This commentary acknowledges the importance of Davey's biocognitive approach to the uneven distribution of fears on the basis of its contribution to a human model for understanding fear. An integrated heredity-environment and developmental transactional approach based on field/system theory is recommended in place of the mechanistic heredity × environment interactionism that Davey uses to explain behavioral ontogeny.

The past 50 years have seen an accumulation of evidence suggesting that associative learning depends on high-level cognitive processes that give rise to propositional knowledge. Yet, many learning theorists maintain a belief in a learning mechanism in which links between mental representations are formed automatically. We characterize and highlight the differences between the propositional and link approaches, and review the relevant empirical evidence. We conclude that learning is the consequence of propositional reasoning processes that cooperate with the unconscious processes involved (...) in memory retrieval and perception. We argue that this new conceptual framework allows many of the important recent advances in associative learning research to be retained, but recast in a model that provides a firmer foundation for both immediate application and future research. (shrink)

Most phobias are focussed on a small number of fear-inducing stimuli (e.g., snakes, spiders). A review of the evidence supporting biological and cognitive explanations of this uneven distribution of phobias suggests that the readiness with which such stimuli become associated with aversive outcomes arises from biases in the processing of information about threatening stimuli rather than from phylogenetically based associative predispositions or “biological preparedness.” This cognitive bias, consisting of a heightened expectation of aversive outcomes following fear-relevant stimuli, generates and maintains (...) robust learned associations between them. Some of the features of such stimuli which determine this expectancy bias are estimates of how dangerous they are, the semiotic similarity between them and their aversive outcomes, and the degree of prior fear they elicit. Ontogenetic and cultural factors influence these features of fear-relevant stimuli and are hence important in determining expectancy bias. The available evidence does not exclude the possibility that both expectancy biases and specific evolved predispositions coexist, but the former can explain a number of important findings that the latter cannot. (shrink)

In his critique of preparedness theory, Davey does not address the limitations of adaptationism. The purpose of this commentary is to outline problems that arise when one assumes that mental illness (e.g., phobic disorder)musthave had adaptive significance for it to have survived the vicissitudes of natural selection.

Failure to find an obvious or linear relationship between a developmental experiential factor and a developmental outcome often leads investigators to posit concepts such as “biological preparedness” and “evolved predispositions” that allude to hypothetical geneticmechanisms that may not exist. However, experiential nonlinearities alone may explain the development of certain instinctive behaviors, as shown by studies on alarm call responsivity in mallard ducklings.

A review of data concerning the uneven distribution of phobias suggests that nonassociative, ethological models can account for most of tile important findings that cannot be attributed to expectancy biases. The origin of a variety of fears that appear in fixed developmental patterns across divergent cultures and species can best be explained by biological models.

Davey reviews evidence purporting to distinguish between two accounts of selective associations – expectancy bias and evolved predispositions, although these hypotheses largely apply to different levels of causal analysis. Criticisms of primate studies in which subjects lack prior exposure to stimuli seem uncompelling. Expectancies may sometimes serve as proximal mediators in selective associations, but other factors, both proximate and ultimate, are clearly also involved.

Davey's discussion of phobias is criticized because of the lack of distinctions between the various classes of phobias. Psychopharmacological evidence indicates differing pathophysiologies. Clinical psychopharmacological distinctions are not congruent with either a strict phylogenetic preparedness model or with cognitive biases. Davey's critique of the laboratory bred animal studies seems far fetched. His hypothesis concerning the importance of historical significance is clearly ad hoc rather than based on comparative data.

There are wide individual differences in the ability to detect a stimulus contingency embedded in a complex paradigm. The present study used a cognitive masking paradigm to better understand individual differences related to contingency learning. Participants were assessed on measures of electrodermal arousal and on working memory capacity before engaging in the contingency learning task. Contingency awareness was assessed both by trial-by-trial verbal reports obtained during the task and by a short post-task recognition questionnaire. Participants who became aware had fewer (...) non-specific skin conductance responses and tended to score higher on a digit span assessment. Skin conductance level was not significantly lower in the aware group than in the unaware group. These findings are consistent with studies showing that lower arousal and greater cognitive processing capacity facilitate conscious perception of a greater breadth of information within a scene or a task. (shrink)

Behavioral research suggests that rule-governed behavior should be less sensitive to environmental changes and thus more resistant to extinction (disconfirmation) than contingency-governed behavior. The opposite is implied in Davey's discussion of ontogenetic and phylogenetic contributions to fear development. The generality of the behavioral findings and their apparent inconsistency with the present article should be further explored with more sensitive research paradigms.

