Study of Cognitive Reactivity and Meta-cognition in Patients with First Episode Major Depressive Disorder and Recurrent Major Depressive Disorder

Background and review of literature

Major depression, characterized as a “common cold” of psychiatry severely limits psychosocial functioning and diminishes quality of life. It is predicted that the burden of Major depressive disorder (MDD) on the modern society will be the largest of all diseases by 2030 (World Health Organization, 2008). The recent National Mental Health Survey (2015-2016) revealed that the lifetime prevalence of depression in India was 5.25% among individuals aged 18 Years and above and the current prevalence was 2.68%.

DSM-5 defines a major depressive episode as a period of two weeks or more in which at least five symptoms are expressed most of the day nearly every day, including either depressed mood or the loss of interest in nearly all activities, weight/appetite disturbance, sleep disturbance, psychomotor agitation/retardation, fatigue, feelings of worthlessness/guilt, decreased concentration/decision-making, and suicidal ideation.

Major depressive episode last for an average of 6 months (Rhebergen et al., 2010) and has high rates of relapse and recurrence (Figueroa et al., 2015). With each depressive episode, an individual’s chance of enduring an additional episode increases by approximately 15% (Seemuller et al., 2010). MDD is a prevalent condition with 12-month estimates being 4.2% in men and 9.9% in women (Maske et al., 2016). Despite wealth of research concerning the assessment, diagnosis, and treatment of depression, limitations in the knowledge regarding relapse are still evident. However, rather than focusing on identifying the causes of first episodes of depression, several researchers have narrowed their search to identify the causes of recurrence in particular, which may be different from the causes of first episodes (Lewinsohn, Allen, Seeley, & Gotlib, 1999).

Cognitive Reactivity and Depression

Cognitive theories of depression show widespread consensus that cognition is an important factor in unipolar depression (Ingram, Miranda, & Segal, 1998). The most central concept is that dysfunctional cognitions are considered to be the key vulnerability factor, both for the first onset and for recurrences of depression (Beck, 1967; Teasdale, 1988; Clark et.al.,1999).

Cognitive reactivity (CR) refers to the ease with which dysfunctional attitudes are activated by sad mood states (Van der Does, 2002). It is defined as the relative ease with which maladaptive cognitions or cognitive styles are triggered by mild (non-pathological) mood fluctuations (Ingram, Miranda & Segal, 1998). From a cognitive science perspective, it has been suggested that sensitization (and increased risk of relapse and recurrence) is brought about by increased cognitive reactivity to small changes in depressed mood (Segal, Williams, Teasdale & Gemar, 1996). Cognitive reactivity is not only an important factor in the onset (Kruijt et al., 2013) and maintenance of depressive symptoms (Struijs et al., 2013) but especially important for depressive relapse/recurrence.

The mechanisms involved in a first onset of depression may differ from those involved in recurrences (Monroe and Harkness, 2011). High cognitive reactivity may also increase the risk of recurrence of depression and two studies using mood induction procedures have shown cognitive reactivity to be a significant predictor of recurrence over periods of 15 and 18 months after remission (Kuyken et al.,2010). Moulds et al., (2008) found that formerly depressed participants had significantly higher LEIDS-R scores than never depressed participants. Segal, Gemar, and Williams (1999) discovered that CR, as measured by the change in Dysfunctional Attitude Scale scores pre/post mood induction procedures, predicted depressive relapse after 31 months, at the same time that they reported that participants treated to remission with CBT showed less CR than those treated to remission with medication.

Metacognition and Depression

Flavell (1979) introduced the concept of meta-cognition and defined it as “cognitions about one’s cognition”. Wells & Cartwright-Hatton, 2004 define meta-cognition as “the psychological structures, knowledge, events, and processes that are involved in the control, modification, and interpretation of thinking itself”.

Meta-cognitions are shown to be unhealthy when operating in a pattern known as the Cognitive Attentional Syndrome (CAS) which consists of worry, rumination, fixed attention, and unhelpful self-regulation strategies or coping behaviors. CAS is conceptualized as ‘‘aspects of cognition that control the way a person thinks and behaves in response to a thought, belief or feeling’’ (Wells 2009).

