Peter F. Lovibond’s research while affiliated with University of South Wales and other places

In this commentary, we propose that occasion setting in humans may be even more widespread than Leising and colleagues assume. In contrast to animal work, our research using the feature negative procedure (A+ AX-) reveals substantial individual differences in what people learn about the feature (X). We discuss findings showing that the majority of participants in our experiments learn something akin to occasion setting, and present reasons for why this may be the case. We conclude that occasion-setting may be the norm in humans because it allows existing learning to be preserved, and for the possibility that the effect of a cue is unique to its accompanying target.

A review of Pavlovian conditioning in animals and humans reveals a critical role for expectancy in the learning of an association between a conditioned stimulus (CS) and an unconditioned stimulus (US), as well as in the expression of this association in a conditioned response (CR). The automatic and involuntary nature of CRs has traditionally been explained in terms of the formation of excitatory or inhibitory links between representations of the CS and US. However, this view has difficulty accounting for the variety of CRs that are observed, some qualitatively different from those elicited by the US, depending on the imminence of the predicted US and the nature of the CS. Furthermore, in humans, the same anticipatory responses are seen when the CS–US relationship is instructed rather than experienced and when the imminent occurrence of the US is directly instructed, without a mediating CS. These findings suggest an alternative explanation in which CRs are anticipatory responses elicited automatically by a specific state of expectancy of the US. The similarity between Pavlovian conditioning in animals and humans in turn suggests a continuity of core mechanisms for learning and performance. We conclude that research and theory in Pavlovian conditioning should go beyond the search for direct CS–US connections and seek to understand the mechanisms that underlie CS–US contingency knowledge, expectancy states, and the generation of anticipatory responses.

People often rely on the covariation between events to infer causality. However, covariation between cues and outcomes may change over time. In the associative learning literature, extinction provides a model to study updating of causal beliefs when a previously established relationship no longer holds. Prediction error theories can explain both extinction and protection from extinction when an inhibitory (preventive) cue is present during extinction. In three experiments using the allergist causal learning task, we found that protection could also be achieved by a hidden cause that was inferred but not physically present, so long as that cause was a plausible preventer of the outcome. We additionally showed complete protection by a physically presented cue that was neutral rather than inhibitory at the outset of extinction. Both findings are difficult to reconcile with dominant prediction error theories. However, they are compatible with the idea of theory protection, where the learner attributes the absence of the outcome to the added cue (when present) or to a hidden cause, and therefore does not need to revise their causal beliefs. Our results suggest that prediction error encourages changes in causal beliefs, but the nature of the change is determined by reasoning processes that incorporate existing knowledge of causal mechanisms and may be biased toward preservation of existing beliefs.

In a causal illusion task, participants rate a cue that has an objectively null contingency with an outcome as causal. Trials are usually organized according to a 2x2 table representing the presence/absence of a binary cue and a binary outcome. Cell A outcomes (cue, outcome) can be attributed to the cue. But how do participants interpret trials from cell C (no cue, outcome), where the cause of the outcome is unspecified? In two experiments we asked participants to provide causal explanations for cell A and C trials in a medicine-recovery causal illusion task. Participants who reported that the cause of cell C outcomes (e.g., strong immunity, spontaneous recovery) did not also apply to cell A outcomes showed the strongest causal illusion. Such a causal reasoning process undermines the logic behind the delta P metric typically used to define a contingency, and thereby provides a potential normative account of causal “illusions”.

The illusory causation effect describes the tendency to judge an unrelated cue and outcome to be causally related. The standard procedure for assessing the illusion is based on the implicit assumptions that participants start as naïve observers with no prior beliefs about the likely relationship between the cue and outcome, and that learning can be adequately captured as a point-estimate causal rating after null contingency training. Here, we use a novel distributional measure to assess participants' beliefs over a range of causal relationships prior to, as well as after, exposure to non-contingent cues and outcomes. Across two experiments with different causal scenarios and 50% cue and outcome density, we show that participants have an initial bias towards expecting a causal relationship between the cue and outcome, and that this bias is mostly corrected after exposure to the null contingency. We conclude that distributional measures of causal beliefs can offer novel insights in understanding the illusory causation effect.

