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Early life events and their consequences for later disease: a life history and evolutionary perspective

Early life events and their consequences for later disease: a life history and evolutionary perspective
Early life events and their consequences for later disease: a life history and evolutionary perspective
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
phenotype, adverse effects, male, early-life, nutrition, origins, diagnosis, female, developmental plasticity, prevention & control, gene, human, epigenetic, life-history, responses, disease, development, health, research, evolution, risk, etiology, maternal exposure, growth, environment, prenatal exposure delayed effects, environmental, review, humans, consequences, epidemiology, energy metabolism, chronic disease, pregnancy, cues
1042-0533
1-19
Gluckman, P.D.
492295c0-ef71-4871-ad5a-771c98e1059a
Hanson, M.A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Beedle, A.S.
214bd9e6-598a-4761-b885-0466521ac623
Gluckman, P.D.
492295c0-ef71-4871-ad5a-771c98e1059a
Hanson, M.A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Beedle, A.S.
214bd9e6-598a-4761-b885-0466521ac623

Gluckman, P.D., Hanson, M.A. and Beedle, A.S. (2007) Early life events and their consequences for later disease: a life history and evolutionary perspective. American Journal of Human Biology, 19 (1), 1-19. (doi:10.1002/ajhb.20590).

Record type: Article

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

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More information

Published date: 2007
Keywords: phenotype, adverse effects, male, early-life, nutrition, origins, diagnosis, female, developmental plasticity, prevention & control, gene, human, epigenetic, life-history, responses, disease, development, health, research, evolution, risk, etiology, maternal exposure, growth, environment, prenatal exposure delayed effects, environmental, review, humans, consequences, epidemiology, energy metabolism, chronic disease, pregnancy, cues

Identifiers

Local EPrints ID: 61155
URI: http://eprints.soton.ac.uk/id/eprint/61155
ISSN: 1042-0533
PURE UUID: 764c4bff-bbc8-471e-8858-bed3c2dbdba5
ORCID for M.A. Hanson: ORCID iD orcid.org/0000-0002-6907-613X

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Date deposited: 02 Sep 2008
Last modified: 16 Mar 2024 03:17

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Contributors

Author: P.D. Gluckman
Author: M.A. Hanson ORCID iD
Author: A.S. Beedle

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