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)

This paper surveys recent philosophy of biology. It aims to introduce outsiders to the field to the recent literature (which is reviewed in the footnotes) and the main recent debates. I concentrate on three of these: recent critiques of the replicator/vehicle distinction and its application to the idea of the gene as the unit of section; the recent defences of group selection and the idea that standard alternatives to group selection are in fact no more than a disguised form of (...) group selection; and recent ideas on the role of selection in evolution, especially the role of selection in structuring the large-scale history of life. The paper connects philosophy of biology to some more general problems in the philosophy of science, and concludes with a few suggestions about unfinished business. (shrink)

This paper attempts to articulate a dispositional account of innateness that applies to cognitive capacities. After criticizing an alternative account of innateness proposed by Cowie (1999) and Samuels (2002), the dispositional account of innateness is explicated and defended against a number of objections. The dispositional account states that an innate cognitive capacity (output) is one that has a tendency to be triggered as a result of impoverished environmental conditions (input). Hence, the challenge is to demonstrate how the input can be (...) compared to the output and shown to be relatively impoverished. I argue that there are robust methods of comparing input to output without measuring them quantitatively. (shrink)

This paper advocates a dispositional account of innate cognitive capacities, which has an illustrious history from Plato to Chomsky. The "triggering model" of innateness, first made explicit by Stich ([1975]), explicates the notion in terms of the relative informational content of the stimulus (input) and the competence (output). The advantage of this model of innateness is that it does not make a problematic reference to normal conditions and avoids relativizing innate traits to specific populations, as biological models of innateness are (...) forced to do. Relativization can be avoided in the case of cognitive capacities precisely because informational content is involved. Even though one cannot measure output relative to input in a precise way, there are indirect and approximate ways of assessing the degree of innateness of a specific cognitive capacity. (shrink)

A fundamental goal of linguistic theory is to explain how natural languages are acquired. This paper describes some recent findings on how learners acquire syntactic knowledge for which there is little, if any, decisive evidence from the environment. The first section presents several general observations about language acquisition that linguistic theory has tried to explain and discusses the thesis that certain linguistic properties are innate because they appear universally and in the absence of corresponding experience. A third diagnostic for innateness, (...) early emergence, is the focus of the second section of the paper, in which linguistic theory is tested against recent experimental evidence on children's acquisition of syntax. (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.

Song in oscine birds (as in human speech and song) relies upon the rare capacity of vocal learning. Transmission can be vertical, horizontal, or oblique. As a rule, memorization and production by a naïve bird are not simultaneous: the long-term storage of song phrases precedes their first vocal rehearsal by months. While a wealth of detail regarding songbird enculturation has been uncovered by focusing on the apprentice, whether observational learning can fully account for the ontogeny of birdsong, or whether there (...) could also be an element of active teaching involved, has remained an open question. Given the paucity of knowledge on animal cultures, I argue for the utility of an inclusive definition of teaching that encourages data be collected across a wide range of taxa. Borrowing insights from musicology, I introduce the Australian pied butcherbird (Cracticus nigrogularis) into the debate surrounding mechanisms of cultural transmission. I probe the relevance and utility of mentalistic, culture-based, and functionalist approaches to teaching in this species. Sonographic analysis of birdsong recordings and observational data (including photographs) of pied butcherbird behavior at one field site provide evidence that I assess based on criteria laid down by Caro and Hauser, along with later refinements to their functionalist definition. The candidate case of teaching reviewed here adds to a limited but growing body of reports supporting the notion that teaching may be more widespread than is currently realized. Nonetheless, I describe the challenges of confirming that learning has occurred in songbird pupils, given the delay between vocal instruction and production, as well as the low status accorded to anecdote and other observational evidence commonly mustered in instances of purported teaching. As a corrective, I press for an emphasis on biodiversity that will guide the study of teaching beyond human accounts and intractable discipline-specific burdens of proof. (shrink)

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.

Controversies over the innateness of cognitive processes, mechanisms, and structures play a persistent role in driving research in philosophy as well as the cognitive sciences, but the appropriate way to understand the category of the innate remains subject to dispute. One venerable approach in philosophy and cognitive science merely contrasts innate features with those that are learned. In fact, Jerry Fodor has recently suggested that this remains our best handle on innateness.

This paper evaluates and criticises the developmental systems conception of evolution and develops instead an extension of the gene's eye conception of evolution. We argue (i) Dawkin's attempt to segregate developmental and evolutionary issues about genes is unsatisfactory. On plausible views of development it is arbitrary to single out genes as the units of selection. (ii) The genotype does not carry information about the phenotype in any way that distinguishes the role of the genes in development from that other factors. (...) (iii) There is no simple and general causal criterion which distinguishes the role of genes in development and evolution. (iv) There is, however, an important sense in which genes but not every other developmental factor represent the phenotype. (v) The idea that genes represent features of the phenotype forces us to recognise that genes are not the only, or almost the only, replicators. Many mechanisms of replication are involved in both development and evolution. (vi) A conception of evolutionary history which recognises both genetic and non-genetic replicators, lineages of replicators and interactors has advantages over both the radical rejection of the replicator/interactor distinction and the conservative restriction of replication to genetic replication. (shrink)

The question of the influence of genes on behavior raises difficult philosophical and social issues. In this paper I delineate what I call the Developmentalist Challenge (DC) to assertions of genetic influence on behavior, and then examine the DC through an indepth analysis of the behavioral genetics of the nematode, C. elegans, with some briefer references to work on Drosophila. I argue that eight "rules" relating genes and behavior through environmentally-influenced and tangled neural nets capture the results of developmental and (...) behavioral studies on the nematode. Some elements of the DC are found to be sound and others are criticized. The essay concludes by examining the relations of this study to Kitcher's antireductionist arguments and Bechtel and Richardson's decomposition and localization heuristics. Some implications for human behavioral genetics are also briefly considered. (shrink)

Cognitive scientists often employ the notion of innateness without defining it. The issue is, how is innateness defined in biology? Some critics contend that innateness is not a legitimate concept in biology. In this paper I will argue that it is. However, neither the concept of high heritability nor the concept of flat norm of reaction define innateness. An adequate account is found in developmental biology. I propose that innateness is best defined in terms of C. H. Waddington's concept of (...) canalization. (shrink)

Recent work in biology and cognitive science depicts a variety of target phenomena as the products of a tangled web of causal influences. Such influences may include both internal and external factors as well as complex patterns of reciprocal causal interaction. Such twisted tales are sometimes seen as a threat to explanatory strategies that invoke notions such as inner programs, genes for and sometimes even internal representations. But the threat, I shall argue, is more apparent than real. Complex causal influence, (...) in and of itself, provides no good reason to reject these familiar explanatory notions. To believe otherwise, I suggest, is generally to commit (at least) one of two seductive errors. The first error is to think that the general notion of a state x coding for an outcome y involves the state's constituting a full description of y. This is what I call the myth of the self-contained code. The second error is to think that the practice of treating certain factors as special (e.g., seeing genes as coding for outcomes in a way environmental factors do not) depends on the (often mistaken) belief that the singled out factor is somehow doing the most real work. Where the amounts of causal influence are evenly spread, it is assumed there can be no reason to treat one factor in a special way. This is what I term the Myth of Explanatory Equality. Avoiding these errors involves reminding ourselves of (1) the rich context-dependence of even standard, unproblematic uses of the notions of code, program and information content (all three make sense only relative to an assumed ecological backdrop) and (2) the difference between explaining why an event occurred and displaying the full workings of a complex causal system. (shrink)

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.

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.

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.

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.