Person:

Nowak, Martin

We constructed a corpus of digitized texts containing about 4% of all books ever printed. Analysis of this corpus enables us to investigate cultural trends quantitatively. We survey the vast terrain of ‘culturomics,’ focusing on linguistic and cultural phenomena that were reflected in the English language between 1800 and 2000. We show how this approach can provide insights about fields as diverse as lexicography, the evolution of grammar, collective memory, the adoption of technology, the pursuit of fame, censorship, and historical epidemiology. Culturomics extends the boundaries of rigorous quantitative inquiry to a wide array of new phenomena spanning the social sciences and the humanities.

Everybody knows that overconfidence can be foolhardy. But a study reveals that having an overly positive self-image might confer an evolutionary advantage if the rewards outweigh the risks.

The problem of achieving widespread immunity to infectious diseases by voluntary vaccination is often presented as a public-goods dilemma, as an individual's vaccination contributes to herd immunity, protecting those who forgo vaccination. The temptation to free-ride brings the equilibrium vaccination level below the social optimum. Here, we present an evolutionary game-theoretic approach to this problem, exploring the roles of individual imitation behaviour and population structure in vaccination. To this end, we integrate an epidemiological process into a simple agent-based model of adaptive learning, where individuals use anecdotal evidence to estimate costs and benefits of vaccination. In our simulations, we focus on parameter values that are realistic for a flu-like infection. Paradoxically, as agents become more adept at imitating successful strategies, the equilibrium level of vaccination falls below the rational individual optimum. In structured populations, the picture is only somewhat more optimistic: vaccination is widespread over a range of low vaccination costs, but coverage plummets after cost exceeds a critical threshold. This result suggests parallels to historical scenarios in which vaccination coverage provided herd immunity for some time, but then rapidly dropped. Our work sheds light on how imitation of peers shapes individual vaccination choices in social networks.

We study the origin of evolution. Evolution is based on replication, mutation, and selection. But how does evolution begin? When do chemical kinetics turn into evolutionary dynamics? We propose “prelife” and “prevolution” as the logical precursors of life and evolution. Prelife generates sequences of variable length. Prelife is a generative chemistry that proliferates information and produces diversity without replication. The resulting “prevolutionary dynamics” have mutation and selection. We propose an equation that allows us to investigate the origin of evolution. In one limit, this “originator equation” gives the classical selection equation. In the other limit, we obtain “prelife.” There is competition between life and prelife and there can be selection for or against replication. Simple prelife equations with uniform rate constants have the property that longer sequences are exponentially less frequent than shorter ones. But replication can reverse such an ordering. As the replication rate increases, some longer sequences can become more frequent than shorter ones. Thus, replication can lead to “reversals” in the equilibrium portraits. We study these reversals, which mark the transition from prelife to life in our model. If the replication potential exceeds a critical value, then life replicates into existence.

We investigate the cooperation dynamics attributed to the interplay between the evolution of individual strategies and evolution of individual partnerships. We focus on the effect of reputation on an individual’s partner-switching process. We assume that individuals can either change their strategies by imitating their partners or adjust their partnerships based on local information about reputations. We manipulate the partner switching in two ways; that is, individuals can switch from the lowest reputation partners, either to their partners’ partners who have the highest reputation (i.e., ordering in partnership) or to others randomly chosen from the entire population (i.e., randomness in partnership). We show that when individuals are able to alter their behavioral strategies and their social interaction partnerships on the basis of reputation, cooperation can prevail. We find that the larger temptation to defect and the denser the partner network, the more frequently individuals need to shift their partnerships in order for cooperation to thrive. Furthermore, an increasing tendency of switching to partners’ partners is more likely to lead to a higher level of cooperation. We show that when reputation is absent in such partner-switching processes, cooperation is much less favored than that of the reputation involved. Moreover, we investigate the effect of discounting an individual’s reputation on the evolution of cooperation. Our results highlight the importance of the consideration of reputation (indirect reciprocity) on the promotion of cooperation when individuals can adjust their partnerships.

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.

Many specific models have been proposed to study evolutionary game dynamics in structured populations, but most analytical results so far describe the competition of only two strategies. Here we derive a general result that holds for any number of strategies, for a large class of population structures under weak selection. We show that for the purpose of strategy selection any evolutionary process can be characterized by two key parameters that are coefficients in a linear inequality containing the payoff values. These structural coefficients, (\sigma1) and (\sigma2), depend on the particular process that is being studied, but not on the number of strategies, (n), or the payoff matrix. For calculating these structural coefficients one has to investigate games with three strategies, but more are not needed. Therefore, (n=3) is the general case. Our main result has a geometric interpretation: Strategy selection is determined by the sum of two terms, the first one describing competition on the edges of the simplex and the second one in the center. Our formula includes all known weak selection criteria of evolutionary games as special cases. As a specific example we calculate games on sets and explore the synergistic interaction between direct reciprocity and spatial selection. We show that for certain parameter values both repetition and space are needed to promote evolution of cooperation.

Cooperation, where one individual incurs a cost to help another, is a fundamental building block of the natural world and human society. It has been suggested that costly punishment can promote the evolution of cooperation, with the threat of punishment deterring free-riders. Recent experiments, however, have revealed the existence of 'antisocial' punishment, where non-cooperators punish cooperators. While various theoretical models find that punishment can promote the evolution of cooperation, these models a priori exclude the possibility of antisocial punishment. Here we extend the standard theory of optional public goods games to include the full set of punishment strategies. We find that punishment no longer increases cooperation, and that selection favours substantial levels of antisocial punishment for a wide range of parameters. Furthermore, we conduct behavioural experiments, showing results consistent with our model predictions. As opposed to an altruistic act that promotes cooperation, punishment is mostly a self-interested tool for protecting oneself against potential competitors.

Major efforts to sequence cancer genomes are now occurring throughout the world. Though the emerging data from these studies are illuminating, their reconciliation with epidemiologic and clinical observations poses a major challenge. In the current study, we provide a novel mathematical model that begins to address this challenge. We model tumors as a discrete time branching process that starts with a single driver mutation and proceeds as each new driver mutation leads to a slightly increased rate of clonal expansion. Using the model, we observe tremendous variation in the rate of tumor development - providing an understanding of the heterogeneity in tumor sizes and development times that have been observed by epidemiologists and clinicians. Furthermore, the model provides a simple formula for the number of driver mutations as a function of the total number of mutations in the tumor. Finally, when applied to recent experimental data, the model allows us to calculate, for the first time, the actual selective advantage provided by typical somatic mutations in human tumors in situ. This selective advantage is surprisingly small, 0.005 +- 0.0005, and has major implications for experimental cancer research.

In-group favoritism is a central aspect of human behavior. People often help members of their own group more than members of other groups. Here we propose a mathematical framework for the evolution of in-group favoritism from a continuum of strategies. Unlike previous models, we do not pre-suppose that players never cooperate with out-group members. Instead, we determine the conditions under which preferential in-group cooperation emerges, and also explore situations where preferential out-group helping could evolve. Our approach is not based on explicit intergroup conflict, but instead uses evolutionary set theory. People can move between sets. Successful sets attract members, and successful strategies gain imitators. Individuals can employ different strategies when interacting with in-group versus out-group members. Our framework also allows us to implement different games for these two types of interactions. We prove general results and derive specific conditions for the evolution of cooperation based on in-group favoritism.