K theory itself has no application to intra-species variation in life history strategy; and third, that genes do not significantly influence where individuals fall on the spectrum of mating strategy.  Upon examination, the bulk of the evidence seems to confirm the first criticism, refute the third, and allow for some degree of subjectivity when considering the second.  Contrary to the opinions of both Rushton and his critics, race may not be a valuable lens through which to consider genetic variation in life history strategy, but genes do seem to play a significant role in determining the predilections of individuals.  Nonetheless, Rushton fails to meaningfully consider the role that environment plays in influencing both present-day choices and relevant physiological developments earlier in life.  Thus, while the various traits evolved in response to ancestral environments appear to have an impact on individual life history strategy, they are only one factor in a complex gene-environment interaction that influences mating behavior.

At heart, Rushton’s “differential K-theory” attempts to employ the biological theory of r and K selection to explain intra-species differences within humans.  First articulated by Robert MacArthur and E.O. Wilson in 1967, r- and K- selection provides a model of how species adapt to static or fluctuating environments through the development of differing life history traits (MacArthur & Wilson, 1967.)   These traits include age at sexual maturity, number of young, reproductive effort, length of inter-birth intervals, and a host of others, but the basis of life history theory at large is that inter-species variation on these dimensions occurs as a direct result of differing environmental pressures (Stearns, 1977.)  Should one species be subject to heavy predation, its environment may select for a lower age at maturity, higher numbers of young per litter, and greater reproductive effort expended by its members.  By these means, they could evolve to devote more energy towards reproduction and persist despite a life-threatening environment.

Where MacArthur and Wilson broke new ground was in their assertions that certain groups of these traits tend to be correlated, that there are two dichotomous extremes of life history strategy, and that they correspond to differing levels of population density and environmental instability.  This dichotomy and these traits were referred to as r- and K-strategy, shorthand for the maximum rate of population growth and the environmental carrying capacity.   By their theory, initially applied to populations of fish colonizing new habitats, organisms in low-density environments naturally pursue reproduction more aggressively than those who have reached their environmental carrying capacity.

Beyond this temporary response to environmental conditions, however, MacArthur and Wilson postulated that species subject to wide fluctuations in population density – whether due to density-independent mortality or regular colonization of new habitats – will evolve permanently towards life history strategies which enable them to repopulate more rapidly.   The life history traits attendant to this strategy include earlier ages of sexual maturity, greater reproductive effort, lower parental investment, and higher birthrates.  On the other hand, species subject to Malthusian environments of high density-dependent mortality will be better served devoting energy to the survival of their offspring than the production of new ones.  These species are more likely to experience competition for resources and thus require greater non-sexual abilities.  K-selected species tend to have delayed ages of maturity, smaller litters, greater parental investment, and more restrained sexuality.  A useful comparison can be made between rabbits and elephants, one of which matures quickly and reproduces often while the other pursues the opposite strategy.  The central question Rushton has posed is whether life history theory accounts for human variation in these traits, and if so, what accounts for variations in individual strategies.

A substantial amount of work has been done in this arena by Alejandro Figueredo, a psychologist at the University of Arizona who has turned to the study of correlations between relevant personality traits in an attempt to identify consistent life history strategies within human populations.  His focus falls on within-group rather than between-group variation, but it nonetheless goes a long way towards establishing a link between genetics and mating strategy.  Given that the two extremes of r- and K- selection revolve, in effect, around effort devoted to reproduction versus effort devoted to parenting, it seems logical that not only biological traits but personality and psychosocial traits as well would develop to facilitate one or the other strategy by influencing the dispositions of individual humans.

In this regard, a large number of relevant traits exist which directly influence one’s particular style of mating and attachment – the sine qua non of human life history strategy.  Figueredo takes cues from some of Eysenck’s work, which demonstrates the association between extraversion and less restricted sexuality, and points to work by Howard Friedman showing the relationship between conscientiousness and long-term strategies (Eysenck 1976; Friedman et al., 1993).  It is Figueredo’s belief that broad life history strategies will underlie functional behavioral composites of correlated behavioral traits, and each strategy will appear as a latent factor correlated with a suite of personality traits which facilitate either greater reproduction or greater parenting abilities.  In identifying these composites and searching for the factors that function beneath them, he attempts to both associate them with life history strategies and argue in favor of their heritability. (Figueredo, Vasquez, Hagenah Brumbach, Sefcek, Kirsner & Jacobs, 2005)

