There's more than one way to aggregate cats

After getting past the provocative title, Robert Axtell’s presentation on the pitfalls of aggregation proved to be very interesting. The slides are posted here:

A comment on my last post on this summed things up pretty well:

… the presentation really focused on the challenges that aggregation brings to the modeling disciplines. Axtell presents some interesting mathematical constructs that could and should form the basis for conversations, thinking, and research in the SD and other aggregate modeling arenas.

It’s worth a look.

Also, as I linked before, check out Hazhir Rahmandad’s work on agent vs. aggregate models of an infection process. His models and articles with John Sterman are here. His thesis is here.

Hazhir’s work explores two extremes – an aggregate model of infection (which is the analog of typical Bass diffusion models in marketing science) compared to agent based versions of the same process. The key difference is that the aggregate model assumes well-mixed victims, while the agent versions explicitly model contacts across various network topologies. The well-mixed assumption is often unrealistic, because it matters who is infected, not just how many. In the real world, the gain of an infection process can vary with the depth of penetration of the social network, and only the agent model can capture this in all circumstances.

However, in modeling there’s often a middle road: an aggregation approach that captures the essence of a granular process at a higher level. That’s fortunate, because otherwise we’d always be building model-maps as big as the territory. I just ran across an interesting example.

A new article in PLoS Computational Biology models obesity as a social process:

Many behavioral phenomena have been found to spread interpersonally through social networks, in a manner similar to infectious diseases. An important difference between social contagion and traditional infectious diseases, however, is that behavioral phenomena can be acquired by non-social mechanisms as well as through social transmission. We introduce a novel theoretical framework for studying these phenomena (the SISa model) by adapting a classic disease model to include the possibility for ‘automatic’ (or ‘spontaneous’) non-social infection. We provide an example of the use of this framework by examining the spread of obesity in the Framingham Heart Study Network. … We find that since the 1970s, the rate of recovery from obesity has remained relatively constant, while the rates of both spontaneous infection and transmission have steadily increased over time. This suggests that the obesity epidemic may be driven by increasing rates of becoming obese, both spontaneously and transmissively, rather than by decreasing rates of losing weight. A key feature of the SISa model is its ability to characterize the relative importance of social transmission by quantitatively comparing rates of spontaneous versus contagious infection. It provides a theoretical framework for studying the interpersonal spread of any state that may also arise spontaneously, such as emotions, behaviors, health states, ideas or diseases with reservoirs.

The very idea of modeling obesity as an infectious social process is interesting in itself. But from a technical standpoint, the interesting innovation is that they capture some of the flavor of a disaggregate representation of the population by introducing an approximation, Continue reading “There's more than one way to aggregate cats”