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Born to fear: non-associative vs associative factors in the etiology of phobias
Behaviour Research and Therapy 40 (2002) 173–184 www.elsevier.com/locate/brat
Born to fear: non-associative vs associative factors in the etiology of phobias Susan Mineka a
¨ hman , Arne O
a,*
b
Department of Psychology, Northwestern University, 2029 Sheridan Road, Swift Hall #102, Evanston, IL 602082710, USA b Psychology Section, Department of Clinical Neuroscience, Karolinska Institute and Hospital, Z6, S-171 76 Stockholm, Sweden
Abstract Poulton and Menzies (Behaviour Research & Therapy 40 (2001) 127–149) review two lines of evidence as supporting a non-associative pathway to the origins of “evolutionary relevant phobias”. First, in retrospective studies of mode of onset some recall they have always had this fear. We review here solid evidence that retrospective recall is notoriously unreliable. Second, they note as many nonphobics recall relevant associative learning experiences as do phobics. We argue such studies are very inconclusive because they fail to consider many experiential and personality vulnerability (and invulnerability) factors that strongly impact the outcome of any putative learning experience. Their argument also does not explain the transition from developmental fears to phobias that is central to their thesis. Overall, we call for major methodological improvements in this area, in the context of theoretical developments pointing to interacting vulnerability and invulnerability factors. 2002 Elsevier Science Ltd. All rights reserved.
Most theories of phobias have taken the seemingly logical route of postulating causal factors such as traumatic events or conditioning episodes to explain the emergence of this relatively common (10–12% of the population) condition. Poulton and Menzies, however, invert this logic by claiming that phobias result not from the presence of positively defined causal factors in the life history of individuals, but rather from the absence of such factors. In particular they argue that phobias result from innate fears shared by all humans. Adult phobias, therefore, are either a result of an enhanced genetic readiness in some individuals to fear particular situations, or reflect a deficit in the (presumably genetically given) mechanisms to get rid of fear responses, such as habituation.
* Corresponding author. E-mail address: [email protected] (S. Mineka).
0005-7967/02/$ - see front matter 2002 Elsevier Science Ltd. All rights reserved. PII: S 0 0 0 5 - 7 9 6 7 ( 0 1 ) 0 0 0 5 0 - X
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To support empirically their position, Poulton and Menzies review a literature consisting of studies that rely very heavily on retrospective recall. They take these studies as showing the absence of conditioning episodes in most phobics who have what they call evolutionary relevant phobias. We may note initially that this is an awkward claim that comes close to the statistical problem of proving the null hypothesis. Logically, it is easier to prove that something has happened than to prove that something has not happened. In the former case any problems of measurement work against the hypothesis, which should give added weight to positive findings. When trying to prove that something has not happened, however, measures that are too insensitive to register an event can provide what falsely is interpreted as support for the hypothesis that no event was present. Thus, one may conclude that there is no evidence of triggering events or conditioning episodes in the life history of a phobic for the simple reason that the method one uses to assess such events lacks the power to pick them up. In this commentary, we start out by discussing the theoretically central thesis of Poulton and Menzies that phobias reflect innate fears from the perspective of what we know about the ontogenesis of fear. We then go on to analyze the methodological soundness of the data base that Poulton and Menzies adduce in support of their theory. We conclude that this theory suffers from logical problems, and remains theoretically unconvincing. Furthermore, the data that are invoked in its support suffer from severe reliability problems that, in effect, provide what falsely appears to be support for the theory. Thus, we do not take the non-associative account as a viable alternative to conditioning (and Rachman’s three pathways) theory as a primary explanation of phobias (Rachman 1977, 1990). At most it may be a fourth pathway to fear, albeit a problematic one from several standpoints. 1. Associative versus nonassociative pathways to fear/phobia acquisition Poulton and Menzies build on earlier work by Menzies and Clarke (1993, 1995) who first argued that non-associative pathways for evolutionary-relevant fears (such as heights and water) provide a superior account for the origins of such fears and phobias. Their strong thesis is that “a non-associative model can provide a more satisfactory account of fear phenomena than conditioning theory” (Poulton & Menzies, 2002) and in many places the authors fail to qualify such broad statements with appropriate caveats (such as that this pathway could only possibly account for a minority of phobias). Their weaker thesis is that a non-associative pathway to fear acquisition constitutes a fourth pathway, adding to the three pathways proposed by Rachman and others. The first of their lines of argument for either of these positions is that the studies they review reveal that some of those reporting fears or phobias of water and heights cannot recall a specific mode of onset and report only that they “always had this fear” or that they “cannot remember”. 1.1. Developmental fears versus phobias The idea that some developmental (or prepotent) fears (as they are often called) are innate (or instinctive) is certainly not new and is indeed widely accepted (e.g., Craske, 1998; Marks, 1987; ¨ hman, Dimberg, & O ¨ st, 1985). Such fears would include height fear, stranger fear, and separO ation anxiety as discussed by Poulton and Menzies (as well as fear of loud noises, the darkness
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and small animals which emerge at different ages) (see Craske, 1998; Marks, 1987). However, the stimuli which evoke such developmental fears constitute only a minority of adult phobias, some of the most common of which are illness/injury, storm, animals and heights (Agras, Sylvester, & Oliveau, 1969).1 Moreover, developmental fears do not generally become phobias but rather are usually outgrown. Poulton and Menzies argue that the adults who have fears or phobias are either the ones whose early fears have failed to habituate (perhaps because of temperamental/personality variables or inadequate exposure), or the ones whose early fear has habituated, but has later become dishabituated through exposure to nonspecific stressors. Although these arguments might be plausible regarding the maintenance or reemergence of a developmental fear, they fail to address why some develop phobias — which are far more intense and disabling than most developmental fears. For example, as noted by Poulton and Menzies virtually every child avoids the deep end in the visual cliff test. However, this avoidance response occurs in the absence of the intense fear reactions seen in a height phobic forced to enter a sixth-floor balcony. One logical possiblity is that adult height phobics have had phobic levels of fear since early childhood, but to be valid such claims must be confirmed, for instance, by parental reports. Any such evidence, however, is not cited by Poulton and Menzies — probably because it does not exist (Ollendick, personal communication, 8/29/00). To us a plausible alternative is that specific negative experiences are likely to play a role in this transition from developmental fears to phobias for the small percent of phobias that may originate from developmental fears. Moreover, because individuals in this category may already have a certain level of fear (i.e., because they are non-habituators), or have habituated or extinguished fear remaining latent (as all extinguished or habituated fears probably are) (cf. Bouton, 1994), it may not take a great deal of negative input to raise the level of fear to a phobia (cf., ¨ hman, 1994; O ¨ hman & Soares, 1998; Seligman, 1971, for disEsteves, Parra, Dimberg, & O cussions of need for only degraded input when dealing with prepared fear learning). Regarding the importance of experiential factors, researchers should be aware that the best behavior genetic evidence shows that although specific phobias have a moderate heritability, there is also a large portion of variance (40–60%) that needs to be accounted for by unique, nonshared environmental factors (Kendler, Neale, Kessler, Heath, & Eaves, 1992; Kendler, Karkowski, & Prescott, 1999). We also note that the evidence cited in studies of height and water fear/phobia at best suggests that a nonassociative pathway is relevant in only a minority of cases. For example, in a study of height fearful students (Menzies & Clarke, 1993) only 30% reported that “it had always been this way” (vs 58% in the associative learning categories combined)2 and a similar study of height phobics reported that only 39% fit in the same non-associative category (Menzies & Clarke, 1995). 1.2. What does it mean when nonphobics and phobics do not differ on prior potential conditioning events? Poulton and Menzies’ second primary argument against associative accounts of fear (or phobia) acquisition comes from studies on this topic that have included nonfearful or nonphobic control 1 Interestingly, water phobia, discussed extensively by Poulton and Menzies as an evolutionary fear, is not even listed among the most common phobias in three major literature reviews we searched (Barlow, 1988; Craske, 1998; Marks, 1987). Moreover, it also seems there is no early widely shared developmental fear of water that is at all analagous to the visual cliff phenomenon for height fear/phobia (Ollendick, personal communication, 8/29/00). 2 See discussion later of interoceptive conditioning for why we included “nonconditioning traumatic events” in this category.
