David Danks

Bayesian models of human learning are becoming increasingly popular in cognitive science. We argue that their purported confirmation largely relies on a methodology that depends on premises that are inconsistent with the claim that people are Bayesian about learning and inference. Bayesian models in cognitive science derive their appeal from their normative claim that the modeled inference is in some sense rational. Standard accounts of the rationality of Bayesian inference imply predictions that an agent selects the option that maximizes the posterior expected utility. Experimental confirmation of the models, however, has been claimed because of groups of agents that probability match the posterior. Probability matching only constitutes support for the Bayesian claim if additional unobvious and untested (but testable) assumptions are invoked. The alternative strategy of weakening the underlying notion of rationality no longer distinguishes the Bayesian model uniquely. A new account of rationality—either for inference or for decision-making—is required to successfully confirm Bayesian models in cognitive science.

In many people, caffeine causes slight muscle tremors, particularly in their hands. In general, the Caffeine → Muscle Tremors causal connection is a noisy one: someone can drink coffee and experience no hand shaking, and there are many other factors that can lead to muscle tremors. Now suppose that Jane drinks several cups of coffee and then notices that her hands are trembling; an obvious question is: did this instance of coffee drinking cause this instance of hand-trembling? Structurally similar questions arise throughout everyday life: Did this pressing of the ‘k’ key cause this change in the pixels on the computer monitor? Did these episodes of smoking cause this lung cancer? Did this studying cause this test score? And so on. These questions all ask about singular causation in a particular situation, in contrast with general causation across multiple cases. They are thus particularly salient in situations in which we care about that specific case, as in many legal contexts, social interactions, physical explanations of anomalous events, and more

There is now substantial agreement about the representational component of a normative theory of causal reasoning: Causal Bayes Nets. There is less agreement about a normative theory of causal discovery from data, either computationally or cognitively, and almost no work investigating how teaching the Causal Bayes Nets representational apparatus might help individuals faced with a causal learning task. Psychologists working to describe how naïve participants represent and learn causal structure from data have focused primarily on learning from single trials under a variety of conditions. In contrast, one component of the normative theory focuses on learning from a sample drawn from a population under some experimental or observational study regime. Through a virtual Causality Lab that embodies the normative theory of causal reasoning and which allows us to record student behavior, we have begun to systematically explore how best to teach the normative theory. In this paper we explain the overall project and report on pilot studies which suggest that students can quickly be taught to (appear to) be quite rational

Our concept of actual causation plays a deep, ever-present role in our experiences. I first argue that traditional philosophical methods for understanding this concept are unlikely to be successful. I contend that we should instead use functional analyses and an understanding of the cognitive bases of causal cognition to gain insight into the concept of actual causation. I additionally provide initial, programmatic steps towards carrying out such analyses. The characterization of the concept of actual causation that results is quite different from many standard views: it is graded, context-sensitive, and extrinsic

Erratum to: Synthese DOI 10.1007/s11229-014-0408-3Appendix 1: NotationLet \(X\) represent a sequence of data, and let \(X_B^t\) represent an i.i.d. subsequence of length \(t\) of data generated from distribution \(B\).We conjecture that the i.i.d. assumption could be eliminated by defining probability distributions over sequences of arbitrary length, though this complication would not add conceptual clarity. Let \(\mathbf{F}\) be a framework (in this case, a set of probability distributions or densities).Let any \(P(\,)\) functions be either a probability distribution function or probability density function, as appropriate. Let \(M_\mathbf{F}\) be a method that takes a data sequence \(X\) as input and outputs a distribution

Even if one can experiment on relevant factors, learning the causal structure of a dynamical system can be quite difficult if the relevant measurement processes occur at a much slower sampling rate than the “true” underlying dynamics. This problem is exacerbated if the degree of mismatch is unknown. This paper gives a formal characterization of this learning problem, and then provides two sets of results. First, we prove a set of theorems characterizing how causal structures change under undersampling. Second, we develop an algorithm for inferring aspects of the causal structure at the “true” timescale from the causal structure learned from the undersampled data. Research on causal learning in dynamical contexts has largely ignored the challenges of undersampling, but this paper provides a framework and foundation for learning causal structure from this type of complex time series data

We evaluate the asymptotic performance of boundedly-rational strategies in multi-armed bandit problems, where performance is measured in terms of the tendency (in the limit) to play optimal actions in either (i) isolation or (ii) networks of other learners. We show that, for many strategies commonly employed in economics, psychology, and machine learning, performance in isolation and performance in networks are essentially unrelated. Our results suggest that the appropriateness of various, common boundedly-rational strategies depends crucially upon the social context (if any) in which such strategies are to be employed.

We argue that current discussions of criteria for actual causation are ill-posed in several respects. (1) The methodology of current discussions is by induction from intuitions about an infinitesimal fraction of the possible examples and counterexamples; (2) cases with larger numbers of causes generate novel puzzles; (3) "neuron" and causal Bayes net diagrams are, as deployed in discussions of actual causation, almost always ambiguous; (4) actual causation is (intuitively) relative to an initial system state since state changes are relevant, but most current accounts ignore state changes through time; (5) more generally, there is no reason to think that philosophical judgements about these sorts of cases are normative; but (6) there is a dearth of relevant psychological research that bears on whether various philosophical accounts are descriptive. Our skepticism is not directed towards the possibility of a correct account of actual causation; rather, we argue that standard methods will not lead to such an account. A different approach is required