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Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity

Developmental plasticity underlies widespread associations between early-life exposures and many components of adult phenotype, including the risk of chronic diseases. Humans take almost two decades to reach reproductive maturity, and yet the ‘critical windows’ of physiological sensitivity that conf...

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Autor principal: Wells, Jonathan C. K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4148720/
https://www.ncbi.nlm.nih.gov/pubmed/25095791
http://dx.doi.org/10.1093/emph/eou019
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author Wells, Jonathan C. K.
author_facet Wells, Jonathan C. K.
author_sort Wells, Jonathan C. K.
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description Developmental plasticity underlies widespread associations between early-life exposures and many components of adult phenotype, including the risk of chronic diseases. Humans take almost two decades to reach reproductive maturity, and yet the ‘critical windows’ of physiological sensitivity that confer developmental plasticity tend to close during fetal life or infancy. While several explanations for lengthy human maturation have been offered, the brevity of physiological plasticity has received less attention. I argue that offspring plasticity is only viable within the niche of maternal care, and that as this protection is withdrawn, the offspring is obliged to canalize many developmental traits in order to minimize environmental disruptions. The schedule of maternal care may therefore shape the duration of critical windows, and since the duration of this care is subject to parent–offspring conflict, the resolution of this conflict may shape the duration of critical windows. This perspective may help understand (i) why windows close at different times for different traits, and (ii) why the duration of critical windows may vary across human populations. The issue is explored in relation to population differences in the association between infant weight gain and later body composition. The occupation of more stable environments by western populations may have favoured earlier closure of the critical window during which growth in lean mass is sensitive to nutritional intake. This may paradoxically have elevated the risk of obesity following rapid infant weight gain in such populations.
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spelling pubmed-41487202014-09-02 Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity Wells, Jonathan C. K. Evol Med Public Health Review Developmental plasticity underlies widespread associations between early-life exposures and many components of adult phenotype, including the risk of chronic diseases. Humans take almost two decades to reach reproductive maturity, and yet the ‘critical windows’ of physiological sensitivity that confer developmental plasticity tend to close during fetal life or infancy. While several explanations for lengthy human maturation have been offered, the brevity of physiological plasticity has received less attention. I argue that offspring plasticity is only viable within the niche of maternal care, and that as this protection is withdrawn, the offspring is obliged to canalize many developmental traits in order to minimize environmental disruptions. The schedule of maternal care may therefore shape the duration of critical windows, and since the duration of this care is subject to parent–offspring conflict, the resolution of this conflict may shape the duration of critical windows. This perspective may help understand (i) why windows close at different times for different traits, and (ii) why the duration of critical windows may vary across human populations. The issue is explored in relation to population differences in the association between infant weight gain and later body composition. The occupation of more stable environments by western populations may have favoured earlier closure of the critical window during which growth in lean mass is sensitive to nutritional intake. This may paradoxically have elevated the risk of obesity following rapid infant weight gain in such populations. Oxford University Press 2014-08-05 /pmc/articles/PMC4148720/ /pubmed/25095791 http://dx.doi.org/10.1093/emph/eou019 Text en © The Author(s) 2014. Published by Oxford University Press on behalf of the Foundation for Evolution, Medicine, and Public Health. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Wells, Jonathan C. K.
Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity
title Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity
title_full Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity
title_fullStr Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity
title_full_unstemmed Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity
title_short Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity
title_sort adaptive variability in the duration of critical windows of plasticity: implications for the programming of obesity
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4148720/
https://www.ncbi.nlm.nih.gov/pubmed/25095791
http://dx.doi.org/10.1093/emph/eou019
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