Literature Review: Incorporating Prior Research

 

Every year, almost ten million adults seek treatment for depression (National Institute, 1).  Each person who experiences an episode of Major Depressive Disorder (MDD) has an increased risk of suicidal behavior, substance abuse, bipolar disorder and poor psychosocial functioning (Birmaher et al., 1996), all of which potentially impact their friends, family and co-workers in negative ways.  Etiological theories, including the Beck’s cognitive diathesis-stress model (1978), Nolen-Hoeksema’s rumination theory (1991), Abramson, Metalsky and Alloy’s hopelessness theory (1989), and Hankin and Abramson’s cognitive vulnerability-transactional stress theory (2001) include negative affect as a common element contributing to the onset of depressive episodes.  Watson and Walker (1996) established that in college students, trait measures of negative affect remain relatively stable in across time spans of six to seven years and retain their power to predict future levels of depression.  Because of this potentially enduring nature of negative affect and the risk of the comorbid dysfunctions listed above, the question of which factors might interact with negative affect to trigger the onset and relapse of MDD is an important one to both sufferers from this disease and society at large. 

            Several etiological theories identify the interaction between dysfunctional cognitions and negative life events as the source of depressive episodes.  The cognitive diathesis-stress theory identifies a person’s thought process, in conjunction with negative life events, as the source of major depression.  A stressful life event can activate a pre-existing negative schema by the affect it induces; this schema then reinforces depressive thought patterns.  According to Kovacs et al. (1978), people respond to events according to cognitive schemas, functional units that organize thoughts.  Beck refers to these thought patterns as a “negative cognitive set,” which he defines as negative views of experience, the future and the self.  The elements of this negative cognitive set, when reinforced by a schema activated by negative affect, contribute to the onset of MDD.   

            The negative cognitive set resembles what Sacco related to Beck in a personal communication (1987), namely, that depressed individuals tend to attribute failure to internal, stable and global attributions.  A pessimistic attributional style has been subsequently linked to a higher risk of future depression when associated with low-levels of stress (Lewinsohn, Joiner & Rohde, 2001), regardless of the number of negative life events experienced (Spence, Sheffield & Donovan, 2002).  Another model of depressive etiology, the information-processing theory (Teasdale, 1983), also takes negative life events into account.  Instead of positing the existence of negative schema, this theory suggests that the ease with which a depressed person accesses negative cognitions increases as a function of depressed mood.  Events that evoke a certain negative affect trigger self-defeating thoughts previously associated with that affect and make it easier for an individual to slip into an episode of MDD when he or she encounters subsequent stressors (Teasdale, 1983). 

The hopelessness theory (Abramson et al., 1988) also links stressful life events, e.g. the failure to achieve a goal, and depression.  The hopelessness results from the depression-prone individual’s negative view of the self, world, and future (Beck’s negative cognitive set).  Rholes, Riskind, and Neville (1985) discovered that, in an undergraduate population, initial levels of hopelessness predicted depression severity six weeks later more accurately than initial levels of depression.  They hypothesized that hopelessness acts as a diathesis that, when combined with negative events, increases vulnerability to a depressive episode.  Emmons and Diener (1986) attributed delayed negative affect to a specific type of stressful event, the failure to achieve an important goal.  Similarly, Ahrens and Abramson’s (1991) studies of college freshmen’s expected versus actual performance on a midterm linked delayed depressive affect to poor performance and lowered expectation standards.  Results of a study of undergraduates by Needles & Abramson (1990) indicate that the interaction between a global, stable attributional style and negative events (like goal failure) contribute to the level of hopelessness and subsequent depression severity six weeks later.  Lastly, Abramson et al.’s (1998) 30-month study of undergraduates at high- and low-cognitive risk for suicide identified hopelessness as a mediator between the vulnerability and suicidal tendency.

Other studies have identified different diatheses and mediators that contribute to the onset of a depressive episode.  A study of adolescents by Spence, Sheffield and Donovan (2002) found that a negative problem solving orientation operated as a diathesis: when combined with higher numbers of stressful life events, it increased chances of more severe depression in the future.  Lewinsohn et al. (2001) identified a mid-range level of dysfunctional attitudes as being related to depressive onset in adolescents.  Abela & D’Alessandro (2002) also pinpointed dysfunctional attitudes, mediated by a negative view of the future, as a diathesis that predicted depressive mood in high school students.  Vazquez, Jimenez, Suara and Avia (2001) identified a different mediator of future depressive mood, namely, the importance that the adolescent places on the stressful event’s outcome.  Another study identified a potential limitation of the diathesis-stress model.  Lewinsohn, Allen, Seeley & Gotlib (1999) differentiated between adolescents with and without a history of depression and discovered that stressful life events only predicted first episodes of MDD.  For those who had experienced an earlier depressive episode, the likelihood of recurrence did not increase as a function of stressful life events but rather as a function of dysphoric mood severity.

