Early life events and their consequences for later disease: a life history and evolutionary perspective
Abstract
Biomedical science has little considered the relevance of life history theory and evolutionary and ecological developmental biology to clinical medicine. However, the observations that early life influences can alter later disease risk—the “developmental origins of health and disease” (DOHaD) paradigm—have led to a recognition that these perspectives can inform our understanding of human biology. We propose that the DOHaD phenomenon can be considered as a subset of the broader processes of developmental plasticity by which organisms adapt to their environment during their life course. Such adaptive processes allow genotypic variation to be preserved through transient environmental changes. Cues for plasticity operate particularly during early development; they may affect a single organ or system, but generally they induce integrated adjustments in the mature phenotype, a process underpinned by epigenetic mechanisms and influenced by prediction of the mature environment. In mammals, an adverse intrauterine environment results in an integrated suite of responses, suggesting the involvement of a few key regulatory genes, that resets the developmental trajectory in expectation of poor postnatal conditions. Mismatch between the anticipated and the actual mature environment exposes the organism to risk of adverse consequences—the greater the mismatch, the greater the risk. For humans, prediction is inaccurate for many individuals because of changes in the postnatal environment toward energy‐dense nutrition and low energy expenditure, contributing to the epidemic of chronic noncommunicable disease. This view of human disease from the perspectives of life history biology and evolutionary theory offers new approaches to prevention, diagnosis and intervention. Am. J. Hum. Biol. 19:1–19, 2007. © 2006 Wiley‐Liss, Inc. © 2006 Wiley‐Liss, Inc.
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Phenotype-environment mismatch can be a source of biologically maladaptive outcomes as a side effect of conditional adaptation.
“Another possible source of biologically maladaptive outcomes is phenotype-environment mismatch, occurring as a side effect of conditional adaptation (e.g., Gluckman et al., 2007).”
From The Adaptive Calibration Model of stress responsivity (2011) · cites this paper as Gluckman et al., 2007
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- Authors
- Gluckman, P. D., Hanson, M. A., & Beedle, A. S.
- Affiliations
- University of Auckland (NZ)
- University of Southampton (GB)
- Corresponding author
- Gluckman, Peter D.
- Venue
- American Journal of Human Biology
- Publisher
- Wiley
- Published
- 2006-12-07
- Volume
- 19
- Issue
- 1
- Pages
- 1-19
- ISSN
- 1042-0533 (ISSN-L)
- 1520-6300
- OpenAlex
- W2050014967
- Cited by
- 1,006
- References
- 163
- Citations by year
- 2026: 23 · 2025: 52 · 2024: 33 · 2023: 42 · 2022: 79 · 2021: 52 · 2020: 63 · 2019: 43 · 2018: 40 · 2017: 47 · 2016: 65 · 2015: 58 · 2014: 67 · 2013: 59 · 2012: 60
- FWCI
- 6.62
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Human Biology (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- ResearchSpace (University of Auckland) (submittedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Life Sciences › Agricultural and Biological Sciences › Ecology, Evolution, Behavior and Systematics › Animal Behavior and Reproduction
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Evolutionary Psychology and Human Behavior
- Keywords
- developmental origins of health and disease, life history theory, developmental plasticity, evolutionary developmental biology, epigenetics, intrauterine environment, developmental programming, environmental mismatch, non-communicable diseases, disease prevention
- MeSH terms
- Chronic Disease, Energy Metabolism, Biological Evolution, Female, Humans, Male, Pregnancy, Prenatal Exposure Delayed Effects, Maternal Exposure
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