Figueredo’s suspicions of a single latent factor underlying the suite of traits associated with life history strategy were ultimately confirmed in a 2005 study (Figueredo  et al., 2005.)  Specifically, they examined the covariance of mating effort, risk-taking attitudes, Machiavellianism, adult attachment to romantic partners, and childhood attachment to and parental investment from the biological or non-biological father figure.  What resulted was a single latent variable associated with reduced mating effort, increased familial attachment, and fewer risk taking attitudes – effectively a latent variable underlying a functional composite of traits associated with K-selected life history strategy.  Referred to by Figueredo et al. as the K-Factor, they found it loaded, “0.36 on childhood attachment to the biological father, -0.36 on childhood attachment to any non-biological father figure, 0.38 on adult romantic partner attachment, -0.51 on mating effort, -0.58 on Machiavellianism, and -0.41 on risk propensity”  (Figueredo et al., 2005.)  Moreover, multiple subsequent studies conducted both in Mexico and the United States found that the common K-Factor accounted for 92% of the variation in life history traits associated with a K-selected strategy ((Tal, Figueredo, Frias-Armenta & Corral-Verdugo, 2006; Figueredo 2005.)  Cumulatively, this evidence suggests strongly that the traits considered part of a K-selection strategy have tended to be inherited together and that this can be attributed to a consistent underlying life history strategy.

Given the likelihood of a consistent and cohesive K-selection life history strategy, at issue is the role genetics play in determining variation between high and low-K traits.  On the subject, Figueredo and company have continued down this path and worked out heritability coefficients for a number of behavioral indicators of a high-K strategy (Figueredo 2004.)  Analyzing archival data on monozygotic and dizygotic twins from the national MIDUS survey, the study found a moderate heritability for most of the life history traits examined.  Foresight and anticipation, for example — a trait logically correlated with a long-term, survival-oriented life history strategy — had a heritability estimate of 0.55; Father relationship quality registered at 0.51 and marital relationship quality at 0.42.  Of all the traits considered, most had a heritability estimate of between 0.30 and 0.50, establishing a moderate heritability for the various behavioral indicators of a high-K strategy.

Perhaps more interesting were the statistics regarding the proportion of genetic covariance between psychometric scales that were accounted for by the K-Factor.  In addition to finding that the heritability estimates of the individual measures were substantial, the 2004 study found that most of the lower order genetic factors loaded highly on the genetic K-factor, ranging between 0.60 and 0.90.  Moreover, the K-Factor was responsible for 82% of the genetic variation among the lower order factors and was itself 68% heritable.  This suggests that not only do the lower order factors covary both phenotypically and genetically, but that there is a strong genetic basis to the higher-order factor which underpins their correlation.  Nonetheless, Figueredo acknowledges that the behavioral traits examined in conjunction with the K-Factor are at best genetically mediated, with regulatory genes interacting with environment to produce personality or psychosocial traits.  While strongly supportive of the role genes play in the development of mating strategy, the evidence herein does not seem sufficient to verify the total primacy of genes Rushton implies in his interpretation of life history theory.

In response, Rushton turns away from the study of the personality traits surrounding K-strategy and towards the physiological.  His reasoning is reminiscent of Turkheimer’s theory of strong and weak biologism, and he accepts that life history strategy, like all behavioral traits, can only be truly attributed to additive genetics when there is a physiological basis for it which is itself subject to the direct influence of specific genes (Turkheimer, 1998.)  To do so, he identifies a number of physiological traits upon which r- and K-selected species consistently differ, finds meaningful approximations of these in humans, and looks to between-group differences for signs of variation in life history strategy.   In this case, he argues that life history events like gestation, ovulation, and menarche are themselves biological events which underlie suites of behavioral traits and which are largely ordered by genetically heritable life history strategies.  This forms the basis of his argument that human variation in these behavioral traits can ultimately be attributed to genetic differences produced by natural selection.

In illustration of this point, Rushton points to a number of main physiological traits associated with life history events which vary between human groups.  The most concrete of these seem to be age of menarche, which Rushton equates with age of sexual maturity, and rates of ovulation, which he considers akin to litter size, differing in degree rather than type.  The latter he examines in terms of differential rates of dizygotic twinning, which suggest that in some small sense, certain women ovulate more frequently than others.  That this is an adaptation consistent with a low-K life history strategy, in which survival is best guaranteed by increased rates of reproduction, is the central presumption of his argument.