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groups. These studies have often found that such nonfearful individuals often report as high or higher rates of traumatic conditioning experiences (direct or indirect or instructional) as do the fearfuls or phobics (e.g., Di Nardo, Guzy, & Bak, 1988; Menzies & Clarke 1993, 1995). Such results have led Poulton and Menzies and others to conclude that the conditioning incidents must not have truly played a causal role for the fearfuls or phobics. However, we have discussed extensively elsewhere that such an argument fails to consider the impact of a wide range of temperamental variables and experiential differences on which individuals undergoing the same trauma are very likely to differ (e.g., Mineka, 1985; Mineka & Zinbarg 1991, 1995, 1996, 1998). For example, a range of theorists from Pavlov (1927) to Eysenck, Kagan, and Gray have all noted individual differences in personality/temperament which affect the speed and strength of conditioning.3 In addition, Mineka and Zinbarg also noted a wide range of experiential differences across individuals that have a major impact on the outcome of direct or indirect conditioning experiences (and therefore why many without phobias will have such histories that theoretically involved conditioning events). Thus these personality and experiential factors may serve as diatheses or vulnerability factors for the development of phobias in certain individuals given appropriate experiential input, just as certain individuals with a variety of diatheses will be more likely than those without the vulnerabilities to develop major depression in response to major life stress (e.g., Monroe & Simons, 1991). One example illustrating these points stems from an experiment by Mineka and Cook (1986) who noted that prior exposure to nonfearful model monkeys behaving nonfearfully with snakes effectively prevented the acquisition of snake fear following later exposure to fearful models behaving fearfully with snakes; moreover this effect was somewhat larger than the effect of latent inhibition (simple exposure to the snakes by themselves). Thus researchers in this area should not only pay attention to whether children have a good deal of experience with, say, heights or water, but also whether they had prior exposure to nonfearful models (e.g., Graham & Gaffan, 1997, found first-born children were more likely to be fearful of water than later born children, presumably because the latter had more opportunity for observational learning of competence and nonfearful behavior). A second example comes from an experiment by Mineka, Gunnar and Champoux (1986) who found that infant monkeys reared with a sense of mastery and control over their environments habituated more quickly to frightening events than did monkeys reared in identical environments except without the experiences with control. Such experimental evidence supports propositions long made by developmental psychologists based on correlational data that infants and children raised in environments where they gain a sense of mastery and control over their environment are less frightened by novel events and better able to cope with frightening situations. Thus, children (or adults) raised with a sense of mastery or control (high self-efficacy) over their environments should be less susceptible to developing fears given identical negative
3 We also note that at least one study reviewed by Poulton and Menzies (Menzies & Parker, 2001) has now added measures of high trait anxiety in their fearful or phobic samples and has not found that the phobics were higher in trait anxiety than the nonphobics. However, the Mineka and Zinbarg model does not predict that all (or even a majority) of phobics will have high levels of trait anxiety or neuroticism; rather, they predict that among those who are high on this personality characteristic and are exposed to the appropriate negative experiential input, fears or phobias will be acquired more readily than among those low on this personalitiy characteristic. That is there should be an interaction between level of trait anxiety or neuroticism at the time of negative experiential input.
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environmental input than are children reared without such a sense of mastery or control (low selfefficacy). (See also Chorpita & Barlow, 1998.) Mineka and Zinbarg (1996, 1998) also discussed how several aspects of the conditioning event itself have a strong impact on how much fear is acquired. For example, having control over a traumatic event itself (such as being able to escape or avoid it) has a major impact on how much fear is conditioned to neutral stimuli paired with that traumatic event, with far less fear being conditioned when the aversive event is controllable than when it is uncontrollable (e.g., Mineka, Cook, & Miller, 1984; Mowrer & Viek, 1948; see Craske, Miller, Rotunda, & Barlow, 1990, for a relevant human study). Additionally, the nature of the object or situation that is paired with negative experiential input must also be taken into consideration when predicting whether fear acquisition will occur. Specifically, evolutionarily fear-relevant (or prepared) stimuli have been shown to support more robust fear acquisition in the laboratory than do fear-irrelevant stimuli ¨ hman et al., 1985; O ¨ hman & Mineka, in press).4 Finally, each of these (and other) experien(e.g., O tial variables and temperamental variables generally should not be seen as operating in isolation (i.e., not as main effects) but rather in a dynamic interaction with each other. That is, they are “stress-in-dynamic-context” models of fear/phobia acquisition rather than the “stress-in-total-isolation” models provided by most researchers and theorists in this area (Mineka & Zinbarg 1996, 1998). Thus, in light of the stress-in-dynamic-context model, studies that have compared rates of traumatic direct or indirect conditioning histories in phobic and nonphobic individuals and found no differences are completely inconclusive. This is because they have generally neglected to include any measures of most of such individual difference variables (with the recent exception of latent inhibition in a few studies) that might account, singly, or more likely in combination, for why only some individuals undergoing a trauma developed a fear or phobia. (See Graham & Gaffan, 1997, for one study that had a more sophisticated approach to understanding multiple interacting causal pathways.) Moreover, somewhat paradoxically it seems quite likely that nonfearful individuals would be expected to be more likely to experience traumas precisely because they are not fearful and therefore are more likely to encounter potentially phobic objects or situations, which in turn could provide the occasion for possible traumas. For example, someone who is not afraid of water (or actually likes it) is much more likely to go swimming or boating and get involved in a water accident than is someone who is more neutral or even mildly cautious about water by virtue of having little direct or vicarious experience with it. Yet because of the nonfearful person’s prior exposure (leading to latent inhibition or immunization) s/he would not be as likely to develop a fear/phobia after such an accident as someone without the prior exposure. Thus, it is not necessarily surprising that some studies have found more nonfearful individuals recalling traumatic incidents than fearful individuals do because the nonfearfuls actually may have had more of them. In summary, we have no argument with the notion that children have a variety of developmental fears, most of which may be largely innate. However, we do not agree with Poulton and Menzies that there is any sound basis on which to conclude that such developmental fears provide a causal pathway to most adult phobias. Moreover, the fact that control groups of nonfearful individuals 4 Although Poulton and Menzies also discuss evolutionary relevant fears as the ones their nonassociative model applies to, they are discussing innate/developmental fears which require only maturational variables for their development. By contrast, prepared fears by definition require at least some amount of negative experiential input to emerge.
