Abstract
The account of cognitive vulnerability to depression offered by Beck's cognitive model is summarised. As this account currently lacks consistent empirical support, an alternative, related, account is presented. This proposes that, once a person is initially depressed, an important factor that determines whether their depression remains mild or transient, or becomes more severe and persistent, is the nature of the negative cognitive processes and constructs that become active and accessible in the depressed state. These interact with the nature of environmental difficulties, available social support, and biological factors, to determine whether a depression-maintaining cognitive-affective vicious cycle will be set up. Results from studies specifically designed to test predictions from this account have yielded positive results. Findings consistent with the hypothesis have also been obtained in other prospective studies which have shown that cognitive measures, administered in the depressed state, predict the future course of depression independently of initial levels of depression. The hypothesis is elaborated to incorporate the demonstrated relationship of elevated neuroticism to risk and persistence of depression. Recent views on the nature of sex differences in rates of depression, and on the relationship of attributional style to depression are also compatible with the hypothesis. It is concluded that the hypothesis has encouraging preliminary support. SUMMARY Two broad aspects of cognitive vulnerability to depression can be distinguished. The first is the tendency to evaluate certain types of life event in ways which will produce intense rather than mild depression. This is the aspect of vulnerability on which Beck's cognitive model appears to concentrate. There are considerable difficulties in assessing this aspect of Beck's model and it is not consistently supported by comparison of recovered depressed patients with control groups. The second aspect of cognitive vulnerability relates to the cognitive processes and constructs that become active and accessible once a person is in a state of depression. Within this approach, vulnerability to onset and vulnerability to persistence of depression can be roughly distinguished, depending on whether the focus is on the period when the depression has been present for only a brief period, or is mild, or whether depression has already existed for some time and reached at least moderate severity. The account presented here proposes that a crucial factor determining whether an initially mild or transient depressed state remains mild or soon disappears, or becomes more severe and persistent, is whether a vicious cycle based on a reciprocally reinforcing relationship between depressed mood and negative cognitive processing can become established. The probability that this cycle will become established is, in turn, a function of a complex interaction between the environmental difficulties facing a person, the support available to them, their biological state, and the nature of the cognitive processes and constructs that are active and accessible in the depressed state. The kind of cognitive process and constructs that are most active and accessible in the depressed state will be a function both of the patterns of cognitive processing that are characteristic of the person in their normal mood state (such as those related to neuroticism), and of the patterns of cognitive processing that become active in the depressed state. It is on these latter that the differential activation hypothesis concentrates. It suggests that individual differences in the cognitive processes and constructs that become active and accessible in the depressed' state can make an important contribution to whether an initial state of depression becomes more intense, or fades away, and whether, once established, depression of moderate severity persists a long time or a short time. In particular, it is proposed that processes and constructs related to global negative characterological evaluations of the self or that, in other ways, lead to interpretations of experience as highly aversive and uncontrollable are likely to act to intensify and maintain depression. Two investigations specifically designed to test predictions from the differential activation hypothesis yielded positive results. Further supportive evidence is available from a number of other studies which have examined the relationship between cognitive measures, administered in the depressed state, and the future course of depression. Such studies haverecurringly found that persistence or return of depression is associated with initially high scores on measures of negative cognition, and this association remains when the effects of initial depression level are partialled out. In addition to this encouraging preliminary empirical support, the differential activation hypothesis has the further attraction that it can incorporate into this account the well established finding that neuroticism is associated with risk of becoming depressed, and of depression persisting. Further, it is quite consistent with recent proposals related to sex differences in rates of depression, and to the relationship of attributional style to depression.