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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 I argue that offspring plasticity is only viable within the niche of maternal care, and that as this protection is withdrawn, the offspring is obliged to canalize many developmental traits in order to minimize environmental disruptions.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.

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