Can Network Theory-based Targeting Increase Technology Adoption?

In order to induce farmers to adopt a productive new agricultural technology, we apply simple and complex contagion diffusion models on rich social network data from 200 villages in Malawi to identify seed farmers to target and train on the new technology. A randomized controlled trial compares these theory-driven network targeting approaches to simpler strategies that either rely on a government extension worker or an easily measurable proxy for the social network (geographic distance between households) to identify seed farmers. Our results indicate that technology diffusion is characterized by a complex contagion learning environment in which most farmers need to learn from multiple people before they adopt themselves. Network theory based targeting can out-perform traditional approaches to extension, and we identify methods to realize these gains at low cost to policymakers. Keywords: Social Learning, Agricultural Technology Adoption, Complex Contagion, Malawi JEL Classification Codes: O16, O13Comment: 61 page

Competition and dual users in complex contagion processes

We study the competition of two spreading entities, for example innovations, in complex contagion processes in complex networks. We develop an analytical framework and examine the role of dual users, i.e. agents using both technologies. Searching for the spreading transition of the new innovation and the extinction transition of a preexisting one, we identify different phases depending on network mean degree, prevalence of preexisting technology, and thresholds of the contagion process. Competition with the preexisting technology effectively suppresses the spread of the new innovation, but it also allows for phases of coexistence. The existence of dual users largely modifies the transient dynamics creating new phases that promote the spread of a new innovation and extinction of a preexisting one. It enables the global spread of the new innovation even if the old one has the first-mover advantage.Comment: 9 pages, 4 figure

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

Think Globally, Act Locally: On the Optimal Seeding for Nonsubmodular Influence Maximization

We study the r-complex contagion influence maximization problem. In the influence maximization problem, one chooses a fixed number of initial seeds in a social network to maximize the spread of their influence. In the r-complex contagion model, each uninfected vertex in the network becomes infected if it has at least r infected neighbors. In this paper, we focus on a random graph model named the stochastic hierarchical blockmodel, which is a special case of the well-studied stochastic blockmodel. When the graph is not exceptionally sparse, in particular, when each edge appears with probability omega (n^{-(1+1/r)}), under certain mild assumptions, we prove that the optimal seeding strategy is to put all the seeds in a single community. This matches the intuition that in a nonsubmodular cascade model placing seeds near each other creates synergy. However, it sharply contrasts with the intuition for submodular cascade models (e.g., the independent cascade model and the linear threshold model) in which nearby seeds tend to erode each others\u27 effects. Finally, we show that this observation yields a polynomial time dynamic programming algorithm which outputs optimal seeds if each edge appears with a probability either in omega (n^{-(1+1/r)}) or in o (n^{-2})

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

From neurons to epidemics: How trophic coherence affects spreading processes

Trophic coherence, a measure of the extent to which the nodes of a directed network are organised in levels, has recently been shown to be closely related to many structural and dynamical aspects of complex systems, including graph eigenspectra, the prevalence or absence of feed-back cycles, and linear stability. Furthermore, non-trivial trophic structures have been observed in networks of neurons, species, genes, metabolites, cellular signalling, concatenated words, P2P users, and world trade. Here we consider two simple yet apparently quite different dynamical models -- one a Susceptible-Infected-Susceptible (SIS) epidemic model adapted to include complex contagion, the other an Amari-Hopfield neural network -- and show that in both cases the related spreading processes are modulated in similar ways by the trophic coherence of the underlying networks. To do this, we propose a network assembly model which can generate structures with tunable trophic coherence, limiting in either perfectly stratified networks or random graphs. We find that trophic coherence can exert a qualitative change in spreading behaviour, determining whether a pulse of activity will percolate through the entire network or remain confined to a subset of nodes, and whether such activity will quickly die out or endure indefinitely. These results could be important for our understanding of phenomena such as epidemics, rumours, shocks to ecosystems, neuronal avalanches, and many other spreading processes