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To explore the mechanistic relationships between aging, frailty and mortality, we developed a computational model in which possible health attributes are represented by the nodes of a complex network, with the connections showing a scale-free distribution. Each node can be either damaged (i.e. a deficit) or undamaged. Damage of connected nodes facilitates local damage and makes local recovery more difficult. Our model demonstrates the known patterns of frailty and mortality without any assumption of programmed aging. It helps us to understand how the observed maximum of the frailty index (FI) might arise. The model facilitates an initial understanding of how local damage caused by random perturbations propagates through a dynamic network of interconnected nodes. Very large model populations (here, 10 million individuals followed continuously) allow us to exploit new analytic tools, including information theory, showing, for example that highly connected nodes are more informative than less connected nodes. This model permits a better understanding of factors that influence the health trajectories of individuals.In a network model of health developed by the authors, individual aging is represented as the spread of deficits through the network.When the most connected nodes (the “mortality” nodes) are damaged, the individual dies.Damage propagates because each time a node is damaged, it becomes easier for its neighbouring nodes to be damaged.Even with no age-dependent terms the model generates characteristic mortality patterns, suggesting that aging is not programmed.The network model shows that at any time people accumulate deficits variably, thereby unifying ageing with frailty.