In this article, 41 models of covariation detection from 2 × 2 contingency tables were evaluated against past data in the literature and against data from new experiments. A new model was also included based on a limiting case of the normative phi‐coefficient under an extreme rarity assumption, which has been shown to be an important factor in covariation detection (McKenzie & Mikkelsen, 2007) and data selection (Hattori, 2002; Oaksford & Chater, 1994, 2003). The results were supportive of the new (...) model. To investigate its explanatory adequacy, a rational analysis using two computer simulations was conducted. These simulations revealed the environmental conditions and the memory restrictions under which the new model best approximates the normative model of covariation detection in these tasks. They thus demonstrated the adaptive rationality of the new model. (shrink)

Information about the structure of a causal system can come in the form of observational data—random samples of the system's autonomous behavior—or interventional data—samples conditioned on the particular values of one or more variables that have been experimentally manipulated. Here we study people's ability to infer causal structure from both observation and intervention, and to choose informative interventions on the basis of observational data. In three causal inference tasks, participants were to some degree capable of distinguishing between competing causal hypotheses (...) on the basis of purely observational data. Performance improved substantially when participants were allowed to observe the effects of interventions that they performed on the systems. We develop computational models of how people infer causal structure from data and how they plan intervention experiments, based on the representational framework of causal graphical models and the inferential principles of optimal Bayesian decision‐making and maximizing expected information gain. These analyses suggest that people can make rational causal inferences, subject to psychologically reasonable representational assumptions and computationally reasonable processing constraints. (shrink)

People are adept at inferring novel causal relations, even from only a few observations. Prior knowledge about the probability of encountering causal relations of various types and the nature of the mechanisms relating causes and effects plays a crucial role in these inferences. We test a formal account of how this knowledge can be used and acquired, based on analyzing causal induction as Bayesian inference. Five studies explored the predictions of this account with adults and 4-year-olds, using tasks in which (...) participants learned about the causal properties of a set of objects. The studies varied the two factors that our Bayesian approach predicted should be relevant to causal induction: the prior probability with which causal relations exist, and the assumption of a deterministic or a probabilistic relation between cause and effect. Adults’ judgments (Experiments 1, 2, and 4) were in close correspondence with the quantitative predictions of the model, and children’s judgments (Experiments 3 and 5) agreed qualitatively with this account. (shrink)

It is argued that causal understanding originates in experiences of acting on objects. Such experiences have consistent features that can be used as clues to causal identification and judgment. These are singular clues, meaning that they can be detected in single instances. A catalog of 14 singular clues is proposed. The clues function as heuristics for generating causal judgments under uncertainty and are a pervasive source of bias in causal judgment. More sophisticated clues such as mechanism clues and repeated interventions (...) are derived from the 14. Research on the use of empirical information and conditional probabilities to identify causes has used scenarios in which several of the clues are present, and the use of empirical association information for causal judgment depends on the presence of singular clues. It is the singular clues and their origin that are basic to causal understanding, not multiple instance clues such as empirical association, contingency, and conditional probabilities. (shrink)

How do human infants learn the causal dependencies between events? Evidence suggests that this remarkable feat can be achieved by observation of only a handful of examples. Many computational models have been produced to explain how infants perform causal inference without explicit teaching about statistics or the scientific method. Here, we propose a spiking neuronal network implementation that can be entrained to form a dynamical model of the temporal and causal relationships between events that it observes. The network uses spike-time (...) dependent plasticity, long-term depression, and heterosynaptic competition rules to implement Rescorla–Wagner-like learning. Transmission delays between neurons allow the network to learn a forward model of the temporal relationships between events. Within this framework, biologically realistic synaptic plasticity rules account for well-known behavioral data regarding cognitive causal assumptions such as backwards blocking and screening-off. These models can then be run as emulators for state inference. Furthermore, this mechanism is capable of copying synaptic connectivity patterns between neuronal networks by observing the spontaneous spike activity from the neuronal circuit that is to be copied, and it thereby provides a powerful method for transmission of circuit functionality between brain regions. (shrink)

How do humans discover causal relations when the effect is not immediately observable? Previous experiments have uniformly demonstrated detrimental effects of outcome delays on causal induction. These findings seem to conflict with everyday causal cognition, where humans can apparently identify long-term causal relations with relative ease. Three experiments investigated whether the influence of delay on adult human causal judgements is mediated by experimentally induced assumptions about the timeframe of the causal relation in question, as suggested by Einhorn and Hogarth (1986). (...) Causal judgements generally decreased when a delay separated cause and effect. This decrease was less pronounced when the thematic context of the causal relation induced participants to expect a delay. Experiment 3 ruled out an alternative explanation of the effect based on variations of cue and outcome saliencies, and showed that detrimental effects of delay are reduced even more when instructions explicitly mentioned the timeframe of the causal relation in question. Knowledge thus mediates the impact of delay on human causal judgement. Implications for contemporary theories of human causal induction are discussed. (shrink)

When a cause interacts with unobserved factors to produce an effect, the contingency between the observed cause and effect cannot be taken at face value to infer causality. Yet, it would be computationally intractable to consider all possible unobserved, interacting factors. Nonetheless, two experiments found that when an unobserved cause is assumed to be fairly stable over time, people can learn about such interactions and adjust their inferences about the causal efficacy of the observed cause. When they observed a period (...) in which a cause and effect were associated followed by a period of the opposite association, rather than concluding a complete lack of causality, subjects inferred an unobserved, interacting cause. The interaction explains why the overall contingency between the cause and effect is low and allows people to still conclude that the cause is efficacious. (shrink)