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sometimes have a greater likelihood of having had relevant traumatic experiences than have phobics does not surprise us. There are wide individual differences (both personality and experiential) which determine the outcome of a conditioning event (direct, vicarious or informational) and nonfearful individuals are undoubtedly more likely to experience such traumas than are those who are neutral or mildly cautious initially (perhaps because they have not had many nonfearful parental or sibling models, cf. Graham & Gaffan, 1997). 2. Problems with the non-associative account 2.1. The definition of conditioning: measurement and assessment issues The results of the studies reviewed could only possibly be as informative as the questionnaires/interviews used to assess individuals’ past experiences (and non-experiences). One primary problem in this regard is that researchers in this area who follow the admonitions of Menzies and Clarke (1995) (see also Poulton & Menzies, 2002) to adhere to their old strict textbook definitions of classical conditioning are clearly not aware of current developments in learning that render some of these definitions outmoded. Such old definitions require that the person be able to recall a completely neutral arbitrary stimulus (CS), that initially elicits no fear whatsoever, as well as a completely arbitrary (UCS) that also must be external and identifiable and with which the CS has been paired. We now cite several such relevant examples of problems with such definitions. In the conditioning literature there are now numerous instances (and likely many more when conditioning occurs in nature) where the CS is not entirely neutral and yet supports associative conditioning. For example, a weak shock or small amount of food (hardly entirely neutral) can serve as a CS for a more intense shock or large amount of food, respectively (e.g., Crowell, 1974; Goddard, 1999). These and other examples like it are often known as US– US conditioning (see Bouton, Mineka, & Barlow, 2001, for a review of definitional issues in conditioning). Another problem with Menzies and Clarke’s definition is that they have excluded from a conditioning category of onset those cases where phobics who could not recall a specific stimulus (UCS) that triggered the fear/panic response (or nonconditioning traumatic event as Poulton and Menzies refer to it) that they had had in the presence of their now phobic object. They argued that such experiences as the basis of the origin of a fear or phobia should be classified as nonas¨ st & Hugdahl, 1981, for a study sociative in nature because of the failure to identify a UCS (see O that included such cases). We strongly disagree because this position does not acknowledge the strong likelihood that such cases do not involve exteroceptive UCSs, but instead involve interoceptive UCSs (which stimulate internal sensory receptors in the gut, lungs, etc.). Interoceptive conditioning was carefully studied early on by the Soviets (e.g., Razran, 1961) but is poorly understood (and generally not recognized) by contemporary clinical researchers. CSs and UCSs can be either interoceptive or exteroceptive in nature, with all four possible combinations of CSs and UCSs producing reliable conditioning; indeed Razran’s (1961) review of the Soviet evidence suggested that interoceptive conditioning is more robust than exteroceptive conditioning and is unconscious in nature. In the case of phobias, this means that the alleged non-associative pathway (Menzies & Clarke 1993, 1995) when subjects can only recall a fear/panic response (but no
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identifiable UCS) is indeed an associative pathway — an example of exteroceptive (CS)–interoceptive (UCS) conditioning (e.g., Barlow, 1988; Bouton et al., 2001; Forsyth & Eifert, 1996; Mineka & Zinbarg, 1996). A related problem with some of the studies reviewed by Poulton and Menzies involves the way researchers have sometimes operationalized what constitutes a UCS in particular studies. Not only can UCSs be interoceptive and unconscious in nature as discussed above, but a UCS also must produce a potentially measurable response (UCR). Thus when Poulton, Thomson, Davies et al. (1997) operationalized the unconditioned stimulus in studies of dental phobia, they used the caries (cavities) level of the children’s teeth as the measure of the intensity of the UCS and UCR (and thereby the opportunity for direct conditioning to take place). Yet this is at best a very imperfect measure of the UCSs and UCRs experienced by a child, both because of individual differences in pain sensitivity and in reactivity to anaesthesia (or even the dentists’ use/nonuse of anaesthesia). Moreover, in their studies of height fear, Poulton, Davies, Menzies, Langley, & Silva (1998) operationalized exposure to a UCS as having a severe fall from a height (i.e., only those leading to a fracture, dislocation, laceration or intracranial injury). This is an overly restrictive definition because even relatively minor falls often create serious distress in children. In summary, there are problems with the instruments used in many of the studies reviewed regarding both definitional issues of what qualifies as a CS and as a UCS, and also in the way certain UCSs are operationalized in terms of being too stringent (e.g., severe falls) or too imprecise (e.g., caries level). 2.2. Unreliability of retrospective recall The second major problem we see in studies supporting the non-associative viewpoint (although to a considerable degree the associative viewpoint as well) concerns the unreliability of retrospective recall. This problem is acknowledged by Poulton and Menzies and by the authors of many of the studies they review, but it is our belief that all these investigators seriously underestimate the degree of these problems, generally only paying lip service to them in their papers. This is a well recognized problem in the stressful life-event literature, in which it is often reported that as much as about half the events are forgotten over a one-year period (e.g., Monroe, 1982), and as a consequence it is often recommended that the required recall intervals should not exceed six months. Unfortunately, however, very few have attempted to estimate the magnitude of this problem with regard to events relevant for fear and anxiety. One exception is a recent study by Taylor, Deane, and Podd (1999) on acquisition of driving fear who found that “retrospective accounts of fear onset may be quite unstable over time” (p. 927). This study provided a one year follow-up to an earlier one in which subjects were assessed for the origins of their fear using a modified version of Menzies and Clarke’s Origins Questionnaire (Menzies & Clarke, 1993). When the phobics were reassessed one year later (using a shorter modified OQ), Taylor et al. found that only 54% of pathway classifications remained the same, with 46% making different pathway ascriptions at one-year follow-up! Moreover, the highest proportion of change occurred within the “cannot remember” group where only 18% of the respondents stayed within this category. This result should of course be replicated in other studies to confirm its reliability but it gives a strong suggestion as to the magnitude of the problem. Some also have suggested the need for corroboration of self-report by others (e.g., Kleinknecht,
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1994). As concrete examples, Kleinknecht reported two case studies of adult injection phobics who had been phobic as long as they could recall, with no memory for any kind of acute onset. However, upon soliciting information from the parents of these two phobics, the parents had very distinct and credible memories of the onset of their (then) child’s phobia. Although the phobics would have been classified in any of the studies in this area as in the “no recall” or “always been this way” (nonassociative) categories, parental reports made it clear this would have been inaccurate and misleading. Another very carefully done prospective and retrospective study of many types of childhood events and family experiences assessed the agreement of retrospective recall at age 18 for childhood variables with the children’s actual recall at ages 9, 11, 13 and 15 of what had happened in the previous two years (i.e., two year retrospective data in a prospective study) (Henry, Moffitt, Caspi, Langley, & Silva, 1994). In the case of memory for childhood major injuries (which could occasion the conditioning of certain fears), the correlation between the retrospective reports at 18 and the actual number of injuries reported at ages 9, 11, 13 and 15 was only 0.42. Moreover, the age 18 retrospective reports were only moderately more accurate than chance alone (=0.34), which provides a far from ringing endorsement of the retrospective methods used in this kind of research on the origins of fears. Finally, a recent study by Kendler et al. (1999) assessed both the short-term and long-term reliability of life-time phobic diagnoses in their large study of female twins. Short-term reliability was obtained for only 192 twin pairs approximately one month after their initial interview and diagnosis; reliability for the diagnosis of specific phobia over the short term was moderate (=0.46). Long-term reliability was assessed 8 years after the initial interview (for 86% of the original sample of 2293 twin pairs) and was only modest (=0.30). When diagnoses are this unreliable over both brief and long term periods, even when using structured interviews, further questions are raised about the usefulness of all the studies such as those reviewed by Poulton and Menzies. Indeed, given all these serious limitations we are somewhat puzzled by why such studies have proliferated at such a rapid pace in recent years. 2.2.1. Superiority of prospective studies? It should also be emphasized that the supposed superiority of the prospective studies by Poulton and his colleagues reviewed here is of somewhat questionable significance (especially unless corroborated by parental reports). As already noted, prospective studies necessarily can only assess subjects every few years and thus they simply rely on shorter-term retrospective recall than the so-called retrospective studies (see also Rutter, Maughn, Pickles, & Simonoff, 1998). However, some of the studies reviewed above suggest the decay in reliability of memories may primarily occur in a matter of weeks or months rather than years. (See also Schacter, 1996). 2.2.2. Characteristics of acquisition that reduce memorability Another relevant issue raised by several authors is that phobias may represent the outcome not of one-trial learning experiences but rather of cumulative more minor experiences that are not very memorable (e.g., Craske, 1998; Graham & Gaffan, 1997). Or in some cases they may be the outcome of second order or sensory preconditioning experiences where the first order pathway may be unmemorable (e.g., Mineka, 1985; Cook & Mineka, 1987). In yet other cases a phobic level fear may be reached following a UCS inflation experience in which memory of the original
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UCS (involved in minor fear conditioning) is altered by subsequent experience with a more intense version of the UCS (not paired with the CS) (e.g., Davey, de Jong, & Tallis, 1993; Mineka, 1985; Mineka & Zinbarg, 1996). Because the more intense UCS was never directly paired with the CS the memorability of this associative pathway to conditioned fear would be very low. 2.2.3. Memory distortions over time In addition to the well-known unreliability of memory simply with the passage of time, there is also now a great deal of research showing how memories often become distorted with the passage of time. Human memory is a constructive process and highly subject to modification or revision based on experiences (including questions and comments by others) happening after an original memory trace was established (e.g, Loftus, Feldman, & Dashiell, 1995; Schacter, Norman, & Koustaal, 1998). Even flashbulb memories of extraordinarily memorable historic events, as well as personally traumatic memories, are subject to distortion over time (see Schacter, 1996, Chapter 7). Thus, the unreliability of retrospective recall is a function of both decay or inadequate retrieval cues, as well as the distortions of memory that can occur due to intervening experiences. Finally, when it comes to memory of early childhood events there is an additional problem of childhood amnesia (cf. Usher & Neisser, 1993) for such events which may further complicate matters in the case of very early onset (see Kleinknecht, 1994). 2.2.4. Explicit vs implicit memories? We also find it surprising that researchers in this area have not considered that many phobic responses may be examples of implicit rather than explicit memory. Implicit memory, by definition, is not available for conscious introspection while explicit memory can be (given adequate retrieval cues). As Kihlstrom, Mulvaney, Tobias, and Tobis (1999) explain it: “emotional response can serve as an index of implicit memory. That is, subjects can display emotional responses that are attributable to some event in their past history, in the absence of conscious recollection of that event”. They cite a case by Bagby (1928) of a woman with a phobia for running water. The person had no memory for how this intense response was acquired but when an aunt visited, the story emerged. As a girl the woman had gone on a picnic with the aunt; the child had strayed and became trapped under a waterfall. The aunt rescued the girl and promised to keep her transgression (straying contrary to instructions) a secret. Conscious memory for the incident was lost but the phobia remained intense — an example of implicit memory (Kihlstrom et al., 1999). (See also Schacter, 1996). This type of dissociation between emotional and conscious memories can be accounted for by the fact that these types of memories are encoded in two independent memory circuits of the brain, one emotional and centered on the amygdala and another cognitive and conscious centered on the hippocampus (LaBar & LeDoux, 2000; LeDoux, 1996). In summary, even if the logic of the non-associative account of phobia acquisition was plausible for more than a few phobias, there are so many problems with the reliance all of these studies place on retrospective recall that these studies seem largely uninformative. Note that this critique of such studies applies to their usefulness in studies supporting both non-associative and associative accounts of the origins of phobias. However, as argued in the introduction, methodological hazards do not risk to generate false support for the associative account to the same degree that they do for the non-associative account.
