Life history and the early origins of health differentials

被引:113
作者
Worthman, CM [1 ]
Kuzara, J [1 ]
机构
[1] Emory Univ, Dept Anthropol, Atlanta, GA 30322 USA
关键词
D O I
10.1002/ajhb.20096
中图分类号
Q98 [人类学];
学科分类号
030303 ;
摘要
Current epidemiologic models concerning the fetal origins of later health risk are evaluated from the perspectives of evolutionary and developmental biology. Claims of adaptive value for and biological status of fetal programming are critically examined. Life history theory is applied to identify key trade-offs in adaptive strategies that constrain developmental design to use information from the environment to guide ontogeny and establish cost-benefit trade-offs that weigh early survival advantage against remote or unlikely future costs. Expectable environments of evolutionary adaptedness, particularly of gestation, are characterized and their impact on human adaptive design discussed. The roles of neuroendocrine mechanisms in scaffolding life course development, negotiating ongoing cost-benefit trade-offs, and mediating their long-term impacts on function and health are reviewed in detail. Overviews of gestational biology and the postnatal physiologic, cognitive-affective, and behavioral effects of gestational stress identify a shared central role for the hypothalamic-pituitary-adrenal (HPA) axis. Rather than merely mediating stress responses, the axis emerges an agent of resource allocation that draws a common thread among conditions of gestation, postnatal environments, and functional and health-related outcomes. The preponderance of evolutionary and developmental analysis identifies environments as agents on both sides of the health risk equation, by influencing vulnerabilities and capacities established in early and later life course development, and determining exposures and demands encountered over the life course. (C) 2004 Wiley-Liss, Inc.
引用
收藏
页码:95 / 112
页数:18
相关论文
共 150 条
  • [11] Barker DJP, 2001, BRIT MED J, V323, P1
  • [12] Costing reproduction
    Barnes, AI
    Partridge, L
    [J]. ANIMAL BEHAVIOUR, 2003, 66 : 199 - 204
  • [13] Emerging and re-emerging infectious diseases: The third epidemiologic transition
    Barrett, R
    Kuzawa, CW
    McDade, T
    Armelagos, GJ
    [J]. ANNUAL REVIEW OF ANTHROPOLOGY, 1998, 27 : 247 - 271
  • [14] Placental 11 beta-hydroxysteroid dehydrogenase: A key regulator of fetal glucocorticoid exposure
    Benediktsson, R
    Calder, AA
    Edwards, CRW
    Seckl, JR
    [J]. CLINICAL ENDOCRINOLOGY, 1997, 46 (02) : 161 - 166
  • [15] BJORNTORP P, 1995, INT J OBESITY, V19, pS6
  • [16] Enzymology and molecular biology of glucocorticoid metabolism in humans
    Blum, A
    Maser, E
    [J]. PROGRESS IN NUCLEIC ACID RESEARCH AND MOLECULAR BIOLOGY, VOL 75, 2003, 75 : 173 - 216
  • [17] Bogin B, 1997, YEARB PHYS ANTHROPOL, V40, P63
  • [18] Bonner JT., 1974, On development: the biology of form
  • [19] Bowlby J., 1969, ATTACHMENT LOSS, V1
  • [20] The evolution of fitness in life-history theory
    Brommer, JE
    [J]. BIOLOGICAL REVIEWS, 2000, 75 (03) : 377 - 404