The current paper synthesizes theory and data from the field of life history (LH) evolution to advance a new developmental theory of variation in human LH strategies. The theory posits that clusters of correlated LH traits (e.g., timing of puberty, age at sexual debut and first birth, parental investment strategies) lie on a slow-to-fast continuum; that harshness (externally caused levels of morbidity-mortality) and unpredictability (spatial-temporal variation in harshness) are the most fundamental environmental influences on the evolution and development of LH strategies; and that these influences depend on population densities and related levels of intraspecific competition and resource scarcity, on age schedules of mortality, on the sensitivity of morbidity-mortality to the organism's resource-allocation decisions, and on the extent to which environmental fluctuations affect individuals versus populations over short versus long timescales. These interrelated factors operate at evolutionary and developmental levels and should be distinguished because they exert distinctive effects on LH traits and are hierarchically operative in terms of primacy of influence. Although converging lines of evidence support core assumptions of the theory, many questions remain unanswered. This review demonstrates the value of applying a multilevel evolutionary-developmental approach to the analysis of a central feature of human phenotypic variation: LH strategy.

No abstract

The National Longitudinal Study of Adolescent Health data were used to test predictions from life history theory. We hypothesized that (1) in young adulthood an emerging life history strategy would exist as a common factor underlying many life history traits (e.g., health, relationship stability, economic success), (2) both environmental harshness and unpredictability would account for unique variance in expression of adolescent and young adult life history strategies, and (3) adolescent life history traits would predict young adult life history strategy. These predictions were supported. The current findings suggest that the environmental parameters of harshness and unpredictability have concurrent effects on life history development in adolescence, as well as longitudinal effects into young adulthood. In addition, life history traits appear to be stable across developmental time from adolescence into young adulthood. KeywordsLife history theory; Add Health; Adolescent health; Environmental harshness; Environmental unpredictability How do developmental experiences and personality processes in adolescence interact to shape quality of life in early adulthood? Life history theory, based in evolutionary biology, provides a powerful framework for addressing this important question. The theory focuses on analyzing individual differences in life history strategies, which constitute overarching patterns of development and behavior that affect many aspects of quality of life (e.g., health, relationship stability, and economic success). The current research tests hypotheses, derived from life history theory, about relations between types of development experience, individual differences in life history strategies, and related life outcomes. Drawing on the National Longitudinal Study of Adolescent Health (Add Health; Udry 2003), we show that

Archival data from the MIDUS survey (Brim et al., 2000), a nationally representative sample, on 309 MZ and 333 DZ twin pairs aged 25-74 years were used to test the psychometrics and behavioral genetics of life history strategy. We organized 253 of the originally administered 2,000 questions into 30 scales measuring life history traits (e.g., quality of family relationships and altruism towards kin), medical symptoms (e.g., thyroid problems), personality traits (e.g., neuroticism, extraversion, conscientiousness), and social background (e.g., financial security). A single higher-order factor, indicating a general life history strategy, composed of three lower-order factors, was replicated. Factor analyses were then performed on the genetic variance-covariance matrices. We found that (a) a single higher-order factor explained the preponderance of the genetic correlations among the scales and (b) this higher-order factor was itself 68 percent heritable and accounted for 82 percent of the genetic variance among the three component lower-order factors.

No abstract