Life history theory

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Life history theory is an analytical framework widely used in animal and human biology, psychology, and evolutionary anthropology which postulates that many of the physiological traits and behaviors of individuals may be best understood in terms of the key maturational and reproductive characteristics that define the life course.

Examples of these characteristics include:

  • Age at weaning
  • Age of sexual maturity or puberty
  • Adult body size
  • Age specific mortality schedules
  • Age specific fecundity
  • Time to first sexual activity or mating
  • Time to first reproduction
  • Duration of gestation
  • Litter size
  • Interbirth interval

Variations in these characteristics reflect differing allocations of an individual's resources (i.e., time, effort, and energy expenditure) to competing life functions, especially growth, body maintenance, and reproduction. For any given individual, available resources in any particular environment are finite. Time, effort, and energy used for one purpose diminishes the time effort, and energy available for another. For example, resources spent growing to a larger body size cannot be spent increasing the number of offspring. In general terms the costs of reproduction may be paid in terms of energy being diverted away from body repair and maintenance and by reducing investment in immunological competence.

Thus the allocation of resources involves trade-offs. These trade-offs and strategies can be compared between species. Two of the most well-known trade-offs involve number of offspring (few or many) and timing of reproduction (accelerated maturation and reproduction versus delayed, allowing for larger size and more complex social supports). The extremes at the species level of these fundamental dimensions of reproduction were recognized long before life history theory, and are traditionally termed r/K selection theory. An r-selection strategy is the production of a large number of offspring (of whom only a minority may survive) as early in life as possible. The K-selection strategy is to produce a smaller number of "fitter" offspring with higher survival chances.

According to life history theory the individuals of a species are able to make limited shifts in reproductive strategies in response to the prevailing environments. Depending on abundance of resources and probable individual longevity, individuals consciously or unconsciously shift their reproductive strategy in one direction or the other to take advantage of available resources or to compensate for resource shortage or uncertainty.

Initially life history theory postulated that life history characteristics were essentially 'extrinsic' (Charnov, 1993, Kozlowski & Wiegert, 1986) and not subject to endogenous processes. However this approach has more recently been found to be theoretically unsatisfying, as there is evidence that higher organisms exert control over virtually all causes of mortality (e.g., by altering patterns of travel to avoid predators, by investing in immune function etc) and these endogenous processes can also be seen at work in the variance in ages of menarché and menopause (Kaplan and Robson, 2002, Kaplan et al, 2003). This argument has some resonance with more recent economic approaches, notably Robert Fogel and Dora Costa’s idea of technophysio evolution (Fogel, 2004).

The traditional life history framework has also been thought to be analytically limited, in that it does not allow for a full understanding of how mortality rates evolve. In reality what varies as a function of ecological factors are not set mortality rates, but rather functional relationships between mortality and efforts allocated to reducing it. Exogenous variation can be thought of in terms of varying 'assault' types and rates (Kaplan et al, 2003).

More recently researchers working in the life history tradition have drawn attention to way the functional relationships described may also be understood in terms of the the fetal programming hypothesis. This hypothesis holds that early growth retardation results in adjustments or impairments in fetal development which have permanent consequences for function and health risk. Programming is thought to occur through "induction, deletion or impaired development of a permanent somatic structure as a result of a stimulus or insult" (Davies and Norman, 2002:386). An accompanying mechanism has also been advanced in an attempt to explain the operation of the programming: the thrifty phenotype hypothesis. The thrifty phenotype process is thought to operate via altered glucose-insulin metabolism (Hales and Barker, 1992, 2001). Although evidence of fetal programming in humans has been questioned on the basis of weaknesses in retrospective epidemiological studies (Huxley et al, 2002), there is very strong evidence from studies of animals to show that poor nutrition in fetal life can have profound effects on metabolic and cardiovascular disease risk in adulthood (Langley-Evans, 2006).

The fetal origins hypothesis has subsequently been developed to include the idea of an 'appropriateness of fit' between the phenotype and its environment. This has resulted in increased attention being drawn to the problems which may occur if there is a mismatch between physiologic capacities established in early development and the environments in which they later function.