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3. Conclusions In this commentary we have argued that as currently articulated the non-associative account of phobia acquisition reviewed by Poulton and Menzies remains unconvincing as an explanation for how the vast majority of, and quite possibly all, phobias develop. At least presently it does not account for the transitions from fears to phobias even for so-called evolutionary relevant phobias, and has difficulty explaining why such phobias are not rather common. Poulton and Menzies also critique associative accounts of phobia acquisition because of findings that as many (or even more) nonphobics recall associative learning experiences as do phobics. However, such studies are seriously flawed, in part because they do not take into account the dynamic context in which aversive experiences occur that strongly impact the outcome of those experiences. In all the psychological disorders that we can think of where stress plays a role in precipitating onset (ranging from schizophrenia to major depression and post-traumatic stress disorder), it is well known that the stress only has this effect in people with certain biological or experiential vulnerabilities. Moreover, other people may have various sources of invulnerability or protective factors which render them unlikely to develop the disorder (e.g., see Carson, Butcher, & Mineka, 2000, for relevant examples). Why this fact has been ignored by phobia researchers for so long is simply astonishing to us. Finally, we also find it unfortunate that insufficient attention has been paid to the major shortcomings of the kinds of studies being done in this area — whether they support non-associative or associative accounts of phobia acquisition. Problems with the unreliability of retrospective recall, especially when it is generally many years after the alleged experience took place (or even several years in prospective studies), are widely known in cognitive psychology; these issues should be far better understood by clinical researchers. We hope that the points raised here will cause researchers in this area to pause before they continue with this line of research — no matter which positions they are taking — unless major improvements in methodology can be developed and theoretical advances as to the nature of interacting causal factors can be explored.
Acknowledgements We thank John Kihlstrom, Kevin LaBar, Tom Ollendick, and Paul Reber for their comments during the preparation of this manuscript.
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Chorpita, B. F., & Barlow, D. H. (1998). The development of anxiety: The role of control in the early environment. Psychological Bulletin, 124, 3–21. Cook, M., & Mineka, S. (1987). Second-order conditioning and overshadowing in the observational conditioning of snake fear in monkeys. Behaviour Research and Therapy, 25, 349–364. Craske, M. (1998). Anxiety disorders: Psychological approaches to theory and treatment. Boulder, CO: Westview Press. Craske, M. G., Miller, P. P., Rotunda, R., & Barlow, D. H. (1990). A descriptive report of features of initial unexpected panic attacks in minimal and extensive avoiders. Behaviour Research & Therapy, 28, 395–400. Crowell, C. R. (1974). Conditioned-aversive aspects of electric shock. Learning and Motivation, 5, 209–220. Davey, G. C. L., de Jong, P. J., & Tallis, F. (1993). UCS inflation in the etiology of a variety of anxiety disorders: some case histories. Behaviour Research and Therapy, 31, 495–498. Di Nardo, P. A., Guzy, L. T., & Bak, R. M. (1988). Anxiety response patterns and etiological factors in dog-fearful and non-fearful subjects. Behaviour Research and Therapy, 26, 245–251. ¨ hman, A. (1994). Nonconscious associative learning: Pavlovian conditioning Esteves, F., Parra, C., Dimberg, U., & O of skin conductance responses to masked fear-relevant facial stimuli. Psychophysiology, 31, 375–385. Forsyth, J. P., & Eifert, G. H. (1996). Systemic alarms in fear conditioning I: A reappraisal of what is being conditioned. Behavior Therapy, 27, 441–462. Goddard, M. J. (1999). The role of US signal value in contingency, drug conditioning, and learned helplessness. Psychonomic Bulletin & Review, 6, 412–423. Graham, J., & Gaffan, E. A. (1997). Fear of water in children and adults: Etiology and familial effects. Behaviour Research and Therapy, 35, 91–108. Henry, B., Moffitt, T. E., Caspi, A., Langley, J. D., & Silva, P. A. (1994). On the “remembrance of things past”: A longitudinal evaluation of the retrospective method. Psychological Assessment, 6, 92–101. Kendler, K. S., Neale, M. C., Kessler, R. C., Heath, A. C., & Eaves, L. J. (1992). The genetic epidemiology of phobias in women: The inter-relationship of agoraphobia, social phobia, situational phobia and simple phobia. Archives of General Psychiatry, 49, 257–266. Kendler, K. S., Karkowski, L. M., & Prescott, C. A. (1999). Fears and phobias: Reliability and heritability. Psychological Medicine, 29, 539–553. Kihlstrom, J., Mulvaney, S., Tobias, B. A., & Tobis, I. P. (1999). The emotional unconscious. In E. Eich, J. F. Kihlstrom, G. H. Bower, J. P. Forgas, & P. M. Niedenthal, Counterpoints: Cognition and Emotion. New York: Oxford University Press. Kleinknecht, R. D. (1994). Acquisition of blood, injury and needle fears and phobias. Behaviour Research and Therapy, 32, 817–823. LaBar, K. S., & LeDoux, J. E. (2000). Coping with danger: The neural basis of defensive behavior and fearful feelings. In B. S. McEwen, Handbook of physiology: Coping with the environment (pp. 139–154). New York: Oxford University Press. LeDoux, J. E. (1996). The emotional brain. New York: Simon & Schuster. Loftus, E. F., Feldman, J., & Dashiell, R. (1995). The reality of illusory memories. In D. Schacter, Memory distortion: How minds, brains, and societies reconstruct the past (pp. 47–68). Cambridge, MA: Harvard University Press. Marks, I. (1987). Fears, phobias, and rituals: Panic, anxiety and their disorders. New York: Oxford University Press. Menzies, R. G., & Clarke, J. C. (1993). The etiology of fear of heights and its relationship to severity and individual response patterns. Behaviour Research and Therapy, 31, 355–365. Menzies, R. G., & Clarke, J. C. (1995). The etiology of phobias: A non-associative account. Clinical Psychology Review, 15, 23–48. Menzies, R. G., & Parker, L. (2001). The origins of height fear: An evaluation of neoconditioning explanations. Behaviour Research and Therapy, 39, 185–199. Mineka, S. (1985). The frightful complexity of the origins of fears. In F. R. Brush, & J. B. Overmier, Affect, conditioning and cognition: Essays on the determinants of behavior (pp. 55–73). Erlbaum. Mineka, S., & Cook, M. (1986). Immunization against the observational conditioning of snake fear in rhesus monkeys. Journal of Abnormal Psychology, 95, 307–318. Mineka, S., & Zinbarg, R. (1991). Animal models of psychopathology. In C. E. Walker, Clinical psychology: Historical and research foundations (pp. 51–86). New York: Plenum Press. Mineka, S., & Zinbarg, R. (1995). Conditioning and ethological models of social phobia. In R. Heimberg, M. Liebowitz,
