When asked to recall specific autobiographical memories of events with a duration of less than 1 day in response to word cues, people sometimes produce overly general responses. For example, the cue “vacation” might prompt the generic recollection “I enjoyed all of my vacations as a child” instead of the required specific response “I remember the day that we went to Disneyland last year.” Williams and Broadbent (1986) serendipitously discovered that this difficulty in producing specific memories was more widespread in their group of depressed parasuicide patients than in a matched control sample. Since this initial study, reduced autobiographical memory specificity (AMS) has been found to be a characteristic of performance on this particular task (the Autobiographical Memory Test [AMT]; Williams & Broadbent, 1986) in a number of clinical groups. These include individuals suffering from clinical depression (e.g., Brewin, Reynolds, & Tata, 1999; Brittlebank, Scott, Williams, & Ferrier, 1993; Kuyken & Dalgleish, 1995; Wessel, Meeren, Peeters, Arntz, & Merckelbach, 2001), posttraumatic stress disorder (PTSD; e.g., McNally, Litz, Prassas, Shin, & Weathers, 1994), acute stress disorder (e.g., Harvey, Bryant, & Dang, 1998), eating disorders (e.g., Dalgleish et al., 2003), and borderline personality disorder (e.g., Startup et al., 2001). Furthermore, reduced AMS has been found to be associated with levels of subclinical depressed mood in both naturalistic (e.g., Ramponi, Barnard, & Nimmo-Smith, 2004) and mood-induction studies (e.g., Au Yeung, Dalgleish, Golden, & Schartau, 2006).
A number of key findings have suggested that reduced AMS is more than simply a cognitive curiosity. Instead, the data indicate that reduced AMS indexes one or more fundamental cognitive processes closely linked to the onset, maintenance, and recovery from a variety of clinical and subclinical states.
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The first such key finding was initially reported by Brittlebank et al. (1993), who showed that reduced AMS predicted later clinical recovery in individuals with major depressive disorder, over and above initial levels of depressive symptoms. This longitudinal effect has been replicated in other depressed samples (e.g., Dalgleish, Spinks, Yiend, & Kuyken, 2001; Hipwell, Reynolds, & Pitts Crick, 2004; Mackinger, Loschin, & Leibetseder, 2000; but see Brewin et al., 1999). Similarly, Harvey et al. (1998) found that reduced AMS posttrauma in motor vehicle accident survivors predicted higher later levels of posttraumatic distress (but see Kangas, Henry, & Bryant, 2005).
The second key finding is that participants in Brittlebank et al.’s (1993) study who recovered from depression still showed reduced AMS relative to control participants, indicating that reduced AMS is a stable marker in recovered or remitted clinical groups and not just a function of acute depressive symptomatology. This was demonstrated more systematically by Mackinger, Pachinger, Leibetseder, and Fartacek (2000), who compared never-depressed and recovered-depressed women on the AMT and found relatively reduced AMS in the recovered sample.
Finally, reduced AMS has been shown to relate to impoverished problem-solving ability, with participants low in specificity finding it difficult to generate solutions on social problem-solving tasks (e.g., Goddard, Dritschel, & Burton, 1996). This fact, along with the related finding that reduced AMS is associated with a difficulty in generating specific simulations of the future (Williams, Ellis, Tyers, MacLeod, & Rose, 1996), suggests that reduced AMS is of potential clinical significance when considering impairments in day-to-day cognitive functioning in some patient groups.
Taken together these key findings suggest that a better understanding of the psychological processes involved in reducing AMS will yield insight into cognitive factors implicated in the onset and maintenance of depressed mood, clinical depression, and other psychopathological states as well as day-to-day cognitive impairments associated with a range of clinical disorders.