As usual, Rushton’s preoccupation is with phenotypic consistency within racial categories, and as evidence, he holds up differences in rates of dizygotic twinning between races.  Rushton reports that, per 100,000 born, Asians give birth to fewer than 4 dizygotic twins, Caucasians approximately 8, and Africans over 16 (Rushton 1995.)  Ignoring the obvious controversy of Rushton’s racial obsessions, it bears acknowledging that, should rate of ovulation qualify as a legitimate indicator of life history strategy, this revelation certainly provides evidence of intra-species variation.  Compounding this evidence is the case for the heritability of spontaneous DZ twinning, and a good deal of research suggests exactly that.  Bulmer deduced that the risk of dizygotic twinning for relatives of mothers with DZ twins is between 1.8 and 2.6 times higher than the general population, and suggested a recessive gene with low penetrance and a gene frequency of 50% that could be responsible.  Surprisingly little work exists concerning the component heritability of twinning rates, but linkage scans have been conducted which identify a number of candidate loci associated with the tendency to conceive dizygotic twins (Painter, Willemsen, Nyholt, Hoekstra, Duffy, Henders, Wallace & Healey, 2010.)  It suffices to say that, despite not having firm figures of heritability, rates of DZ twinning have been shown to cluster within families, which suggests some degree of genetic influence.

Comparatively more work has been done to demonstrate the influence of genes on age of menarche, and heritability estimates tend to fall consistently around 0.50 (Towne, Czerwinski, Demerath, Blangero , Roche & Siervogel, 2005.)  Establishing a genetic basis for age of sexual maturation could go a long way towards substantiating Rushton’s theory that intra-species differences in life history strategy exist, and that the physiological developments indicative of different strategies originate in the genes.  Rushton consistently pays only lip service to the significance of individual variation and the role played by environment, however, and it is difficult to argue that a 0.50 heritability estimate justifies this.

While a good deal of evidence exists to support Rushton’s claims about these biological traits and their basis in genetics, his theory begins to unravel under closer scrutiny.  He fails to address the question of whether biological traits like age at menarche or rates of ovulation covary consistently with one another and thus never substantiates his assumption that there is a latent variable connecting them that we can reasonably identify as the K-Factor.  In fact, race is the only real factor he holds up to link them together, and he seems to make the circular argument that racial minorities are low-K because they have higher incidences of these biological traits — which are themselves low-K because they are collectively found in racial minorities.  His reasoning rests on the assumption that, for example, rates of ovulation are genuinely akin to differences in litter size — a legitimately biological life history trait — but this remains an unfalsifiable assumption, and without actually demonstrating a correlation between twinning rates and some sort of higher order factor, an assumption is all it amounts to.

Beyond the error of relegating substantial within-group variation in mating strategy to a concessionary footnote, Rushton’s great fault lies in ignoring more recent evidence that the physiological traits he considers incontrovertible evidence of genetic determinism are in fact heavily subject to environmental influence.  He addresses variation in ovulation and age of menarche, but prefers to attribute it to tectonic evolutionary shifts over individual adaptation.  The capacity of individuals to adapt is considerable, however, and a number of studies confirm the short-sightedness of Rushton’s approach.   A good deal of work has been done to show that pubertal timing is fundamentally responsive to numerous ecological factors, whether related to health, familial stress, or the social environment.  Findings show that both parental supportiveness and time spent by the father in child care are statistically significant predictors of a daughter’s pubertal timing, each correlated positively with later ages of menarche (Ellis, 2004.)  Similarly, girls raised in the absence of their fathers tend to experience menarche earlier.  This may well be an evolutionary adaptation to uncertainty of environmental stability, but if so, it serves only to confirm the capacity of individuals to adapt their life history strategies and counters the argument that these adaptations have their root in additive genetics.

If we accept Rushton’s argument that genetics affect life history strategy indirectly through the direction of relevant physiological events like menarche, ovulation, and gestation, then the revelation of a strong environmental influence obliges us to concede that environment can affect life history strategy through exactly the same means and possibly to a greater degree.  If individual mating decisions are a product of both contextual decision making and biological predilection, then this biological predilection is subject to the influence of not only additive genetics but of the developmental environment, which strongly affects a number of the factors examined.   It certainly bears mentioning that several of the social predictors for later pubertal timing (e.g. strength of relationship with a biological father figure) were themselves indicators of Figueredo’s K-Factor, which suggests a complex interaction between genes and environment in determining life history strategy.