In life history terms, fetal programming works to 'configure' our somatic system so that in conditions of good maternal health, low juvenile morbidity rates, and sustained normal nutrition the 'settings' work just so as to increase overall productivity and reduce the relative cost of maintenance (the meaning of 'good health', 'low juvenile morbity' and 'normal nutrition' should be understood in terms of the pre-historic foraging environment where our biology effectively evolved). From this initial 'setting' any sustained increase in nutritional energy input (or reduction in the disease load on the immune system) tends towards increased growth and accelerated maturation (this incidentally may help understand those puzzling long-term fluctuations in population sizes and final heights which characterised the pre-industrial period). Such improved environmental circumstances are also know to operate indirectly on age at maturity since they act as a signal that resource availability is reliably good and that mortality risk is low. Hence it has been found that the norm of reaction for timing of maturation in humans is large, and documented population median ages at menarche range from 12.3–18 years (Eveleth and Tanner, 1990), and the mean age at menarche has been falling steadily in modern growth environments (Weil, 2005).

Thus the trade-offs identified by life history can be interpreted as implying that the present health consequences of differential fetal outcomes represent the resurfacing of costs deferred in early trade-offs. According to the fetal programming hypothesis permanent alterations in metabolic regulation under early conditions of adversity could be seen as adaptive in virtue the overarching need to produce an energy-sparing phenotype (Hales and Barker, 2001). The resulting conceptual problem has been to clarify why such permanent changes should be adaptive if they yield little in the way of future benefits, yet do exact a future cost.

Life history theory has provided new perspectives in understanding many aspects of human reproductive behavior, such as the relationship between poverty and fertility. A number of statistical predictions have been confirmed by social data, though not always reproducibly. The implications for social policy have been hotly debated because statistical associations are not always causal, and a preferred interpretation may be a more minor factor than another unpalatable relationship.

[edit] See also

[edit] References

  • Charnov, E. L. (1993). Life history invariants. Oxford, England: Oxford University Press.
  • Davies M.J., Norman R.J. 2002. "Programming and reproductive functioning". Trends Endocrinol Metab 13: 386–392.
  • Eveleth P., and J Tanner, 1990. Worldwide variation in human growth. New York: Cambridge University Press.
  • Fogel, Robert W, 2001. Biotechnology and the burden of age-related diseases, Chicago Centre For Population Econonics, Working Paper WP- 200 -2
  • Hales CN, Barker DJP. 2001. "The thrifty phenotype hypothesis". Br Med Bull 60:5–20
  • Hales CN, Barker DJP. 1992. Type 2 (non-insulindependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia 35:595–601.
  • Huxley R., Neil A., Colins R. 2002. Unravelling the fetal origins hypothesis: is there really an inverse association between birthweight and subsequent blood pressure? Lancet 360: 659-665.
  • Kozlowski, J and Wiegert, RG 1986. Optimal allocation to growth and reproduction. Theoretical Population, 29, 16-37.
  • Kaplan, H.S., and AJ Robson, 2002. The emergence of humans: The coevolution of intelligence and longevity with intergenerational transfers. PNAS 99(15):10221-10226.
  • Kaplan, H.S., Lancaster, J.B., & Robson, 2003. Embodied Capital and the Evolutionary Economics Of the Human Lifespan. In: Lifespan: Evolutionary, Ecology and Demographic Perspectives, J.R. Carey & S. Tuljapakur (eds.) Population and Development Review 29, Supplement 2003, Pp. 152-182.
  • Langley-Evans, S.C. (2006). Developmental programming of health and disease. Proceedings of the Nutrition Society 65: 97-105.
  • Roff, D. (1992). The evolution of life histories: Theory and analysis. New York:Chapman & Hall.
  • Selander, Robert K. (Sep., 1967). Why There are no Subspecies of North American House Sparrows Systematic Zoology Vol. 16, No. 3, pp. 286-287
  • Stearns, S. (1992). The evolution of life histories. Oxford, England: Oxford University Press.
  • Weil, David N, 2005, Accounting for the Effect of Health on Economic Growth, NBER Working Paper No. 11455

[edit] Further reading

  • Langley-Evans, S.C. (2004). Fetal nutrition and adult disease; programming of chronic disease through fetal exposure to undernutrition. CABI Publishing, Wallingford, UK.
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