The thrifty phenotype hypothesis is widely used to interpret associations between early nutritional experience and degenerative disease risks. However, it remains unclear what is adaptive about early life thrift, and biomedical approaches struggle to explain why associations between early growth and later disease hold across the entire range of birth size. This issue can be addressed using a simple model, attributing disease to a high metabolic load (large tissue masses, rich diet, and sedentary lifestyle) relative to metabolic capacity (physiological traits contingent on fetal/infant development). In this context, different hypotheses regarding the long-term functions of thrift can be examined. The “predictive adaptive response” hypothesis considers thrift to involve metabolic adaptations (insulin resistance and central adiposity) that emerge in anticipation of a poor quality adult breeding environment. The competing “maternal capital” hypothesis considers thrift to involve reductions in lean mass and organ phenotype arising through constraints on maternal phenotype, reflecting both maternal developmental experience and current ecological conditions. This hypothesis assumes offspring developmental responses to stresses such as temperature, altitude, and nutritional ecology occur under the influence of maternal capital indices, including size, physiology, reproductive history and social status. I argue that insulin resistance only emerges after infancy, and far from being anticipatory of a low nutritional plane, indicates perturbations of metabolism. Following exposure of early thrifty growth to the obesogenic niche. Thrift as early growth variability represents a plausible profile of developmental plasticity for human evolutionary history, aiding understand how the modern obesogenic environment interacts with physiological variability to induce disease. Am. J. Hum. Biol., 2011. © 2010 Wiley-Liss, Inc.