When is it better to use agent based (AB) models, and when should differential equation (DE) models be used? Where DE models assume homogeneity and perfect mixing within compartments, AB models can capture heterogeneity in agent attributes and in the network of interactions among them. Using contagious disease as an example, we contrast the dynamics of AB models with those of the corresponding mean-field DE model, specifically, comparing the standard SEIR model-a nonlinear DE-to an explicit AB model of the same system. We examine both agent heterogeneity and the impact of different network structures, including fully connected, random, Watts-Strogatz small world, scale-free, and lattice networks. Surprisingly, in many conditions the AB and DE dynamics are quite similar. Differences between the DE and AB models are not statistically significant on key metrics relevant to public health, including diffusion speed, peak load on health services infrastructure and total disease burden. We explore the conditions under which the AB and DE dynamics differ, and consider implications for managing infectious disease. The results extend beyond epidemiology: from innovation adoption to the spread of rumor and riot to financial panics, many important social phenomena involve analogous processes of diffusion and social contagion.

When is it better to use agent based (AB) models, and when should differential equation (DE) models be used? Where DE models assume homogeneity and perfect mixing within compartments, AB models can capture heterogeneity in agent attributes and in the network of interactions among them. Using contagious disease as an example, we contrast the dynamics of AB models with those of the corresponding mean-field DE model, specifically, comparing the standard SEIR model-a nonlinear DE-to an explicit AB model of the same system. We examine both agent heterogeneity and the impact of different network structures, including fully connected, random, Watts-Strogatz small world, scale-free, and lattice networks. Surprisingly, in many conditions the AB and DE dynamics are quite similar. Differences between the DE and AB models are not statistically significant on key metrics relevant to public health, including diffusion speed, peak load on health services infrastructure and total disease burden. We explore the conditions under which the AB and DE dynamics differ, and consider implications for managing infectious disease. The results extend beyond epidemiology: from innovation adoption to the spread of rumor and riot to financial panics, many important social phenomena involve analogous processes of diffusion and social contagion.

Reproducibility of research is critical for the healthy growth and accumulation of reliable knowledge, and simulation-based research is no exception. However, studies show many simulation-based studies in the social sciences are not reproducible. Better standards for documenting simulation models and reporting results are needed to enhance the reproducibility of simulation-based research in the social sciences. We provide an initial set of Reporting Guidelines for Simulation-based Research (RGSR) in the social sciences, with a focus on common scenarios in system dynamics research. We discuss these guidelines separately for reporting models, reporting simulation experiments, and reporting optimization results. The guidelines are further divided into minimum and preferred requirements, distinguishing between factors that are indispensable for reproduction of research and those that enhance transparency. We also provide a few guidelines for improved visualization of research to reduce the costs of reproduction. Suggestions for enhancing the adoption of these guidelines are discussed at the end.Acknowledgments: We would like to thank Mohammad Jalali for providing excellent research assistance for this paper. We thank David Lane for his helpful suggestions.

Background Depression is a complex public health problem with considerable variation in treatment response. The systemic complexity of depression, or the feedback processes among diverse drivers of the disorder, contribute to the persistence of depression. This paper extends prior attempts to understand the complex causal feedback mechanisms that underlie depression by presenting the first broad boundary causal loop diagram of depression dynamics. Method We applied qualitative system dynamics methods to map the broad feedback mechanisms of depression. We used a structured approach to identify candidate causal mechanisms of depression in the literature. We assessed the strength of empirical support for each mechanism and prioritized those with support from validation studies. Through an iterative process, we synthesized the empirical literature and created a conceptual model of major depressive disorder. Results The literature review and synthesis resulted in the development of the first causal loop diagram of reinforcing feedback processes of depression. It proposes candidate drivers of illness, or inertial factors, and their temporal functioning, as well as the interactions among drivers of depression. The final causal loop diagram defines 13 key reinforcing feedback loops that involve nine candidate drivers of depression. Conclusions Future research is needed to expand upon this initial model of depression dynamics. Quantitative extensions may result in a better understanding of the systemic syndrome of depression and contribute to personalized methods of evaluation, prevention and intervention.

Effective responses to the COVID-19 pandemic require integrating behavioral factors such as risk-driven contact reduction, improved treatment, and adherence fatigue with asymptomatic transmission, disease acuity, and hospital capacity. We build one such model and estimate it for all 92 nations with reliable testing data. Cumulative cases and deaths through 22 December 2020 are estimated to be 7.03 and 1.44 times official reports, yielding an infection fatality rate (IFR) of 0.51 percent, which has been declining over time. Absent adherence fatigue, cumulative cases would have been 47 percent lower. Scenarios through June 2021 show that modest improvement in responsiveness could reduce cases and deaths by about 14 percent, more than the impact of vaccinating half of the population by that date. Variations in responsiveness to risk explain two orders of magnitude difference in per-capita deaths despite reproduction numbers fluctuating around one across nations. A public online simulator facilitates scenario analysis over the coming months.