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ObjectivesEpisodes of ill‐health in childhood can predispose affected individuals to further periods of illness and early adult mortality. This study uses nonspecific indicators of stress to examine how growth disruptions during infancy/early childhood, and late childhood/early adolescence affected adult longevity in later medieval and post‐medieval London.Materials and MethodsHazards analysis was used to evaluate the effect of linear enamel hypoplasia (LEH) and the size of the anteroposterior (AP) and transverse (TR) diameters of the vertebral neural canal (VNC) on adult age‐at‐death. This was applied to skeletal samples from later medieval (n = 461) and post‐medieval (n = 480) London.ResultsGrowth disruptions during infancy/early childhood (LEH and AP VNC diameters) were not associated with longevity, or with impaired growth at later stages of development (TR VNC diameters). Growth disruptions during late childhood/early adolescence (TR VNC diameters) were associated with a significantly increased risk of adult mortality.DiscussionMacroscopic hypoplasia represent short periods of stress during infancy/early childhood which did not disrupt future investments in growth or cause long‐term damage to health. Small TR diameters represent chronic stress during late childhood/early adolescence which resulted in greater susceptibility to infections and increased risk of mortality. These interactions were influenced by sex and socioeconomic status, suggesting that socioeconomic circumstances in both childhood and adult life could influence exposure and resistance to stressors. Am J Phys Anthropol 158:569–580, 2015. © 2015 Wiley Periodicals, Inc.

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