Desktop version

Home arrow History

  • Increase font
  • Decrease font

<<   CONTENTS   >>

What Drives Life History Variation?

Mortality, specifically its predictability and controllability, is what drives the life history of a species (Charnov 1993; Hewlett et al. 2000). Extrinsic mortality is that which can neither be predicted nor controlled; intrinsic mortality can be both predicted and controlled (Griskevicius et al. 2011). High rates of extrinsic mortality promote faster life histories

© The Author(s) 2016 27

S.C. Hertler, Life History Evolution and Sociology,

DOI 10.1007/978-3-319-48784-7_5

(Chisholm 1999). Extrinsic mortality induces faster intergenerational baton passing, selecting for disposable somas, large broods, and little parental investment (Promislow and Harvey 1990). Risk of lineage extinction is thereby diversified. Alternatively, a relative exchange of extrinsic for intrinsic mortality promotes a K-selected life history, with its slower intergenerational baton passing, selection for durable somas, small broods, and high parental investment (Quinlan 2007). Investing in the maintenance of oneself, and the care of offspring, only rewards to the extent that it works. To clarify the relationship between mortality and life history, consider an analogy: An investor with little knowledge of stock trends (extrinsic mortality) invests little across many stocks, which functions as a bet-hedging device in the absence of predictive power (fast life history). Alternatively, a seasoned trader with inside information (intrinsic mortality) invests much in a few stocks, which are known to have a high likelihood of return (slow life history). The predictability and controllability of the investment, like the predictability and controllability of mortality, determines the strategy that is adopted.

When experimentally amplifying rates of extrinsic mortality, senescence specifically, and life history speed generally, augments in fruit flies, guppies, and bacteria (Rauser et al. 2009). Briefly, fruit flies, in a series of experiments by Stephen Stearns, have assumed greatly exaggerated lifespans as extrinsic mortality is dialed down. In these, and in similar experiments (Rose 1984; Partridge and Fowler 1992; Zwan et al. 1995; Burke and Rose 2009), artificially controlled mortality regimes were responsible for this remarkable divergence (Stearns et al. 1998, 2000). Conversely, experimentally augmented extrinsic mortality rates within a naturalistic setting increased guppy fecundity and maturation speed, while experimentally augmented extrinsic mortality rates within the laboratory setting “allowed for the invasion of a more rapidly aging morph”1 (Rauser et al. 2009, p. 565; Walsh and Reznick 2011). Ackermann et al. (2007), experimentally manipulating “asymmetrically fissile bacteria,2 found rapid aging in response to high extrinsic mortality (Rauser et al. 2009). Related experiments, manipulating mortality regime or its correlates, have shown experimental associations between mortality and life history speed (Dowling 2012) across species of beetle (Maklakov et al. 2007), nematode (Chen and Maklakov 2012), birds (Alonso-Alvarez et al. 2006), and flies (Martin and Hosken

2003). Moving from experimentation to observation, those organisms possessing extrinsic mortality reducing adaptations show slower life histories: Quahog clams (Bodnar 2009; Philipp and Abele 2009), tortoises and turtles (Gibbons 1987), elephants (Wiese and Willis 2004), arboreal primates (van Schaik and Isler 2012), bats (Wilkinson and South 2002; van Schaik and Isler 2012), and birds, specifically parrots and cockatoos (Young et al. 2012). In common, all of these animals have some means of limiting extrinsic mortality, be it by shell, bulk, tree, or wing. With these adaptations providing effective predator defense, life becomes less precarious, and life histories can slow. Beyond experimental manipulation and evolved adaptations, climate can greatly alter the mortality regime. To this end, consider that geographically mapped selections of long-lived organisms (Sussman et al. 2014) show a disproportionate number concentrated in desert, polar, and subalpine biomes wherein extrinsic mortality imposed by biotic competition is limited by the harshness imparted by high altitude, latitude, or aridity: Creosote and Yucca of the Mojave Desert (Sussman et al. 2014; Bellingham and Sparrow 2000), the many succulent species within the Grand Canyon of Arizona (Bowers et al. 1995), cave salamanders (Speakman and Selman 2011), Siberian actinobacteria (Sussman et al. 2014), and the great majority of Antarctic plant species (Green et al. 2007).

