The evidence from randomized controlled trials (RCTs) is widely regarded as supplying the ‘gold standard’ in medicine—we may sometimes have to settle for other forms of evidence, but this is always epistemically second-best. But how well justified is the epistemic claim about the superiority of RCTs? This paper adds to my earlier (predominantly negative) analyses of the claims produced in favour of the idea that randomization plays a uniquely privileged epistemic role, by closely inspecting three related arguments from leading contributors (...) to the burgeoning field of probabilistic causality—Papineau, Cartwright and Pearl. It concludes that none of these further arguments supplies any practical reason for thinking of randomization as having unique epistemic power. IntroductionWhy the issue is of great practical importance—the ECMO casePapineau on the ‘virtues of randomization’Cartwright on causality and the ‘ideal’ randomized experimentPearl on randomization, nets and causesConclusion. (shrink)

In clinical and agricultural trials, there is the danger that an experimental outcome appears to arise from the causal process or treatment one is interested in when, in reality, it was produced by some extraneous variation in the experimental conditions. The remedy prescribed by classical statisticians involves the procedure of randomization, whose effectiveness and appropriateness is criticized. An alternative, Bayesian analysis of experimental design, is shown, on the other hand, to provide a coherent and intuitively satisfactory solution to the problem.

When two causally independent processes each have a quantity that increases monotonically (either deterministically or in probabilistic expectation), the two quantities will be correlated, thus providing a counterexample to Reichenbach's principle of the common cause. Several philosophers have denied this, but I argue that their efforts to save the principle are unsuccessful. Still, one salvage attempt does suggest a weaker principle that avoids the initial counterexample. However, even this weakened principle is mistaken, as can be seen by exploring the concepts (...) of homology and homoplasy used in evolutionary biology. I argue that the kernel of truth in the principle of the common cause is to be found by separating metaphysical and epistemological issues; as far as the epistemology is concerned, the Likelihood Principle is central. (shrink)

For nearly as long as the word “correlation” has been part of statistical parlance, students have been warned that correlation does not prove causation, and that only experimental studies, e.g., randomized clinical trials, can establish the existence of a causal relationship. Over the last few decades, somewhat of a consensus has emerged between statisticians, computer scientists, and philosophers on how to represent causal claims and connect them to probabilistic relations. One strand of this work studies the conditions under which evidence (...) accumulated from non-experimental (observational) studies can be used to infer a causal relationship. In this paper, I compare the typical conditions required to infer that one variable is a direct cause of another in observational and experimental studies. I argue that they are essentially the same. (shrink)

Peter Urbach has argued, on Bayesian grounds, that experimental randomization serves no useful purpose in testing causal hypothesis. I maintain that he fails to distinguish general issues of statistical inference from specific problems involved in identifying causes. I concede the general Bayesian thesis that random sampling is inessential to sound statistical inference. But experimental randomization is a different matter, and often plays an essential role in our route to causal conclusions.

Traditional analyses of the curve fitting problem maintain that the data do not indicate what form the fitted curve should take. Rather, this issue is said to be settled by prior probabilities, by simplicity, or by a background theory. In this paper, we describe a result due to Akaike [1973], which shows how the data can underwrite an inference concerning the curve's form based on an estimate of how predictively accurate it will be. We argue that this approach throws light (...) on the theoretical virtues of parsimoniousness, unification, and non ad hocness, on the dispute about Bayesianism, and on empiricism and scientific realism. * Both of us gratefully acknowledge support from the Graduate School at the University of Wisconsin-Madison, and NSF grant DIR-8822278 (M.F.) and NSF grant SBE-9212294 (E.S.). Special thanks go to A. W. F. Edwards.William Harper. Martin Leckey. Brian Skyrms, and especially Peter Turney for helpful comments on an earlier draft. (shrink)

This survey presents some of the main principles involved in discovering causal relations. They belong to a large array of possible assumptions and conditions about causal relations, whose various combinations limit the possibilities of acquiring causal knowledge in different ways. How much and in what detail the causal structure can be discovered from what kinds of data depends on the particular set of assumptions one is able to make. The assumptions considered here provide a starting point to explore further the (...) foundations of causal discovery procedures, and how they can be improved. (shrink)

Evidence-based medicine (EBM) makes use of explicit procedures for grading evidence for causal claims. Normally, these procedures categorise evidence of correlation produced by statistical trials as better evidence for a causal claim than evidence of mechanisms produced by other methods. We argue, in contrast, that evidence of mechanisms needs to be viewed as complementary to, rather than inferior to, evidence of correlation. In this paper we first set out the case for treating evidence of mechanisms alongside evidence of correlation in (...) explicit protocols for evaluating evidence. Next we provide case studies which exemplify the ways in which evidence of mechanisms complements evidence of correlation in practice. Finally, we put forward some general considerations as to how the two sorts of evidence can be more closely integrated by EBM. (shrink)

Causality offers the first comprehensive coverage of causal analysis in many sciences, including recent advances using graphical methods. Pearl presents a unified account of the probabilistic, manipulative, counterfactual and structural approaches to causation, and devises simple mathematical tools for analyzing the relationships between causal connections, statistical associations, actions and observations. The book will open the way for including causal analysis in the standard curriculum of statistics, artificial intelligence, business, epidemiology, social science and economics.