More than any other species, humans form social ties to individuals who are neither kin nor mates, and these ties tend to be with similar people. Here, we show that this similarity extends to genotypes. Across the whole genome, friends genotypes at t
he SNP level tend to be positively correlated (homophilic); however, certain genotypes are negatively correlated (heterophilic). A focused gene set analysis suggests that some of the overall correlation can be explained by specific systems; for example, an olfactory gene set is homophilic and an immune system gene set is heterophilic. Finally, homophilic genotypes exhibit significantly higher measures of positive selection, suggesting that, on average, they may yield a synergistic fitness advantage that has been helping to drive recent human evolution.
Here, we review the research we have done on social contagion. We describe the methods we have employed (and the assumptions they have entailed) in order to examine several datasets with complementary strengths and weaknesses, including the Framingha
m Heart Study, the National Longitudinal Study of Adolescent Health, and other observational and experimental datasets that we and others have collected. We describe the regularities that led us to propose that human social networks may exhibit a three degrees of influence property, and we review statistical approaches we have used to characterize inter-personal influence with respect to phenomena as diverse as obesity, smoking, cooperation, and happiness. We do not claim that this work is the final word, but we do believe that it provides some novel, informative, and stimulating evidence regarding social contagion in longitudinally followed networks. Along with other scholars, we are working to develop new methods for identifying causal effects using social network data, and we believe that this area is ripe for statistical development as current methods have known and often unavoidable limitations.
Understanding how and how far information, behaviors, or pathogens spread in social networks is an important problem, having implications for both predicting the size of epidemics, as well as for planning effective interventions. There are, however,
two main challenges for inferring spreading paths in real-world networks. One is the practical difficulty of observing a dynamic process on a network, and the other is the typical constraint of only partially observing a network. Using a static, structurally realistic social network as a platform for simulations, we juxtapose three distinct paths: (1) the stochastic path taken by a simulated spreading process from source to target; (2) the topologically shortest path in the fully observed network, and hence the single most likely stochastic path, between the two nodes; and (3) the topologically shortest path in a partially observed network. In a sampled network, how closely does the partially observed shortest path (3) emulate the unobserved spreading path (1)? Although partial observation inflates the length of the shortest path, the stochastic nature of the spreading process also frequently derails the dynamic path from the shortest path. We find that the partially observed shortest path does not necessarily give an inflated estimate of the length of the process path; in fact, partial observation may, counterintuitively, make the path seem shorter than it actually is.
Current methods for the detection of contagious outbreaks give contemporaneous information about the course of an epidemic at best. Individuals at the center of a social network are likely to be infected sooner, on average, than those at the peripher
y. However, mapping a whole network to identify central individuals whom to monitor is typically very difficult. We propose an alternative strategy that does not require ascertainment of global network structure, namely, monitoring the friends of randomly selected individuals. Such individuals are known to be more central. To evaluate whether such a friend group could indeed provide early detection, we studied a flu outbreak at Harvard College in late 2009. We followed 744 students divided between a random group and a friend group. Based on clinical diagnoses, the progression of the epidemic in the friend group occurred 14.7 days (95% C.I. 11.7-17.6) in advance of the randomly chosen group (i.e., the population as a whole). The friend group also showed a significant lead time (p<0.05) on day 16 of the epidemic, a full 46 days before the peak in daily incidence in the population as a whole. This sensor method could provide significant additional time to react to epidemics in small or large populations under surveillance. Moreover, the method could in principle be generalized to other biological, psychological, informational, or behavioral contagions that spread in networks.
Theoretical models suggest that social networks influence the evolution of cooperation, but to date there have been few experimental studies. Observational data suggest that a wide variety of behaviors may spread in human social networks, but subject
s in such studies can choose to befriend people with similar behaviors, posing difficulty for causal inference. Here, we exploit a seminal set of laboratory experiments that originally showed that voluntary costly punishment can help sustain cooperation. In these experiments, subjects were randomly assigned to a sequence of different groups in order to play a series of single-shot public goods games with strangers; this feature allowed us to draw networks of interactions to explore how cooperative and uncooperative behavior spreads from person to person to person. We show that, in both an ordinary public goods game and in a public goods game with punishment, focal individuals are influenced by fellow group members contribution behavior in future interactions with other individuals who were not a party to the initial interaction. Furthermore, this influence persists for multiple periods and spreads up to three degrees of separation (from person to person to person to person). The results suggest that each additional contribution a subject makes to the public good in the first period is tripled over the course of the experiment by other subjects who are directly or indirectly influenced to contribute more as a consequence. These are the first results to show experimentally that cooperative behavior cascades in human social networks.
Social networks exhibit strikingly systematic patterns across a wide range of human contexts. While genetic variation accounts for a significant portion of the variation in many complex social behaviors, the heritability of egocentric social network
attributes is unknown. Here we show that three of these attributes (in-degree, transitivity, and centrality) are heritable. We then develop a mirror network method to test extant network models and show that none accounts for observed genetic variation in human social networks. We propose an alternative Attract and Introduce model with two simple forms of heterogeneity that generates significant heritability as well as other important network features. We show that the model is well suited to real social networks in humans. These results suggest that natural selection may have played a role in the evolution of social networks. They also suggest that modeling intrinsic variation in network attributes may be important for understanding the way genes affect human behaviors and the way these behaviors spread from person to person.