Metacognitions about worry have also been proposed as a promising vulnerability marker of depressive relapse (Halvorsen et al., 2015). Individuals with a history of depression tend to worry about relapsing (Sarisoy et al., 2013) Sarisoy et al., (2013) found that ‘Negative beliefs about worry concerning uncontrollability and danger’ was elevated both in unipolar and bipolar depressed individuals compared to the non-depressed control group. Meta-cognitive beliefs are significantly effective on prediction of depression and anxiety. Moreover, out of meta-cognitive elements, only general negative beliefs, in comparison with other elements, may predict the depression (Delavar et al.,2014)

Beliefs About Rumination and Meta-cognition:

The Meta-cognitive Model suggests that depressed individuals use rumination to deal with stress and trigger thoughts. Rumination is a thinking style that typifies depression and has been linked to the maintenance of depressive episodes (Nolen-Hoeksema, 1991; Teasdale & Barnard, 1993) but may also represent a strategy intended to cope with depression. Rumination is defined as self-focused, persistent, recurrent, negative thinking (Papageorgiou & Wells, 2004).

Active and perseverative thinking, in the form of rumination or worry, is linked to positive and negative metacognitive beliefs about these processes (Cartwright-Hatton & Wells, 1997; Wells & Papageorgiou, 1998). Positive beliefs about rumination motivate individuals to engage in rumination as they may believe that analyzing why they are depressed will help them to snap out of their depression. However, rumination leads to distress which again activates negative beliefs about this mental process such as having no control of one’s thinking and fearing the mental, physical, and interpersonal consequences of rumination. Papageorgiou and Wells (1999) found that depressed patients believed that rumination was helpful for solving problems and understanding depression, but also that rumination was uncontrollable and dangerous. In a longitudinal study by Matsumoto & Mochizuki, 2018, negative meta-beliefs predicted high depressive symptoms, and depressive symptoms predicted high negative meta-beliefs. Negative meta-beliefs predicted high uncontrollability of rumination, whereas uncontrollability of rumination did not predict depressive symptoms.

Cognitive Coping:

Dysregulation of emotions typically characterizes mood and anxiety disorders (Gross and Thompson, 2007). Cognitive coping is defined as the conscious, mental strategies individuals use to handle the intake of emotionally arousing information (Garnefski et al., 2001). Two major strategies that have been particularly studied are cognitive reappraisal and expressive suppression (Gross and John, 1998). Cognitive reappraisal is defined as the attempt to reinterpret an emotion-eliciting situation in a way that alters its meaning and changes its emotional impact (Gross and John, 2003). Expressive suppression is defined as the attempt to hide, inhibit or reduce ongoing emotion-expressive behavior (Gross and John, 2003). People who experience depression rely more on expressive suppression than cognitive reappraisal to evade adverse emotional states. Therefore they may experience increased depression in the long term (Campbell & Barlow, 2007). Findings have indicated that expressive suppression is associated with increased depression symptoms (Joormann & Gotlib, 2010). Moreover, emotion suppression has been associated with increased use of rumination (Liverant, Kamholz, Sloan, & Brown, 2011). Indeed, recent studies demonstrate that voluntary changes of the interpretation of a situation can change the intensity of an emotional reaction (Gross, 1998; Ochsner, Bunge, Gross, & Gabrieli, 2002; Ochsner et al., 2004). Habitual use of reappraisal vs. expressive suppression has been shown to be associated with the experience and expression of greater positive affect and lesser negative affect, better interpersonal functioning, and increased well-being (Gross & John, 2003).

Save your time!
We can take care of your essay

• Proper editing and formatting
• Free revision, title page, and bibliography
• Flexible prices and money-back guarantee

Place Order

In summary, Cognitive Reactivity is an important cognitive feature in depression as it predicts the onset, relapse or recurrence of a depressive episode. However, it has mostly been studied in patients with previous depressive episodes and healthy groups. Therefore, the relationship between cognitive reactivity and currently symptomatic groups is being entailed in this study. Existing literature also reveals that there exists a relationship between meta-cognition and depression. Nevertheless, existing studies have focused either on healthy samples or already depressed individuals (Sarisoy et al. 2013) or have compared depressed patients with those having anxiety disorders. None of the studies investigated the presence of meta-cognitions in individuals in different phases of Major Depressive Disorder.