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D. Hope, & F. Schneier, Social phobia: Diagnosis, assessment and treatment (pp. 134–162). New York: Guilford Press. Mineka, S., & Zinbarg, R. (1996). Conditioning and ethological models of anxiety disorders: stress-in-dynamic-context anxiety models. In D. Hope, Perspectives on Anxiety, Panic, and Fear. 43rd Annual Nebraska Symposium on Motivation (pp. 135–211). Lincoln, NE: University of Nebraska Press. Mineka, S., & Zinbarg, R. (1998). Experimental approaches to understanding the mood and anxiety disorders. In J. Adair, D. Belanger, & K. Dion, Advances in psychological science: social, personal, and cultural aspects. Proceedings of the XXVI International Congress of Psychology (Vol. 1, pp. 429–454). Psychology Press. Mineka, S., Cook, M., & Miller, S. (1984). Fear conditioned with escapable and inescapable shock: Effects of a feedback stimulus. Journal of Experimental Psychology: Animal Behavior Processes, 10, 307–323. Mineka, S., Gunnar, M., & Champoux, M. (1986). Control and early socioemotional development: Infant rhesus monkeys reared in controllable versus uncontrollable environments. Child Development, 57, 1241–1256. Monroe, S. M. (1982). Assessment of life events. Archives of General Psychiatry, 39, 606–610. Mowrer, O. H., & Viek, P. (1948). An experimental analogue of fear from a sense of helplessness. Journal of Abnormal Social Psychology, 83, 193–200. ¨ hman, A., Dimberg, U., & O ¨ st, L.-G. (1985). Animal and social phobias: Biological constraints on learned fear O responses. In S. Reiss, & R. R. Bootzin, Theoretical issues in behavior therapy (pp. 123–178). New York: Academic Press. ¨ hman, A., & Soares, J. J. F. (1998). Emotional conditioning to masked stimuli: Expectancies for aversive outcomes O following nonrecognized fear-relevant stimuli. Journal of Experimental Psychology: General, 127, 69–82. ¨ hman, A., & Mineka, S. (2001). Fears, phobias, and preparedness: Toward an evolved module of fear learning. O Psychological Review. ¨ st, L-G., & Hugdahl, K. (1981). Acquisition of phobias and anxiety response patterns in clinical patients. Behaviour O Research and Therapy, 19, 439–447. Pavlov, I. P. (1927). Conditioned reflexes. London: Oxford University Press. Poulton, R., Davies, S., Menzies, R. G., Langley, J., & Silva, P. A. (1998). Evidence for a non-associative model of the acquisition of a fear of heights. Behaviour Research and Therapy, 36, 537–544. Poulton, R. & Menzies, R. G. (2002). Non-associative fear acquisition: A review of the evidence from retrospective and longitudinal research. Behaviour Research and Therapy, 40, 127–149. Poulton, R., Thomson, W. M., & Davies, S. et al. (1997). Good teeth, bad teeth and fear of the dentist. Behaviour Research and Therapy, 35, 327–334. Rachman, S. (1977). The conditioning theory of fear-acquisition: A critical examination. Behaviour Research and Therapy, 15, 375–387. Rachman, S. (1990). Fear and courage. New York: Freeman. Razran, G. (1961). The observable unconscious and the inferable conscious in current Soviet psychophysiology: Interoceptive conditioning, semantic conditioning, and the orienting reflex. Psychological Review, 68, 81–147. Rutter, M., Maughn, B., Pickles, A., & Simonoff, E. (1998). Retrospective recall recalled. In R. B. Cairns, L. R. Bergman, & J. Kagan, Methods and models for studying the individual (pp. 219–241). Thousand Oaks, CA: Sage. Schacter, D. L. (1996). Searching for memory: The brain, the mind and the past. New York: Basic Books. Schacter, D. L., Norman, K. A., & Koustaal, W. (1998). The cognitive neuroscience of constructive memory. In J. T. Spence, J. Darley, & D. J. Foss, Annual Review of Psychology (pp. 289–318). Palo Alto, CA: Annual Reviews. Seligman, M. E. P. (1971). Phobias and preparedness. Behavior Therapy, 2, 307–320. Taylor, J. E., Deane, F. P., & Podd, J. V. (1999). Stability of driving fear acquisition pathways over one year. Behaviour Research and Therapy, 37, 927–939. Usher, J. A., & Neisser, U. (1993). Childhood amnesia and the beginnings of memory for four real life events. Journal of Experimental Psychology: General, 122, 155–165.
Born to fear: non-associative vs associative factors in the etiology of phobias Susan Mineka a
¨ hman , Arne O
a,*
b
Department of Psychology, Northwestern University, 2029 Sheridan Road, Swift Hall #102, Evanston, IL 602082710, USA b Psychology Section, Department of Clinical Neuroscience, Karolinska Institute and Hospital, Z6, S-171 76 Stockholm, Sweden
Abstract Poulton and Menzies (Behaviour Research & Therapy 40 (2001) 127–149) review two lines of evidence as supporting a non-associative pathway to the origins of “evolutionary relevant phobias”. First, in retrospective studies of mode of onset some recall they have always had this fear. We review here solid evidence that retrospective recall is notoriously unreliable. Second, they note as many nonphobics recall relevant associative learning experiences as do phobics. We argue such studies are very inconclusive because they fail to consider many experiential and personality vulnerability (and invulnerability) factors that strongly impact the outcome of any putative learning experience. Their argument also does not explain the transition from developmental fears to phobias that is central to their thesis. Overall, we call for major methodological improvements in this area, in the context of theoretical developments pointing to interacting vulnerability and invulnerability factors. 2002 Elsevier Science Ltd. All rights reserved.
Most theories of phobias have taken the seemingly logical route of postulating causal factors such as traumatic events or conditioning episodes to explain the emergence of this relatively common (10–12% of the population) condition. Poulton and Menzies, however, invert this logic by claiming that phobias result not from the presence of positively defined causal factors in the life history of individuals, but rather from the absence of such factors. In particular they argue that phobias result from innate fears shared by all humans. Adult phobias, therefore, are either a result of an enhanced genetic readiness in some individuals to fear particular situations, or reflect a deficit in the (presumably genetically given) mechanisms to get rid of fear responses, such as habituation.
* Corresponding author. E-mail address: [email protected] (S. Mineka).