Illusory causation is a phenomenon in which people mistakenly perceive a causal relationship between a cue and outcome even though the contingency between them is actually zero. Illusory causation studies typically use a unidirectional causal rating scale, where one endpoint refers to no relationship and the other to a strongly positive causal relationship. This procedure may bias mean causal ratings in a positive direction, either by censoring negative ratings or by discouraging participants from giving the normative rating of zero which is at the bottom extreme of the scale. To test this possibility, we ran two experiments that directly compared the magnitude of causal illusions when assessed with a unidirectional (zero - positive) versus a bidirectional (negative - zero - positive) rating scale. Experiment 1 used high cue and outcome densities (both 75%) whereas Experiment 2 used neutral cue and outcome densities (both 50%). Across both experiments, we observed a larger illusory causation effect in the Unidirectional group compared to the Bidirectional group, despite both groups experiencing the same training trials. The causal illusions in Experiment 2 were observed despite participants accurately learning the conditional probabilities of the outcome occurring in both the presence and absence of the cue, suggesting that the illusion is driven by the inability to accurately integrate conditional probabilities to infer causal relationships. Our results indicate that although illusory causation is a genuine phenomenon that is observable with either a undirectional or bidirectional rating scale, its magnitude may be overestimated when unidirectional rating scales are used.

Individuals differ in their sensitivity to the adverse consequences of their actions, leading some to persist in maladaptive behaviors. Two pathways have been identified for this insensitivity: a motivational pathway based on excessive reward valuation and a behavioral pathway based on autonomous stimulus-response mechanisms. Here, we identify a third, cognitive pathway based on differences in punishment knowledge and use of that knowledge to suppress behavior. We show that distinct phenotypes of punishment sensitivity emerge from differences in what people learn about their actions. Exposed to identical punishment contingencies, some people (sensitive phenotype) form correct causal beliefs that they use to guide their behavior, successfully obtaining rewards and avoiding punishment, whereas others form incorrect but internally coherent causal beliefs that lead them to earn punishment they do not like. Incorrect causal beliefs were not inherently problematic because we show that many individuals benefit from information about why they are being punished, revaluing their actions and changing their behavior to avoid further punishment (unaware phenotype). However, one condition where incorrect causal beliefs were problematic was when punishment is infrequent. Under this condition, more individuals show punishment insensitivity and detrimental patterns of behavior that resist experience and information-driven updating, even when punishment is severe (compulsive phenotype). For these individuals, rare punishment acted as a "trap," inoculating maladaptive behavioral preferences against cognitive and behavioral updating.

Inhibitory stimuli are slow to acquire excitatory properties when paired with the outcome in a retardation test. However, this pattern is also seen after simple non-reinforced exposure: latent inhibition. It is commonly assumed that retardation would be stronger for a conditioned inhibitor than for a latent inhibitor, but there is surprisingly little empirical evidence comparing the two in either animals or humans. Thus, retardation after inhibitory training could in principle be attributable entirely to latent inhibition. We directly compared the speed of excitatory acquisition after conditioned inhibition and matched latent inhibition training in human causal learning. Conditioned inhibition training produced stronger transfer in a summation test, but the two conditions did not differ substantially in a retardation test. We offer two explanations for this dissociation. One is that learned predictiveness attenuated the latent inhibition that otherwise would have occurred during conditioned inhibition training, so that retardation in that condition was primarily due to inhibition. The second explanation is that inhibitory learning in these experiments was hierarchical in nature, similar to negative occasion-setting. By this account, the conditioned inhibitor was able to negatively modulate the test excitor in a summation test, but was no more retarded than a latent inhibitor in its ability to form a direct association with the outcome.