Bibliography

1. American Psychiatric Association (2000). Diagnostic and statistical manual of mental disorders (text revision – fourth). Washington, D.C.: American Psychiatric Association.
2. American Psychiatric Association [APA]. (2013). Diagnostic and statistical manual of mental disorders (DSM 5) (5th ed.). Washington, DC: American Psychiatric Association.
3. Campbell-Sills, L., and Barlow, D.H. “Incorporating emotion regulation into conceptualizations and treatments of anxiety and mood disorders”. In J.J. Gross (Ed.), Handbook of emotion regulation (pp. 542-559), 2007. New York: Guilford Press.
4. Cartwright-Hatton, S., & Wells, A. (1997). Beliefs about worry and intrusions: The Meta-Cognitions Questionnaire and its correlates. Journal of Anxiety Disorders, 11, 279-296.
5. Clark, D.A., Beck, A.T., Alford, B.A.,1999.Scientific Foundations of Cognitive Theory and Therapy of Depression. John Wiley & Sons Inc., Hoboken, NJ, US.
6. Figueroa, C. A., Ruhé, H. G., Koeter, M. W., Spinhoven, P., van der Does, W., Bockting, C.L., & Schene, A. H. (2015). Cognitive reactivity versus dysfunctional cognitions and the prediction of relapse in recurrent major depressive disorder. The Journal of Clinical Psychiatry, 76, 1306-1312. DOI: 10.4088/JCP.14m09268
7. Flavell, J. H. (1979). Metacognition and cognitive monitoring: A new area of cognitive-developmental inquiry. American Psychologist, 34(10), 906–911.
8. Garnefski, N., Kraaij, V., & Spinhoven, P. (2001). Negative life events, cognitive emotion regulation, and depression. Personality and Individual Differences, 30, 1311–1327.
9. Gross, J. J., and John, O. P. (1998). Mapping the domain of emotional expressivity: multi-method evidence for a hierarchical model. J. Pers. Soc. Psychol. 74, 170– 191. DOI: 10.1037//0022-3514.74.1.170
10. Gross, J. J., and John, O. P. (2003). Individual differences in two emotion regulation processes: implications for affect, relationships, and well-being. J. Pers. Soc. Psychol. 85, 348–362. DOI: 10.1037/0022-3514.85.2.348
11. Gross, J. J., and Thompson, R. A. (2007). “Emotion regulation: conceptual foundations,” in Handbook of Emotion Regulation, ed J. J. Gross (New York: Guilford Press), 3–24.
12. Halvorsen M., Hagen R., Hjemdal O., Eriksen M. S., Sørli Å. J., Waterloo K., et al. (2015). Metacognitions and thought control strategies in unipolar major depression: a comparison of currently depressed, previously depressed, and never depressed individuals. Cogn. Ther. Res. 39, 31–40. 10.1007/s10608-014-9638-4
13. Ingram, R. E., Miranda, J., & Segal, Z. V. (1998) Cognitive vulnerability to depression. New York: Guilford Press.
14. Joormann, J. (2010). Cognitive inhibition and emotion regulation in depression. Current Directions in Psychological Science, 19, 161–166. doi:10.1177/0963721410370293
15. Kuyken,W., Watkins,E., Holden,E., White,K., Taylor,R.S., Byford,S., Dalgleish,T., et al.,2010.How does mindfulness-based cognitive therapy work? Behaviour Research Therapy.48(11),11051112. http://dx.doi.org/10.1016/j.brat.2010.08.003.
16. Kruijt, A. W., Antypa, N., Booij, L., de Jong, P. J., Glashouwer, K., Penninx, B. W. J. H., et al. (2013). Cognitive reactivity, implicit associations, and the incidence of depression: A two-year prospective study. PLoS ONE, 8, e70245. DOI: 10.1371/journal.pone.0070245.
17. Lewinsohn PM, Allen NB, Seeley JR, Gotlib IH. First onset versus recurrence of depression: Differential processes of psychosocial risk. Journal of Abnormal Psychology. 1999;108(3):483–489.
18. Liverant, G. I., Kamholz, B. W., Sloan, D. M., & Brown, T. A. (2011). Rumination in clinical depression: A type of emotional suppression? Cognitive Therapy and Research, 35, 253–265. doi:10.1007/s10608-010-9304-4
