Jacob Stegenga

The value-free ideal for science holds that values should not influence the core features of scientific reasoning. We defend the difference-to-inference model of value-permeation, which holds that value-permeation in science is problematic when values make a difference to the inferences made about a hypothesis. This view of value-permeation is superior to existing views, and it suggests a corresponding maxim—namely, that scientists should strive to eliminate differences to inference. This maxim is the basis of a novel value-free ideal for science.

If scientists violate principles and practices of routine science to quickly develop interventions against catastrophic threats, they are engaged in what I call fast science. The magnitude, imminence, and plausibility of a threat justify engaging in and acting on fast science. Yet, that justification is incomplete. I defend two principles to assess fast science, which say: fast science should satisfy as much as possible the reliability-enhancing features of routine science, and the fast science developing an intervention against a threat should not depend on the same problematic assumptions as the fast science which estimates the magnitude, imminence, and plausibility of the threat.

It is a plausible speculation that conventional choices in outcome measures might influence the results of meta-analyses. We test that speculation by simulating data from trials on antidepressants. We vary real drug effectiveness while modulating conventional values for outcome measures. We had previously shown that one conventional choice used in meta-analyses of antidepressants falls in a narrow range of values that maximize estimates of effectiveness. Our present analysis investigates why this phenomenon occurs. Moreover, our results suggest the superiority of absolute outcome measures over relative measures. This research program can be extended to test numerous other aspects of clinical research.

There are two competing views regarding the role of mechanistic knowledge in inferences about the effectiveness of interventions. One view holds that inferences about the effectiveness of interventions should be based only on data from population-level studies (often statistical evidence from randomised trials). The other view holds that such inferences must be based in part on mechanistic evidence. The competing views are local principles of inference, the plausibility of which can be assessed by a more general normative principle of inference. Bayesianism tells us to base inferences on both the ‘likelihood’ and the ‘prior’. The likelihood represents statistical evidence. One influence on the prior probability of a hypothesis like ‘d causes x’ is mechanistic knowledge of how d causes x. Thus, reasoning about such inferences by appealing to both statistical and mechanistic evidence is vindicated by our best general theory of inference. The primary contribution of this paper is to assess the merits and weaknesses of the arguments on both sides of the debate, using the Bayesian framework. This analysis lends support to those who argue that we should base our causal inferences about interventions in part on mechanistic evidence.

We provide a novel articulation of the epistemic peril of p-hacking using three resources from philosophy: predictivism, Bayesian confirmation theory, and model selection theory. We defend a nuanced position on p-hacking: p-hacking is sometimes, but not always, epistemically pernicious. Our argument requires a novel understanding of Bayesianism, since a standard criticism of Bayesian confirmation theory is that it cannot represent the influence of biased methods. We then turn to pre-analysis plans, a methodological device used to mitigate p-hacking. Some say that pre-analysis plans are epistemically meritorious while others deny this, and in practice pre-analysis plans are often violated. We resolve this debate with a modest defence of pre-analysis plans. Further, we argue that pre-analysis plans can be epistemically relevant even if the plan is not strictly followed—and suggest that allowing for flexible pre-analysis plans may be the best available policy option.

Drug regulation is fraught with inductive risk. Regulators must make a prediction about whether or not an experimental pharmaceutical will be effective and relatively safe when used by typical patients, and such predictions are based on a complex, indeterminate, and incomplete evidential basis. Such inductive risk has important practical consequences. If regulators reject an experimental drug when it in fact has a favourable benefit/harm profile, then a valuable intervention is denied to the public and a company’s material interests are needlessly thwarted. Conversely, if regulators approve an experimental drug when it in fact has an unfavourable benefit/harm profile, then resources are wasted, people are needlessly harmed, and other potentially more effective treatments are underutilized. Given that such regulatory decisions have these practical consequences, non-epistemic values about the relative importance of these consequences impact the way such regulatory decisions are made (similar to the analysis of laboratory studies on the toxic effects of dioxins presented in Douglas [2000]). To balance the competing demands of the pertinent non-epistemic values, regulators must perform what I call an “inductive risk calculus.” At least in the American context this inductive risk calculus is not well-managed.

Debates about the genuine disease status of controversial diseases rely on intuitions about a range of factors. Adopting tools from experimental philosophy, this paper explores some of the factors that influence judgments about whether low sexual desire should be considered a disease and whether it should be medically treated. Drawing in part on some assumptions underpinning a divide in the literature between viewing low sexual desire as a genuine disease and seeing it as improperly medicalized, we investigate whether health and disease judgments are affected by factors such as an individual’s gender, the cause of the low desire, whether the desire is high or low, and both personal and societal valuations of the condition. Our main findings indicate that (a) the cause of a condition influences whether it is judged a disorder, (b) how the individual values the condition influences whether the condition is seen as a proper target of medical intervention, and (c) perceived dysfunction influences judgments regarding health, disorder classification, medicalization, and medical intervention. Our findings help further illuminate the intricate interplay of factors that influence judgments about health and disease in controversial conditions.

A stereotype is a belief or claim that a group of people has a particular feature. Stereotypes are expressed by sentences that have the form of generic statements, like “Canadians are nice.” Recent work on generics lends new life to understanding generics as statements involving probabilities. I argue that generics (and thus sentences expressing stereotypes) can take one of several forms involving conditional probabilities, and these probabilities have what I call a naturalness requirement. This is the natural probability theory of stereotypes. Each of the two components of the theory entails a family of fallacies that contributes to the spurious reinforcement of stereotypes: inferential slippage within and between the different generic forms, and inferential slippage from facts about frequencies of group traits to beliefs about natural propensities or dispositions of groups. Empirical research suggests that we often commit these fallacies. Moreover, this theory can referee a vitriolic debate between some psychologists, who hold that stereotypes are always false and stereotyping is always wrong, and other psychologists, who hold that stereotypes are often accurate and stereotyping is often reasonable.