Dataset Information

Structural diversity in social contagion.

ABSTRACT: The concept of contagion has steadily expanded from its original grounding in epidemic disease to describe a vast array of processes that spread across networks, notably social phenomena such as fads, political opinions, the adoption of new technologies, and financial decisions. Traditional models of social contagion have been based on physical analogies with biological contagion, in which the probability that an individual is affected by the contagion grows monotonically with the size of his or her "contact neighborhood"--the number of affected individuals with whom he or she is in contact. Whereas this contact neighborhood hypothesis has formed the underpinning of essentially all current models, it has been challenging to evaluate it due to the difficulty in obtaining detailed data on individual network neighborhoods during the course of a large-scale contagion process. Here we study this question by analyzing the growth of Facebook, a rare example of a social process with genuinely global adoption. We find that the probability of contagion is tightly controlled by the number of connected components in an individual's contact neighborhood, rather than by the actual size of the neighborhood. Surprisingly, once this "structural diversity" is controlled for, the size of the contact neighborhood is in fact generally a negative predictor of contagion. More broadly, our analysis shows how data at the size and resolution of the Facebook network make possible the identification of subtle structural signals that go undetected at smaller scales yet hold pivotal predictive roles for the outcomes of social processes.

SUBMITTER: Ugander J

PROVIDER: S-EPMC3341012 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature

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Structural diversity in social contagion.

Ugander Johan J Backstrom Lars L Marlow Cameron C Kleinberg Jon J

Proceedings of the National Academy of Sciences of the United States of America 20120402 16

The concept of contagion has steadily expanded from its original grounding in epidemic disease to describe a vast array of processes that spread across networks, notably social phenomena such as fads, political opinions, the adoption of new technologies, and financial decisions. Traditional models of social contagion have been based on physical analogies with biological contagion, in which the probability that an individual is affected by the contagion grows monotonically with the size of his or ...[more]

PMID: 22474360

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Project description: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. The interaction assumptions of the model are validated using longitudinal network transmission data. We find that the current rate of becoming obese is 2 per year and increases by 0.5 percentage points for each obese social contact. The rate of recovering from obesity is 4 per year, and does not depend on the number of non-obese contacts. The model predicts a long-term obesity prevalence of approximately 42, and can be used to evaluate the effect of different interventions on steady-state obesity. Model predictions quantitatively reproduce the actual historical time course for the prevalence of obesity. 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.

Dataset Information

Structural diversity in social contagion.

Publications

Structural diversity in social contagion.

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