Thus, experimental manipulations, cross-species comparisons, and geographic surveys establish as causal, the degree of predictability and controllability of mortality. Humans are not exempt from this calculus. Life history variation results. Consider the comparison of 170 nations conducted by Low et al. (2008) who found that nearly three quarters of the variation in age at first birth related to life expectancy in the predicted direction. Consider too, the study of Chicago neighborhoods by Wilson and Daly (1997), wherein variation in life expectancy related to a nearly five year differential in age at first birth, again in the predicted direction (Griskevicius et al. 2011). Again, this is because humans are subject to the same inescapable calculus. As described by Gladden et al. (2009), expressing the future orientation of the K selected, and all the biological and cultural behaviors that follow from it, would be incongruous and maladaptive under conditions of high extrinsic mortality. As these authors state, “planning for the future or delaying reproduction,” “would likely be wasted in an unpredictable environment where mortality risk is high.” The relative inability to protect offspring against extrinsic mortality results in the r selected bet-hedging against lineage extinction via reproducing early and often (Chisholm 1999). The rapidity of the r selected life is not an expression of pathology. A person or party may value the K strategy over the r strategy, but, from an evolutionary perspective, each is an adaptation to past and prevailing conditions.

With the causal link between mortality and life history in mind, consider Fishtown and Belmont. Eighty percent of white federal prisoners between the ages 20-49 came from Fishtown, while 2 % came from Belmont. Furthermore, the 2,392,000 white parolees recorded in 2008 were overwhelmingly residents of Fishtown. It is then important to note that, “the levels of arrests in Fishtown, especially for violent crime, remain far above their levels of earlier decades” (Murray 2012, p. 194). Violent crime is the modern societal proxy for extrinsic mortality (Ellis et al. 2009). Controlling for SES and almost irrespective of property crime, violent crime informs, for instance, cross-national trends toward early childbirth (Griskevicius et al. 2011). In Fishtown, it seems that “persistent mortality cues and persistent resource scarcity appear to lead people to adopt faster life history strategies” (Griskevicius et al. 2011). Such conditions combine to make the future an uncertain prospect, and thereby select for the faster life histories, which emphasize the certainty of the present. On the other side, as Fishtown residents suffer from high extrinsic mortality, they could be thought of as enjoying low intrinsic mortality. The disability services, Medicaid, Social Security Income benefits, and unemployment assistance funded by wealth transfer payments from higher income strata limit intrinsic mortality; they insulate from the Malthusian3 state of nature that is red in tooth and claw.

The opposite holds true for Belmont residents. They enjoy extremely low levels of violent crime and have sufficient law enforcement, health behaviors, and medical coverage to regard a single prime-aged adult death as a news capturing tragedy (Hewlett et al. 2000).4 While residents of Belmont benefit from what is possibly the lowest rate ofextrinsic mortality that any set of interbreeding humans ever experienced, they in some subjective sense also still operate under high levels of intrinsic mortality. Certainly, they will not die from cold or starvation, even should they stop working all together; and so despite any behavioral changes, current Belmont residents will still be part of the national population. However, it does not follow that they will be part of the insular, interbreeding Belmont population. To gain entry into Belmont, and stay within it, one must surmount the economic barriers imposed by astronomical real estate taxes and exorbitant home sale prices, while paying rates of payroll, income, inheritance, and sales tax that not only scale linearly with income but increase the bracket at which one are taxed. Belmonters also fund much of the wealth transfer payments made to Fishtowners. All of this requires planning, hard work, and delay of gratification. Just as violent crime is a modern proxy for extrinsic mortality, this kind of hardship is a modern proxy for intrinsic mortality. The Belmont resident may not be under the yoke laboring against the cold to survive, but he is at the desk laboring against the odds to survive as a Belmonter.

<<   CONTENTS   >>

Related topics