Humans diverge from most mammals, including nonhuman primates, by depositing significant quantities of body fat in utero and are consequently one of the fattest species on record at birth. While explanations for the fat layer of human neonates have commonly assumed that it serves as insulation to compensate for hairlessness, empirical support for this hypothesis is presently weak. Whether the tissue's abundance at birth and growth changes in adiposity during infancy and childhood might be explained in light of its role as energy buffer has not been assessed, and this possibility is explored through development of a model of fat function and growth centered on two related hypotheses. The first is that the greater adiposity of human neonates is at least partially explainable as an accompaniment of the enlarged human brain, which demands a larger energy reserve to ensure that its obligatory needs are met when the flow of resources from mother or other caretakers is disrupted. The second is that age-related changes in the likelihood of experiencing such disruption have influenced the pattern of investment in the tissue, reflected today in peak adiposity during infancy and a decline to a leaner childhood period. Nutritional disruption is common at birth and until lactation is established, during which time human newborns survive from fats deposited prenatally, suggesting one possible explanation for the early onset of fat deposition. At weaning, the transition from breast milk to supplemental foods and the parallel transition from maternal to endogenous immune protection interact to increase the frequency and impact of nutritional disruption, and this may help explain why newborns devote roughly 70% of growth expenditure to fat deposition during the early postnatal months. Evidence is presented that fat stores are mobilized during infections, hinting at one possible mechanism underlying the association between nutritional status and infectious morbidity and mortality among infants in nutritionally stressed human populations. Consistent with the proposed hypothesis, well-fed infants acquire peak fat reserves by an age of peak prevalence of malnutrition, infectious disease, and fat reserve depletion in less-buffered contexts, and childhood--characterized by minimal investment in the tissue--is a stage of reduced risk of energy stress. The model presented here foregrounds energy storage in adipose tissue as an important life-history strategy and a means to modify mortality risk during the nutritionally turbulent period of infancy.