  To explore the mechanistic relationships between ageing, frailty and
mortality, we developed a computational model in which possible health
attributes are represented by the nodes of a complex network. Each node can be
either damaged (i.e. a deficit) or undamaged. Damage of connected nodes
facilitates further local damage. Our model recovers the known patterns of
frailty and mortality without any programmed ageing. It helps us to understand
how the observed maximum of the frailty index (FI) might arise, and allows us
to start to understand how health deficits accumulate. Large model populations
allow us to exploit new analytic tools, including information theory. This will
allow us to systematically characterize the effects of sudden changes in the
health trajectories of individuals and serve as a way to evaluate large
clinical and population databases.