0005-7967/02/$ - see front matter 2002 Elsevier Science Ltd. All rights reserved. PII: S 0 0 0 5 - 7 9 6 7 ( 0 1 ) 0 0 0 5 0 - X
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To support empirically their position, Poulton and Menzies review a literature consisting of studies that rely very heavily on retrospective recall. They take these studies as showing the absence of conditioning episodes in most phobics who have what they call evolutionary relevant phobias. We may note initially that this is an awkward claim that comes close to the statistical problem of proving the null hypothesis. Logically, it is easier to prove that something has happened than to prove that something has not happened. In the former case any problems of measurement work against the hypothesis, which should give added weight to positive findings. When trying to prove that something has not happened, however, measures that are too insensitive to register an event can provide what falsely is interpreted as support for the hypothesis that no event was present. Thus, one may conclude that there is no evidence of triggering events or conditioning episodes in the life history of a phobic for the simple reason that the method one uses to assess such events lacks the power to pick them up. In this commentary, we start out by discussing the theoretically central thesis of Poulton and Menzies that phobias reflect innate fears from the perspective of what we know about the ontogenesis of fear. We then go on to analyze the methodological soundness of the data base that Poulton and Menzies adduce in support of their theory. We conclude that this theory suffers from logical problems, and remains theoretically unconvincing. Furthermore, the data that are invoked in its support suffer from severe reliability problems that, in effect, provide what falsely appears to be support for the theory. Thus, we do not take the non-associative account as a viable alternative to conditioning (and Rachman’s three pathways) theory as a primary explanation of phobias (Rachman 1977, 1990). At most it may be a fourth pathway to fear, albeit a problematic one from several standpoints. 1. Associative versus nonassociative pathways to fear/phobia acquisition Poulton and Menzies build on earlier work by Menzies and Clarke (1993, 1995) who first argued that non-associative pathways for evolutionary-relevant fears (such as heights and water) provide a superior account for the origins of such fears and phobias. Their strong thesis is that “a non-associative model can provide a more satisfactory account of fear phenomena than conditioning theory” (Poulton & Menzies, 2002) and in many places the authors fail to qualify such broad statements with appropriate caveats (such as that this pathway could only possibly account for a minority of phobias). Their weaker thesis is that a non-associative pathway to fear acquisition constitutes a fourth pathway, adding to the three pathways proposed by Rachman and others. The first of their lines of argument for either of these positions is that the studies they review reveal that some of those reporting fears or phobias of water and heights cannot recall a specific mode of onset and report only that they “always had this fear” or that they “cannot remember”. 1.1. Developmental fears versus phobias The idea that some developmental (or prepotent) fears (as they are often called) are innate (or instinctive) is certainly not new and is indeed widely accepted (e.g., Craske, 1998; Marks, 1987; ¨ hman, Dimberg, & O ¨ st, 1985). Such fears would include height fear, stranger fear, and separO ation anxiety as discussed by Poulton and Menzies (as well as fear of loud noises, the darkness
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and small animals which emerge at different ages) (see Craske, 1998; Marks, 1987). However, the stimuli which evoke such developmental fears constitute only a minority of adult phobias, some of the most common of which are illness/injury, storm, animals and heights (Agras, Sylvester, & Oliveau, 1969).1 Moreover, developmental fears do not generally become phobias but rather are usually outgrown. Poulton and Menzies argue that the adults who have fears or phobias are either the ones whose early fears have failed to habituate (perhaps because of temperamental/personality variables or inadequate exposure), or the ones whose early fear has habituated, but has later become dishabituated through exposure to nonspecific stressors. Although these arguments might be plausible regarding the maintenance or reemergence of a developmental fear, they fail to address why some develop phobias — which are far more intense and disabling than most developmental fears. For example, as noted by Poulton and Menzies virtually every child avoids the deep end in the visual cliff test. However, this avoidance response occurs in the absence of the intense fear reactions seen in a height phobic forced to enter a sixth-floor balcony. One logical possiblity is that adult height phobics have had phobic levels of fear since early childhood, but to be valid such claims must be confirmed, for instance, by parental reports. Any such evidence, however, is not cited by Poulton and Menzies — probably because it does not exist (Ollendick, personal communication, 8/29/00). To us a plausible alternative is that specific negative experiences are likely to play a role in this transition from developmental fears to phobias for the small percent of phobias that may originate from developmental fears. Moreover, because individuals in this category may already have a certain level of fear (i.e., because they are non-habituators), or have habituated or extinguished fear remaining latent (as all extinguished or habituated fears probably are) (cf. Bouton, 1994), it may not take a great deal of negative input to raise the level of fear to a phobia (cf., ¨ hman, 1994; O ¨ hman & Soares, 1998; Seligman, 1971, for disEsteves, Parra, Dimberg, & O cussions of need for only degraded input when dealing with prepared fear learning). Regarding the importance of experiential factors, researchers should be aware that the best behavior genetic evidence shows that although specific phobias have a moderate heritability, there is also a large portion of variance (40–60%) that needs to be accounted for by unique, nonshared environmental factors (Kendler, Neale, Kessler, Heath, & Eaves, 1992; Kendler, Karkowski, & Prescott, 1999). We also note that the evidence cited in studies of height and water fear/phobia at best suggests that a nonassociative pathway is relevant in only a minority of cases. For example, in a study of height fearful students (Menzies & Clarke, 1993) only 30% reported that “it had always been this way” (vs 58% in the associative learning categories combined)2 and a similar study of height phobics reported that only 39% fit in the same non-associative category (Menzies & Clarke, 1995). 1.2. What does it mean when nonphobics and phobics do not differ on prior potential conditioning events? Poulton and Menzies’ second primary argument against associative accounts of fear (or phobia) acquisition comes from studies on this topic that have included nonfearful or nonphobic control 1 Interestingly, water phobia, discussed extensively by Poulton and Menzies as an evolutionary fear, is not even listed among the most common phobias in three major literature reviews we searched (Barlow, 1988; Craske, 1998; Marks, 1987). Moreover, it also seems there is no early widely shared developmental fear of water that is at all analagous to the visual cliff phenomenon for height fear/phobia (Ollendick, personal communication, 8/29/00). 2 See discussion later of interoceptive conditioning for why we included “nonconditioning traumatic events” in this category.
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groups. These studies have often found that such nonfearful individuals often report as high or higher rates of traumatic conditioning experiences (direct or indirect or instructional) as do the fearfuls or phobics (e.g., Di Nardo, Guzy, & Bak, 1988; Menzies & Clarke 1993, 1995). Such results have led Poulton and Menzies and others to conclude that the conditioning incidents must not have truly played a causal role for the fearfuls or phobics. However, we have discussed extensively elsewhere that such an argument fails to consider the impact of a wide range of temperamental variables and experiential differences on which individuals undergoing the same trauma are very likely to differ (e.g., Mineka, 1985; Mineka & Zinbarg 1991, 1995, 1996, 1998). For example, a range of theorists from Pavlov (1927) to Eysenck, Kagan, and Gray have all noted individual differences in personality/temperament which affect the speed and strength of conditioning.3 In addition, Mineka and Zinbarg also noted a wide range of experiential differences across individuals that have a major impact on the outcome of direct or indirect conditioning experiences (and therefore why many without phobias will have such histories that theoretically involved conditioning events). Thus these personality and experiential factors may serve as diatheses or vulnerability factors for the development of phobias in certain individuals given appropriate experiential input, just as certain individuals with a variety of diatheses will be more likely than those without the vulnerabilities to develop major depression in response to major life stress (e.g., Monroe & Simons, 1991). One example illustrating these points stems from an experiment by Mineka and Cook (1986) who noted that prior exposure to nonfearful model monkeys behaving nonfearfully with snakes effectively prevented the acquisition of snake fear following later exposure to fearful models behaving fearfully with snakes; moreover this effect was somewhat larger than the effect of latent inhibition (simple exposure to the snakes by themselves). Thus researchers in this area should not only pay attention to whether children have a good deal of experience with, say, heights or water, but also whether they had prior exposure to nonfearful models (e.g., Graham & Gaffan, 1997, found first-born children were more likely to be fearful of water than later born children, presumably because the latter had more opportunity for observational learning of competence and nonfearful behavior). A second example comes from an experiment by Mineka, Gunnar and Champoux (1986) who found that infant monkeys reared with a sense of mastery and control over their environments habituated more quickly to frightening events than did monkeys reared in identical environments except without the experiences with control. Such experimental evidence supports propositions long made by developmental psychologists based on correlational data that infants and children raised in environments where they gain a sense of mastery and control over their environment are less frightened by novel events and better able to cope with frightening situations. Thus, children (or adults) raised with a sense of mastery or control (high self-efficacy) over their environments should be less susceptible to developing fears given identical negative
3 We also note that at least one study reviewed by Poulton and Menzies (Menzies & Parker, 2001) has now added measures of high trait anxiety in their fearful or phobic samples and has not found that the phobics were higher in trait anxiety than the nonphobics. However, the Mineka and Zinbarg model does not predict that all (or even a majority) of phobics will have high levels of trait anxiety or neuroticism; rather, they predict that among those who are high on this personality characteristic and are exposed to the appropriate negative experiential input, fears or phobias will be acquired more readily than among those low on this personalitiy characteristic. That is there should be an interaction between level of trait anxiety or neuroticism at the time of negative experiential input.
