There is now much evidence that early life undernutrition elevates risk of diseases like cardiovascular disease. Less clear is whether the underlying developmental plasticity in metabolism and physiology evolved to serve an adaptive function, beyond these effects on pathophysiology. This review builds from principles of life history theory to propose a functional model linking early environments with adult biology. An organism has metabolic potential in excess of survival requirements, called productivity, that supports growth before being shunted into reproduction after growth ceases. This concept from inter-specific studies leads to the prediction that plasticity in growth rate will be positively correlated with components of future adult reproductive expenditure. Consistent with this idea, evidence is reviewed that early nutrition or growth rate predict offspring size in females, and increased somatic investment related to reproductive strategy in males. Thus, population birth weight and sexual size dimorphism are predicted to increase in response to improvements in early nutrition. A striking feature of the continuity of metabolic production is its perpetuation not merely during the lifecycle but across generations: in females, growth rate predicts future nutritional investment in reproduction, which in turn determines fetal growth rate in the next generation. Growth and reproduction serve as mutually-defining templates, thus creating a phenotypic bridge allowing ecologic information to be maintained during ontogeny and transmitted to offspring. Resetting of metabolic production in response to maternal nutritional cues may serve a broader goal of integrating nutritional information within the matriline, thus providing a more reliable basis for adjusting long-term strategy. Am. J. Hum. Biol., 2007. © 2007 Wiley-Liss, Inc.