            Hammen’s (1991) stress generation hypothesis offers an explanation of the relationship between stress and depression that differs from the diathesis-stress model discussed above.  Hammen studied stress generation in depressed individuals and discovered that the interpersonal deficits caused by depressive affect and behaviors generated new sources of dependent stress that, in turn, fueled the depression.  Hokanson, Rubert, Welker, Hollander and Hedeen (1989) discovered over an eight-month study that the roommates of clinically depressed college students reported more aggressive feelings toward their roommate and less enjoyment of their company.  Siegel and Alloy (1990) reported that dysphoric students and their roommates tended to have more negative relationships than two non-depressed individuals.  A subsequent study of women by Harkness et al. (2001) examined the link between comorbid anxiety, dysthymia, and dependent stressful life events, and reported that the presence of these two factors increased the threat of events like interpersonal difficulties.  These difficulties strain the depressed individual’s relationships and subsequently deepen and maintain the depressed emotions.

            A 1995 study of college students by Potthoff, Holahan, and Joiner integrated the stress generation hypothesis with Coyne’s (1976) interpersonal theory of depression.  The interpersonal theory asserts that individuals with a reassurance-seeking style of interpersonal communication will experience more interpersonal difficulties and, as a result, an increase in depressive symptoms.  Negative affect can cause individuals to engage in reassurance seeking behaviors that strain relationships and subsequently deepen and maintain the depressed emotions.  Potthoff et al. (1995) discovered a positive relationship between reassurance-seeking and depressive symptoms; they proposed that stress generation mediates between the reassurance-seeking behavior and the depression that potentially results, highlighting the importance of interpersonal factors in depression’s development. 

            Nolen-Hoeksema’s (1991) rumination theory places less emphasis on external events than the diathesis-stress or stress-generation hypotheses.  It proposes that people tend to cope with stressors in a consistent manner (as supported by Nolen-Hoeksema, Morrow, and Fredrickson, 1993) and that individuals who cope by focusing on their negative emotions instead of distracting themselves have an increased chance of experiencing a longer, more severe depressive episode, regardless of stressful life events or social support.  The ruminative response style causes the individual to focus on the negative affect, which increases the severity of the depressed emotions.  A prospective study of college students by Just & Alloy (1997) reports that trait ruminative response styles predict when a nondepressed individual will experience a depressive episode and that rumination increases the severity of the episode.  Other studies of undergraduates indicate that individuals with moderate levels of depression tend to cope by ruminating and subsequently experience more stress (Arthur, 1998; Forsythe and Compas, 1987).  Rumination has since been associated with cognitive inflexibility that might contribute to the perseverance of the negative affect (Davis & Nolen-Hoeksema, 2000).  Although rumination is proposed as a maintenance rather than etiological theory, it is possible that a person experiencing mid-range levels of dysphoria who ruminates instead of actively coping will be at greater risk of experiencing a full-blown depressive episode. 

            Hankin et al.’s (2001) cognitive vulnerability-transactional stress theory combines several of these existing etiological models into a more cohesive form.  It takes the cognitive diathesis-stress model (Beck, 1987) and posits negative affect as a mediating factor between the stressor and the cognition, because the negative affect only endures in those who are already cognitively vulnerable.  It incorporates a ruminative response style (Nolen-Hoeksema, 1991) and other non-depression specific cognitive vulnerabilities, increasing the number of chances they have to interact with affect and negative life events.  Also, as suggested by Potthoff et al. (1995), Hammen (1991) and Coyne (1976), this theory allows for the possibility that depressed individuals might create stressful interpersonal situations that exacerbate their condition (Hankin et al., 2001).

            According to the literature reviewed above, the following have been proposed as risk factors for depression onset: negative attributional style, stressful life events, interpersonal deficits, dysfunctional attitudes, reassurance-seeking behaviors and coping style.  However, no prospective study has been conducted that examines a non-clinical population with elevated negative affect to determine what factors interact with that affect and induce a full depressive episode.  I plan to administer measures evaluating the above factors to male and female college students with mid-range levels of dysphoria.  After two months have passed, I will re-administer the measures and determine which students experienced a depressive episode during the elapsed time.  By comparing the scores of participants who had an episode of MDD with those who did not, I can determine what factors, if any, contributed to students with elevated negative affect experiencing depression. 

  

 

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