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Theoretical attempts to understand the source of reduced AMS in the affective science and abnormal psychology literature have been strongly influenced by another aspect of the AMS data—the relationship between reduced AMS and a history of trauma. The prototypical study in this area was by Kuyken and Brewin (1995), who examined AMT performance in depressed women with and without a reported history of childhood abuse. Women with a history of abuse showed reduced AMS relative to those women who had not been abused. Furthermore, increased levels of current intrusion and avoidance symptoms concerning the abuse correlated positively with the reduction in AMS. Since this initial study, this relationship between reduced AMS and both a history of trauma and greater intrusive and avoidant symptomatology following trauma has been replicated several times and for various kinds of traumatic experience (e.g., Dalgleish et al., 2003; de Decker, Hermans, Raes, & Eelen, 2003; Henderson, Hargreaves, Gregory, & Williams, 2002; though see Kuyken, Howell, & Dalgleish, 2006).
Building on these findings, the most consensual theoretical explanation of reduced AMS to date has been the affect regulation hypothesis (Williams, Stiles, & Shapiro, 1999). The affect regulation hypothesis accounts for reduced AMS in terms of difficulties in searching a self-memory system (M. A. Conway & Pleydell-Pearce, 2000). The proposal is that to recall a specific autobiographical memory to a cue word, one’s first step is to generate a restricted set of categorical descriptors constrained by the cue word. These descriptors are then used to search the memory system for memories that relate to that cue word. Subsequent sets of descriptors are then generated iteratively, allowing an increasingly refined search of this categorical subset of memories in order to retrieve specific episodes that comply with the task instructions. Williams, Stiles, and Shapiro (1999) proposed that to progress beyond the categorical descriptor stage during memory search to a more refined interrogation of the specific memory database, one must inhibit unneeded categorical descriptors in some way.1 Failure to inhibit these descriptors, it is proposed, will lead to the generation of overly general responses (reduced AMS) to cue words.
Williams has further suggested that children learn to inhibit irrelevant descriptors during memory search as a function of normal development but that trauma in childhood impairs this learning (Williams et al., in press). The heart of the affect regulation hypothesis is that painful emotional information is avoided by aborting memory search processes at a nonspecific level of analysis. Consequently, the argument goes, individuals with a history of childhood trauma will be less able to inhibit categorical descriptors during memory search and will therefore produce relatively reduced AMS on the AMT. As childhood trauma is a key correlate of depression and other clinical states (e.g., Boudewyn & Liem, 1995), the affect regulation hypothesis provides a plausible account of reduced AMS in a range of clinical conditions.
Although the affect regulation hypothesis has clear face validity as an account of reduced AMS, it seems unlikely to be a complete account. For example, it is difficult to see how the affect regulation hypothesis can offer a plausible conceptualization of reduced AMS following a negative mood induction in healthy individuals with no history of depression (Au Yeung et al., 2006) or in healthy individuals following category generation on related themes (Barnard, Watkins, & Ramponi, 2006). An additional or possibly alternative explanation for reduced AMS, and one that has the benefit of parsimony in that it is consistent with the wider theoretical literature on depression (and indeed other forms of emotional disorder), is that the phenomenon results from relatively poor executive or attentional control on the part of depressed individuals in the face of a cognitively demanding task—in this case the AMT.
Although there is limited consensus about exactly which cognitive operations fall under the rubric of executive control, let alone about which processes might underpin executive control within a psychological system (see Miyake & Shah, 1999, Question 2), it is generally agreed that executive control broadly encapsulates the set of cognitive processes that are responsible for the planning, initiation, sequencing, and monitoring of complex goal-directed behavior in the face of distracting information. Relatively impaired executive control in depression is a key empirical finding in the literature (see Burt, Zembar, & Niederehe, 1995; Hartlage, Alloy, Vazquez, & Dykman, 1993, for reviews) and a prominent feature of a number of influential theoretical models of the disorder (Barrett, Tugade, & Engle, 2004; Ellis & Ashbrook, 1988; Hasher & Zacks, 1979; Hertel & Rude, 1991).2
A prototypical model of impaired executive control in depression has been articulated by Hertel and colleagues (e.g., Hertel & Hardin, 1990; Hertel & Rude, 1991; see Hertel, 2000, for an overview) in their cognitive-initiative account. The central thesis of the cognitive-initiative approach is that where executive control processes are poorly constrained by a given task (for example the AMT), depressed individuals should exhibit impaired performance due to a deficit in the ability to initiate relevant strategies or generate appropriate hypotheses when performing the task. Within this type of executive control framework, reduced AMS on the AMT may be a consequence of impoverished retrieval strategies during memory search in certain individuals or groups, a difficulty in maintaining or applying the task instructions to be specific during the task itself, and/or problems with inhibiting inappropriate (i.e., overgeneral) candidate memory responses on the task.
