Heterogeneity and network structure in the dynamics of diffusion Hazhir Rahmandad , John Sterman. MANAGEMENT SCIENCE Vol. 5. No. 5. May 2008

Abstract

When is it better to use agent-based (AB) models, and when should differential equation (DE) models be used? Whereas DE models assume homogeneity and perfect mixing within compartments, AB models can capture heterogeneity across individuals and in the network of interactions among them. AB models relax aggregation assumptions, but entail computational and cognitive costs that may limit sensitivity analysis and model scope. Because resources are limited, the costs and benefits of such disaggregation should guide the choice of models for policy analysis. Using contagious disease as an example, we contrast the dynamics of a stochastic AB model with those of the analogous deterministic compartment DE model. We examine the impact of individual heterogeneity and different network topologies, including fully connected, random, Watts-Strogatz small world, scale-free, and lattice networks. Obviously, deterministic models yield a single trajectory for each parameter set, while stochastic models yield a distribution of outcomes. More interestingly, the DE and mean AB dynamics differ for several metrics relevant to public health, including diffusion speed, peak load on health services infrastructure, and total disease burden. The response of the models to policies can also differ even when their base case behavior is similar. In some conditions, however, these differences in means are small compared to variability caused by stochastic events, parameter uncertainty, and model boundary. We discuss implications for the choice among model types, focusing on policy design. The results apply beyond epidemiology: from innovation adoption to financial panics, many important social phenomena involve analogous processes of diffusion and social contagion.


Heterogeneity and network structure in the dynamics of diffusion

Contents

1. INTRODUCTION
2. A SPECTRUM OF AGGREGATION ASSUMPTIONS
3. MODEL STRUCTURE
4. EXPERIMENTAL DESIGN
 4.1 Network Topology
 4.2 Individual Heterogeneity
    4.3 Calibrating the DE Model
5. RESULTS
 5.1 Fully Connected Network
 5.2 Random Network
    5.3 Scale-Free Network
    5.4 Small World Network
    5.5 Ring Lattice Network
    5.6 Calibrated DE Model
    5.7 Sensitivity to Population Size
    5.8 Sensitivity to R0
    5.9 Sensitivity to Disease Natural History
    5.10 Policy Analysis and Sensitivity to Model Boundary
6. DISCUSSION AND CONCLUSIONS
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