Davey suggests that increased resistance to extinction of CRs conditioned to fear-relevant stimuli may be due to more persistent expectancies of the UCS following these stimuli. However, this viewpoint is contradicted by existing empirical evidence that fear-relevant CRs survive an extinction trials series producing extinction of expectancies whereas CRs conditioned to non-fear-relevant CSs do not.

Studies on associative learning in normals and patients need appropriate dependent measures which are sensitive enough to reflect stimulus-specific responses and also consider the context in which the conditioning takes place. Patient's fear responses, once acquired, seem to be maintained by specific cognitive biases such as individual belief systems and a tendency to stay consistent with their previous judgments.

We endorse Davey's view that expectancy processes are intimately involved in fear reactions, but question his model on three grounds. First, the mechanism for generating expectancy bias to both ontogenetic and phylogenetic stimuli is not spelled out. Second, the selective association component is unnecessary. Third, the model fails to provide a clear explanation for the irrationality of phobic reactions.

This commentary focuses upon two issues raised by Davey's target article: (1) whether there are certain core features of stimuli we learn to fear, rather than specific types of objects or situations, which implies some element of innateness; and (2) whether expectancy biases serve to maintain rather than generate anxiety.

Davey has failed to clarify the critical evidence that could corroborate the expectancy bias hypothesis and refute preparedness theory. Such a clarification is necessary because each theory could potentially allow for multiple distal and proximal influences on selective associations. Expectancies are not the only proximal mediators. Our recent findings indicate that affective response matching may be an additional factor promoting such associations.

The present commentary emphasizes that the acquisition of fear always involves complex changes in several quasi-independent response systems. Stimulus-specific electrodermal response differentiation as well as the bias to overestimate the belongingness of certain stimulus pairs mainly indicates cognitive processes of selective orienting and attention. Emotion, however, also involves the activation of subcortical motivational circuits. Why certain stimuli acquire rapid access to these basic motivational systems is not explained by the expectancy bias model.

According to Davey, generalized expectancy biases cause fearrelevant behavior and may complement Seligman's biological preparedness model. Expectancy biases do not explain the preparedness phenomenon, because such cognitive (or covert behavioral) processes are themselves controlled by social and other environmentally based contingencies. Davey's own examination of the importance of cross-cultural factors can show the relationship between FR stimuli and behavior without needing cognitive agency to explain the behavioral phenomenon.

Expectations can facilitate rapid fear conditioning and this may explain some phenomena that have been attributed to preparedness. However, preparedness remains the best explanation for some aspects of clinical phobias and the difficulty of creating fears of modern dangers. Rapid fear conditioning based on expectancy is not an alternative to an evolutionary explanation, but has, like preparedness, been shaped by natural selection.

In this response, we provide further clarification of the propositional approach to human associative learning. We explain why the empirical evidence favors the propositional approach over a dual-system approach and how the propositional approach is compatible with evolution and neuroscience. Finally, we point out aspects of the propositional approach that need further development and challenge proponents of dual-system models to specify the systems more clearly so that these models can be tested.

Because of their evolutionary importance, threat-detection mechanisms are likely to exist at a variety of levels. A recent study of face recognition suggests that novel stimuli receive enhanced processing when presented as fear-related. This suggests the existence of a complex, context-dependent threat-detection mechanism that can adaptively respond to spatiotemporally varying and unique environmental features.

The evolutionary origin of phobias is strongly supported by behavioral genetics and monkey vicarious conditioning data. Prepared Pavlovian conditioning may be only one of the mechanisms mediating the evolutionarily determined outcome in phobias, avoidance. Davey's alternative biased expectancy hypothesis has merit in accounting for some aspects of laboratory data, but it is insufficient to explain the unconscious origin of phobic fear.

Many now consider “instinct” and “learning” opposite poles of a unidimensional continuum. An alternative model with two independently varying parameters predicts different selective pressures. Behavioral adaptation matches the organism's utilizations of stimuli and responses to their ecological validities: the mean validity over evolutionary time specifies the optimal initial potency of the prepared association; the variance specifies the optimal prepared plasticity.

Additional support is presented for the necessity of awareness of the CS-US relation in human autonomic conditioning. However, possible limitations and exceptions regarding this general rule are discussed. Limitations include the lack of relationship between conditioned response (CR) strength and degree of awareness, and an important exception may be the finding of conditioning with backwardly masked CSs of a biologically prepared nature.