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environmental input than are children reared without such a sense of mastery or control (low selfefficacy). (See also Chorpita & Barlow, 1998.) Mineka and Zinbarg (1996, 1998) also discussed how several aspects of the conditioning event itself have a strong impact on how much fear is acquired. For example, having control over a traumatic event itself (such as being able to escape or avoid it) has a major impact on how much fear is conditioned to neutral stimuli paired with that traumatic event, with far less fear being conditioned when the aversive event is controllable than when it is uncontrollable (e.g., Mineka, Cook, & Miller, 1984; Mowrer & Viek, 1948; see Craske, Miller, Rotunda, & Barlow, 1990, for a relevant human study). Additionally, the nature of the object or situation that is paired with negative experiential input must also be taken into consideration when predicting whether fear acquisition will occur. Specifically, evolutionarily fear-relevant (or prepared) stimuli have been shown to support more robust fear acquisition in the laboratory than do fear-irrelevant stimuli ¨ hman et al., 1985; O ¨ hman & Mineka, in press).4 Finally, each of these (and other) experien(e.g., O tial variables and temperamental variables generally should not be seen as operating in isolation (i.e., not as main effects) but rather in a dynamic interaction with each other. That is, they are “stress-in-dynamic-context” models of fear/phobia acquisition rather than the “stress-in-total-isolation” models provided by most researchers and theorists in this area (Mineka & Zinbarg 1996, 1998). Thus, in light of the stress-in-dynamic-context model, studies that have compared rates of traumatic direct or indirect conditioning histories in phobic and nonphobic individuals and found no differences are completely inconclusive. This is because they have generally neglected to include any measures of most of such individual difference variables (with the recent exception of latent inhibition in a few studies) that might account, singly, or more likely in combination, for why only some individuals undergoing a trauma developed a fear or phobia. (See Graham & Gaffan, 1997, for one study that had a more sophisticated approach to understanding multiple interacting causal pathways.) Moreover, somewhat paradoxically it seems quite likely that nonfearful individuals would be expected to be more likely to experience traumas precisely because they are not fearful and therefore are more likely to encounter potentially phobic objects or situations, which in turn could provide the occasion for possible traumas. For example, someone who is not afraid of water (or actually likes it) is much more likely to go swimming or boating and get involved in a water accident than is someone who is more neutral or even mildly cautious about water by virtue of having little direct or vicarious experience with it. Yet because of the nonfearful person’s prior exposure (leading to latent inhibition or immunization) s/he would not be as likely to develop a fear/phobia after such an accident as someone without the prior exposure. Thus, it is not necessarily surprising that some studies have found more nonfearful individuals recalling traumatic incidents than fearful individuals do because the nonfearfuls actually may have had more of them. In summary, we have no argument with the notion that children have a variety of developmental fears, most of which may be largely innate. However, we do not agree with Poulton and Menzies that there is any sound basis on which to conclude that such developmental fears provide a causal pathway to most adult phobias. Moreover, the fact that control groups of nonfearful individuals 4 Although Poulton and Menzies also discuss evolutionary relevant fears as the ones their nonassociative model applies to, they are discussing innate/developmental fears which require only maturational variables for their development. By contrast, prepared fears by definition require at least some amount of negative experiential input to emerge.
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sometimes have a greater likelihood of having had relevant traumatic experiences than have phobics does not surprise us. There are wide individual differences (both personality and experiential) which determine the outcome of a conditioning event (direct, vicarious or informational) and nonfearful individuals are undoubtedly more likely to experience such traumas than are those who are neutral or mildly cautious initially (perhaps because they have not had many nonfearful parental or sibling models, cf. Graham & Gaffan, 1997). 2. Problems with the non-associative account 2.1. The definition of conditioning: measurement and assessment issues The results of the studies reviewed could only possibly be as informative as the questionnaires/interviews used to assess individuals’ past experiences (and non-experiences). One primary problem in this regard is that researchers in this area who follow the admonitions of Menzies and Clarke (1995) (see also Poulton & Menzies, 2002) to adhere to their old strict textbook definitions of classical conditioning are clearly not aware of current developments in learning that render some of these definitions outmoded. Such old definitions require that the person be able to recall a completely neutral arbitrary stimulus (CS), that initially elicits no fear whatsoever, as well as a completely arbitrary (UCS) that also must be external and identifiable and with which the CS has been paired. We now cite several such relevant examples of problems with such definitions. In the conditioning literature there are now numerous instances (and likely many more when conditioning occurs in nature) where the CS is not entirely neutral and yet supports associative conditioning. For example, a weak shock or small amount of food (hardly entirely neutral) can serve as a CS for a more intense shock or large amount of food, respectively (e.g., Crowell, 1974; Goddard, 1999). These and other examples like it are often known as US– US conditioning (see Bouton, Mineka, & Barlow, 2001, for a review of definitional issues in conditioning). Another problem with Menzies and Clarke’s definition is that they have excluded from a conditioning category of onset those cases where phobics who could not recall a specific stimulus (UCS) that triggered the fear/panic response (or nonconditioning traumatic event as Poulton and Menzies refer to it) that they had had in the presence of their now phobic object. They argued that such experiences as the basis of the origin of a fear or phobia should be classified as nonas¨ st & Hugdahl, 1981, for a study sociative in nature because of the failure to identify a UCS (see O that included such cases). We strongly disagree because this position does not acknowledge the strong likelihood that such cases do not involve exteroceptive UCSs, but instead involve interoceptive UCSs (which stimulate internal sensory receptors in the gut, lungs, etc.). Interoceptive conditioning was carefully studied early on by the Soviets (e.g., Razran, 1961) but is poorly understood (and generally not recognized) by contemporary clinical researchers. CSs and UCSs can be either interoceptive or exteroceptive in nature, with all four possible combinations of CSs and UCSs producing reliable conditioning; indeed Razran’s (1961) review of the Soviet evidence suggested that interoceptive conditioning is more robust than exteroceptive conditioning and is unconscious in nature. In the case of phobias, this means that the alleged non-associative pathway (Menzies & Clarke 1993, 1995) when subjects can only recall a fear/panic response (but no
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identifiable UCS) is indeed an associative pathway — an example of exteroceptive (CS)–interoceptive (UCS) conditioning (e.g., Barlow, 1988; Bouton et al., 2001; Forsyth & Eifert, 1996; Mineka & Zinbarg, 1996). A related problem with some of the studies reviewed by Poulton and Menzies involves the way researchers have sometimes operationalized what constitutes a UCS in particular studies. Not only can UCSs be interoceptive and unconscious in nature as discussed above, but a UCS also must produce a potentially measurable response (UCR). Thus when Poulton, Thomson, Davies et al. (1997) operationalized the unconditioned stimulus in studies of dental phobia, they used the caries (cavities) level of the children’s teeth as the measure of the intensity of the UCS and UCR (and thereby the opportunity for direct conditioning to take place). Yet this is at best a very imperfect measure of the UCSs and UCRs experienced by a child, both because of individual differences in pain sensitivity and in reactivity to anaesthesia (or even the dentists’ use/nonuse of anaesthesia). Moreover, in their studies of height fear, Poulton, Davies, Menzies, Langley, & Silva (1998) operationalized exposure to a UCS as having a severe fall from a height (i.e., only those leading to a fracture, dislocation, laceration or intracranial injury). This is an overly restrictive definition because even relatively minor falls often create serious distress in children. In summary, there are problems with the instruments used in many of the studies reviewed regarding both definitional issues of what qualifies as a CS and as a UCS, and also in the way certain UCSs are operationalized in terms of being too stringent (e.g., severe falls) or too imprecise (e.g., caries level). 2.2. Unreliability of retrospective recall The second major problem we see in studies supporting the non-associative viewpoint (although to a considerable degree the associative viewpoint as well) concerns the unreliability of retrospective recall. This problem is acknowledged by Poulton and Menzies and by the authors of many of the studies they review, but it is our belief that all these investigators seriously underestimate the degree of these problems, generally only paying lip service to them in their papers. This is a well recognized problem in the stressful life-event literature, in which it is often reported that as much as about half the events are forgotten over a one-year period (e.g., Monroe, 1982), and as a consequence it is often recommended that the required recall intervals should not exceed six months. Unfortunately, however, very few have attempted to estimate the magnitude of this problem with regard to events relevant for fear and anxiety. One exception is a recent study by Taylor, Deane, and Podd (1999) on acquisition of driving fear who found that “retrospective accounts of fear onset may be quite unstable over time” (p. 927). This study provided a one year follow-up to an earlier one in which subjects were assessed for the origins of their fear using a modified version of Menzies and Clarke’s Origins Questionnaire (Menzies & Clarke, 1993). When the phobics were reassessed one year later (using a shorter modified OQ), Taylor et al. found that only 54% of pathway classifications remained the same, with 46% making different pathway ascriptions at one-year follow-up! Moreover, the highest proportion of change occurred within the “cannot remember” group where only 18% of the respondents stayed within this category. This result should of course be replicated in other studies to confirm its reliability but it gives a strong suggestion as to the magnitude of the problem. Some also have suggested the need for corroboration of self-report by others (e.g., Kleinknecht,