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It is interesting to note that in the same essay in which Williams (1996) proposed the affect regulation hypothesis he also highlighted a putative role for executive processes in defining the reduced AMS effect. It was assumed that once memory search had been aborted, further iterations of the retrieval process would give rise to the activation of other intermediate descriptions. After a number of such iterations a more highly elaborated network of categoric memories would exist so that, under conditions in which executive control was compromised, such information would be more likely to be generated as responses on future memory searches (Williams, 1996).
Despite these predictions, a clear empirical link between reduced AMS and executive control has yet to be established. The results from the handful of studies relevant to this issue have generally been negative, mixed, or inconclusive. For example, Williams and Broadbent (1986) found that reduced AMS was not associated with category fluency (for vegetables or boys’ names) or processing speed (the time taken to judge a series of 50 “silly sentences” as true or false; Baddeley, Emslie, & Nimmo-Smith, 1992). Other studies found a negative association between performance in a word fluency task and reduced AMS (e.g., Williams & Dritschel, 1992). Still others indicated some role for general cognitive ability (including executive control processes) in AMT performance but have suggested that such processes offer a far-from-complete explanation of the reduced AMS effect. For example, Park, Goodyer, and Teasdale (2002) matched two samples of adolescents for IQ but still found that individuals in the depressed group gave significantly fewer specific responses. Similarly, Wessel et al. (2001) found that educational level contributed significantly to the prediction of AMS but that between-group differences remained after controlling for this variable.
One reason for the equivocal nature of the findings to date may be that the research seeking to account for the reduced AMS effect has not focused clearly enough or exclusively on tasks that load heavily on executive control. In fact, depression (and indeed other forms of psychopathology) does not seem to be associated with impairments on all forms of cognitive task but rather seems to relate specifically to tasks in which effective executive control is particularly important (e.g., Hartlage et al., 1993). The rationale for the present series of studies was therefore to investigate systematically for the first time the extent to which reduced AMS on the AMT is an example of poor task performance on a paradigm that loads significantly on executive control and that is associated with depressed mood and/or various clinical states.
To this end, in the first study we sought to examine, through reanalysis of existing data in patients with eating disorders, the relationship between AMT performance and verbal fluency—a classic executive control measure (Rosen & Engle, 1997). We also included a mediational analysis in Study 1 in order to investigate whether the relationship between both an eating disorder diagnosis and depressed mood, on the one hand, and reduced AMS, on the other, was significantly accounted for by verbal fluency scores.
The aim behind Studies 2-4 was to further establish a nomological net (Cronbach & Meehl, 1955) for the AMT by demonstrating a clear relationship (independent of depression) between AMT performance and performance on other nonautobiographical and generally emotion-unrelated tasks that themselves depend on executive control processes. In these three studies we therefore exploited naturally occurring individual differences in executive control capabilities in unselected samples to establish the existence of such a relationship, and in each case depressed mood was included as a covariate in the key analyses.
Having established that the AMT is a task associated with other executive control measures independent of depression (Studies 1-4) and that executive control mediates the relationship between depression (as well as eating disorder diagnosis) and reduced AMS in a clinical sample, in Studies 5-8 we sought to further show that the diminished executive control routinely associated with depressed mood (e.g., Hartlage et al., 1993) is an important factor in determining the patterns of AMT performance in depression. To do this we first replicated the significant association between depressed mood and AMT performance in a stratified dysphoric sample, using the standard version of the AMT from the extant literature (Study 5). We then manipulated the task parameters of this standard AMT in ways that would interact with individual differences in executive control (such as those that occur naturally in correspondence with individual differences in levels of depressed mood; Studies 6-8). In these latter four studies, levels of depressed mood were not included as a covariate, because the nature and direction of the relationship between depression and AMS, in the face of variations of the AMT parameters, were the key variables of interest.
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