Complex Contagions in Kleinberg's Small World Model

Complex contagions describe diffusion of behaviors in a social network in settings where spreading requires the influence by two or more neighbors. In a $k$-complex contagion, a cluster of nodes are initially infected, and additional nodes become infected in the next round if they have at least $k$ already infected neighbors. It has been argued that complex contagions better model behavioral changes such as adoption of new beliefs, fashion trends or expensive technology innovations. This has motivated rigorous understanding of spreading of complex contagions in social networks. Despite simple contagions ($k=1$) that spread fast in all small world graphs, how complex contagions spread is much less understood. Previous work~\cite{Ghasemiesfeh:2013:CCW} analyzes complex contagions in Kleinberg's small world model~\cite{kleinberg00small} where edges are randomly added according to a spatial distribution (with exponent $\gamma$) on top of a two dimensional grid structure. It has been shown in~\cite{Ghasemiesfeh:2013:CCW} that the speed of complex contagions differs exponentially when $\gamma=0$ compared to when $\gamma=2$. In this paper, we fully characterize the entire parameter space of $\gamma$ except at one point, and provide upper and lower bounds for the speed of $k$-complex contagions. We study two subtly different variants of Kleinberg's small world model and show that, with respect to complex contagions, they behave differently. For each model and each $k \geq 2$, we show that there is an intermediate range of values, such that when $\gamma$ takes any of these values, a $k$-complex contagion spreads quickly on the corresponding graph, in a polylogarithmic number of rounds. However, if $\gamma$ is outside this range, then a $k$-complex contagion requires a polynomial number of rounds to spread to the entire network.Comment: arXiv admin note: text overlap with arXiv:1404.266

Long ties accelerate noisy threshold-based contagions

Network structure can affect when and how widely new ideas, products, and behaviors are adopted. In widely-used models of biological contagion, interventions that randomly rewire edges (generally making them "longer") accelerate spread. However, there are other models relevant to social contagion, such as those motivated by myopic best-response in games with strategic complements, in which an individual's behavior is described by a threshold number of adopting neighbors above which adoption occurs (i.e., complex contagions). Recent work has argued that highly clustered, rather than random, networks facilitate spread of these complex contagions. Here we show that minor modifications to this model, which make it more realistic, reverse this result: we allow very rare below-threshold adoption, i.e., rarely adoption occurs when there is only one adopting neighbor. To model the trade-off between long and short edges we consider networks that are the union of cycle-power-$k$ graphs and random graphs on $n$ nodes. Allowing adoptions below threshold to occur with order $1/\sqrt{n}$ probability along some "short" cycle edges is enough to ensure that random rewiring accelerates spread. Simulations illustrate the robustness of these results to other commonly-posited models for noisy best-response behavior. Hypothetical interventions that randomly rewire existing edges or add random edges (versus adding "short", triad-closing edges) in hundreds of empirical social networks reduce time to spread. This revised conclusion suggests that those wanting to increase spread should induce formation of long ties, rather than triad-closing ties. More generally, this highlights the importance of noise in game-theoretic analyses of behavior

Disconnected, fragmented, or united? A trans-disciplinary review of network science

During decades the study of networks has been divided between the efforts of social scientists and natural scientists, two groups of scholars who often do not see eye to eye. In this review I present an effort to mutually translate the work conducted by scholars from both of these academic fronts hoping to continue to unify what has become a diverging body of literature. I argue that social and natural scientists fail to see eye to eye because they have diverging academic goals. Social scientists focus on explaining how context specific social and economic mechanisms drive the structure of networks and on how networks shape social and economic outcomes. By contrast, natural scientists focus primarily on modeling network characteristics that are independent of context, since their focus is to identify universal characteristics of systems instead of context specific mechanisms. In the following pages I discuss the differences between both of these literatures by summarizing the parallel theories advanced to explain link formation and the applications used by scholars in each field to justify their approach to network science. I conclude by providing an outlook on how these literatures can be further unified