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1994). As concrete examples, Kleinknecht reported two case studies of adult injection phobics who had been phobic as long as they could recall, with no memory for any kind of acute onset. However, upon soliciting information from the parents of these two phobics, the parents had very distinct and credible memories of the onset of their (then) child’s phobia. Although the phobics would have been classified in any of the studies in this area as in the “no recall” or “always been this way” (nonassociative) categories, parental reports made it clear this would have been inaccurate and misleading. Another very carefully done prospective and retrospective study of many types of childhood events and family experiences assessed the agreement of retrospective recall at age 18 for childhood variables with the children’s actual recall at ages 9, 11, 13 and 15 of what had happened in the previous two years (i.e., two year retrospective data in a prospective study) (Henry, Moffitt, Caspi, Langley, & Silva, 1994). In the case of memory for childhood major injuries (which could occasion the conditioning of certain fears), the correlation between the retrospective reports at 18 and the actual number of injuries reported at ages 9, 11, 13 and 15 was only 0.42. Moreover, the age 18 retrospective reports were only moderately more accurate than chance alone (=0.34), which provides a far from ringing endorsement of the retrospective methods used in this kind of research on the origins of fears. Finally, a recent study by Kendler et al. (1999) assessed both the short-term and long-term reliability of life-time phobic diagnoses in their large study of female twins. Short-term reliability was obtained for only 192 twin pairs approximately one month after their initial interview and diagnosis; reliability for the diagnosis of specific phobia over the short term was moderate (=0.46). Long-term reliability was assessed 8 years after the initial interview (for 86% of the original sample of 2293 twin pairs) and was only modest (=0.30). When diagnoses are this unreliable over both brief and long term periods, even when using structured interviews, further questions are raised about the usefulness of all the studies such as those reviewed by Poulton and Menzies. Indeed, given all these serious limitations we are somewhat puzzled by why such studies have proliferated at such a rapid pace in recent years. 2.2.1. Superiority of prospective studies? It should also be emphasized that the supposed superiority of the prospective studies by Poulton and his colleagues reviewed here is of somewhat questionable significance (especially unless corroborated by parental reports). As already noted, prospective studies necessarily can only assess subjects every few years and thus they simply rely on shorter-term retrospective recall than the so-called retrospective studies (see also Rutter, Maughn, Pickles, & Simonoff, 1998). However, some of the studies reviewed above suggest the decay in reliability of memories may primarily occur in a matter of weeks or months rather than years. (See also Schacter, 1996). 2.2.2. Characteristics of acquisition that reduce memorability Another relevant issue raised by several authors is that phobias may represent the outcome not of one-trial learning experiences but rather of cumulative more minor experiences that are not very memorable (e.g., Craske, 1998; Graham & Gaffan, 1997). Or in some cases they may be the outcome of second order or sensory preconditioning experiences where the first order pathway may be unmemorable (e.g., Mineka, 1985; Cook & Mineka, 1987). In yet other cases a phobic level fear may be reached following a UCS inflation experience in which memory of the original
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UCS (involved in minor fear conditioning) is altered by subsequent experience with a more intense version of the UCS (not paired with the CS) (e.g., Davey, de Jong, & Tallis, 1993; Mineka, 1985; Mineka & Zinbarg, 1996). Because the more intense UCS was never directly paired with the CS the memorability of this associative pathway to conditioned fear would be very low. 2.2.3. Memory distortions over time In addition to the well-known unreliability of memory simply with the passage of time, there is also now a great deal of research showing how memories often become distorted with the passage of time. Human memory is a constructive process and highly subject to modification or revision based on experiences (including questions and comments by others) happening after an original memory trace was established (e.g, Loftus, Feldman, & Dashiell, 1995; Schacter, Norman, & Koustaal, 1998). Even flashbulb memories of extraordinarily memorable historic events, as well as personally traumatic memories, are subject to distortion over time (see Schacter, 1996, Chapter 7). Thus, the unreliability of retrospective recall is a function of both decay or inadequate retrieval cues, as well as the distortions of memory that can occur due to intervening experiences. Finally, when it comes to memory of early childhood events there is an additional problem of childhood amnesia (cf. Usher & Neisser, 1993) for such events which may further complicate matters in the case of very early onset (see Kleinknecht, 1994). 2.2.4. Explicit vs implicit memories? We also find it surprising that researchers in this area have not considered that many phobic responses may be examples of implicit rather than explicit memory. Implicit memory, by definition, is not available for conscious introspection while explicit memory can be (given adequate retrieval cues). As Kihlstrom, Mulvaney, Tobias, and Tobis (1999) explain it: “emotional response can serve as an index of implicit memory. That is, subjects can display emotional responses that are attributable to some event in their past history, in the absence of conscious recollection of that event”. They cite a case by Bagby (1928) of a woman with a phobia for running water. The person had no memory for how this intense response was acquired but when an aunt visited, the story emerged. As a girl the woman had gone on a picnic with the aunt; the child had strayed and became trapped under a waterfall. The aunt rescued the girl and promised to keep her transgression (straying contrary to instructions) a secret. Conscious memory for the incident was lost but the phobia remained intense — an example of implicit memory (Kihlstrom et al., 1999). (See also Schacter, 1996). This type of dissociation between emotional and conscious memories can be accounted for by the fact that these types of memories are encoded in two independent memory circuits of the brain, one emotional and centered on the amygdala and another cognitive and conscious centered on the hippocampus (LaBar & LeDoux, 2000; LeDoux, 1996). In summary, even if the logic of the non-associative account of phobia acquisition was plausible for more than a few phobias, there are so many problems with the reliance all of these studies place on retrospective recall that these studies seem largely uninformative. Note that this critique of such studies applies to their usefulness in studies supporting both non-associative and associative accounts of the origins of phobias. However, as argued in the introduction, methodological hazards do not risk to generate false support for the associative account to the same degree that they do for the non-associative account.
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3. Conclusions In this commentary we have argued that as currently articulated the non-associative account of phobia acquisition reviewed by Poulton and Menzies remains unconvincing as an explanation for how the vast majority of, and quite possibly all, phobias develop. At least presently it does not account for the transitions from fears to phobias even for so-called evolutionary relevant phobias, and has difficulty explaining why such phobias are not rather common. Poulton and Menzies also critique associative accounts of phobia acquisition because of findings that as many (or even more) nonphobics recall associative learning experiences as do phobics. However, such studies are seriously flawed, in part because they do not take into account the dynamic context in which aversive experiences occur that strongly impact the outcome of those experiences. In all the psychological disorders that we can think of where stress plays a role in precipitating onset (ranging from schizophrenia to major depression and post-traumatic stress disorder), it is well known that the stress only has this effect in people with certain biological or experiential vulnerabilities. Moreover, other people may have various sources of invulnerability or protective factors which render them unlikely to develop the disorder (e.g., see Carson, Butcher, & Mineka, 2000, for relevant examples). Why this fact has been ignored by phobia researchers for so long is simply astonishing to us. Finally, we also find it unfortunate that insufficient attention has been paid to the major shortcomings of the kinds of studies being done in this area — whether they support non-associative or associative accounts of phobia acquisition. Problems with the unreliability of retrospective recall, especially when it is generally many years after the alleged experience took place (or even several years in prospective studies), are widely known in cognitive psychology; these issues should be far better understood by clinical researchers. We hope that the points raised here will cause researchers in this area to pause before they continue with this line of research — no matter which positions they are taking — unless major improvements in methodology can be developed and theoretical advances as to the nature of interacting causal factors can be explored.
Acknowledgements We thank John Kihlstrom, Kevin LaBar, Tom Ollendick, and Paul Reber for their comments during the preparation of this manuscript.
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