This interaction would seem to make sense in light of the historical data, and Rushton’s insistence on a biologically hardwired life history strategy falls apart when confronted with the obvious reality that strategies change dramatically across generations in genetically consistent populations.  Historical records show a birth rate of 49.2 per thousand in the newly founded Bay Colony of 17th Century Massachusetts, beating out today’s Niger, Mali, and Uganda and outpacing any country currently in existence (Anderson & Thomas, 1973.)  An average family size of 7.13 children would certainly seem indicative of an r-selected mating strategy, and all that remains is for Rushton to verify the inborn criminality, low-IQ, and unrestricted sexuality of the Brownists who stood behind the Salem witch trials.  More likely, ancestral environments selected for an adaptive life history strategy, whereby the physiological and behavioral life history traits of individuals are capable of developing in response to changing environments.  This could explain the apparent gene-environment interaction responsible for the physiological traits that underlie life history strategy, and could be an area of potential future study.

The most significant lesson to be drawn from the realization that both genes and environment influence this strategy, however, is that it must now be subject to intervention.  Rushton seems preoccupied throughout his work with the role played by the K-Factor in the production of complex civilization, due to its emphasis on sexual repression and encouragement of long-term planning.  Whatever his motivation for saying this, there may be some wisdom in developing a collective awareness of the importance of parental investment and future time-orientation to the maintenance of civilization.  A casual observation of American society suggests that participation in the post-industrial economy requires ever-increasing degrees of K-strategy, while the collapse of a common dogma surrounding sexual mores has produced a public which is increasingly r-oriented with each generation.  Ultimately, Rushton’s work comes off fatalistic for its belief in the immutability of genetic predisposition to underlying life history strategy.  The conclusion that environment plays just as strong a role in the formation of these strategies contradicts this belief, and may well be cause for optimism.

Works Cited

  1. Anderson, T., & Thomas, R. P. (1973). White population, labor force and extensive growth of the new england economy in the seventeenth century. Journal of Economic History34(3), 634-667.
  2. Bulmer MG (1970): “The Biology of Twinning in Man.” London: Oxford University Press, pp 113-137.
  3. Buss, D., & Shackleford, T. (2008). Attractive women want it all: Good genes, economic investment, parenting proclivities, and emotional commitment. Evolutionary Psychology6(1), 134-146.
  4. Ellis, B. J. (2004). Timing of pubertal maturation in girls: An integrated life history approach. Psychological Bulletin6(130), 920-958.
  5. Figueredo, A. J., Vasquez, G., Brumbach, B. H., & Schneider, S. M. (2004). The heritability of life history strategy: The k-factor, covitality, and personality. Social Biology3-4(51), 121-143.
  6. Figueredo, A. J., Vasquez, G., Hagenah Brumbach, B., Sefcek, J. A., Kirsner, B., & Jacobs, W. J. (2005). The k-factor: Individual differences in life history strategy. Personality and Individual Differences,2005(39), 1349-1360.
  7. MacArthur, R. H. and Wilson, E. O. 1967. The Theory of Island Biogeography. Princeton, N.J.: Princeton University Press.
  8. Painter, J., Willemsen, G., Nyholt, D., Hoekstra, C., Duffy, D., Henders, A., Wallace, L., & Healey, S. (2010). A genome wide linkage scan for dizygotic twinning in 525 families of mothers of dizygotic twins.Human Reproduction6(25), 1569-1580.
  9. Stearns, S. (1977). The evolution of life history traits: A critique of the theory and a review of the data.Annual Review of Ecology and Systematics,8(1977), 145-171.
  10. Tal, I., Figueredo, A. J., Frias-Armenta, M., & Corral-Verdugo, V. (2006). An evolutionary approach to explaining water conservation behavior. Medio Ambiente y Comportamiento Humano7(1), 7-27.
  11. Towne, B., Czerwinski, S., Demerath, E., Blangero , J., Roche, A., & Siervogel, R. (2005). Heritability of age at menarche in girls from the fels longitudinal study. American Journal of Physical Anthropology, (128), 210-219.
  12. Turkheimer, E. (1998). Heritability and biological explanation.Psychological Review105(4), 782-791.

That’s it.  Any feedback welcome.

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