19. Maske, U. E., Buttery, A. K., Beesdo-Baum, K., Riedel-Heller, S., Hapke, U., & Busch, M. A. (2016). Prevalence and correlates of DSM-IV-TR major depressive disorder, self-reported diagnosed depression, and current depressive symptoms among adults in Germany. Journal of affective disorders, 190, 167-177.
20. Matsumoto, N., & Mochizuki,S., (2018). Why do People Overthink? A Longitudinal Investigation of a Meta-Cognitive Model and Uncontrollability of Rumination. Behavioral and Cognitive Psychotherapy: page 1 of 6. doi:10.1017/S1352465818000103
21. Monroe, S.M., Harkness, K.L.,2011.Recurrence in major depression: a conceptual analysis. Psychol.Rev.118(4),655–674. http://dx.doi.org/10.1037/a0025190.
22. Moulds, M. L., Kandris, E., Williams, A. D., Lang, T., Yap, C., & Hoffmeister, K. (2008). An Investigation of the Relationship Between Cognitive Reactivity and Rumination. Behavior Therapy, 39(1), 65.
23. National Mental Health Survey of India, 2015–16. Prevalence, Pattern, and Outcomes. Bengaluru: National Institute of Mental Health and Neuro Sciences; 2016
24. Nolen-Hoeksema, S. (1991). Responses to depression and their effects on the duration of depressive episodes. Journal of Abnormal Psychology, 100, 569-582.
25. Papageorgiou, C., & Wells, A. (1999). Process and metacognitive dimensions of depressive and anxious thoughts and relationships with emotional intensity. Clinical Psychology and Psychotherapy, 6, 156-162.
26. Papageorgiou, C., & Wells, A. (2001). Positive beliefs about depressive rumination: Development and preliminary validation of a self-report scale. Behavior Therapy, 32, 13–26.
27. Pageorgiou, C.,& Wells, A. (2009). An Empirical Test of clinical meta-cognition model of Rumination and Depression. Cogn Ther and Res; 27(3): 261-273.
28. Rhebergen, D., Beekman, A. T., deGraaf, R., Nolen, W. A., Spijker, J., Hoogendijk, W.J., & Penninx, W. (2010). Trajectories of recovery of social and physical functioning in major depression, dysthymic disorder and double depression: A 3-year follow-up. Journal of Affective Disorders, 124, 148-156.
29. Sarisoy, G., Pazvantoglu, O., Ozturan, D. D., Ay, N. D., Yilman, T., Mor, S., et al. (2013). Metacognitive beliefs in unipolar and bipolar depression: A comparative study. Nordic Journal of Psychiatry.Published online August 1, 2013. doi:10.3109/08039488.2013.814710.
30. Seemuller, F., Riedel, M., Obermeier, M., Bauer, M., Adli, M., Kronmuller, K.,Mooler, H.J. (2010). Outcomes of 1014 naturalistically treated in-patients with major depressive episodes. European Neuropsychopharmacology, 20(5), 346-355.
31. Segal, Z. V., Williams, J. M. G., Teasdale, J. D., & Gemar, M. (1996). A cognitive science perspective on kindling and episode sensitization in recurrent affective disorder. Psychological Medicine, 26, 371– 380.
32. Segal, Z. V., Gemar, M., & Williams, S. (1999). Differential cognitive response to a mood challenge following successful cognitive therapy or pharmacotherapy for unipolar depression. Journal of Abnormal Psychology, 108(1), 3-10.
33. Struijs, S. Y., Groenewold, N. A., Voshaar, R. C. O., & de Jonge, P. (2013). Cognitive vulnerability differentially predicts symptom dimensions of depression. Journal of Affective Disorders, 92–99.
34. Teasdale, J.D.,1988.Cognitive vulnerability to persistent depression.Cogn.Emot.2 (3), 247–274.
35. Teasdale, J. D., & Barnard, R J. (1993). Affect, cognition and change: Re-modelling depressive thought. Hove, UK: Lawrence Erlbaum Associates.
36. Van der Does, A. J. W. (2002). Cognitive reactivity to a sad mood: Structure and validity of a new measure. Behaviour Research and Therapy, 40, 105– 120.
37. Wells, A. and Cartwright-Hatton, S. (2004) A Short form of the Metacognition Questionnaire: Properties of the MCQ- 30. Behaviour Research and Therapy, 42, 385-396. http://dx.doi.org/10.1016/S0005-7967(03)00147-5
38. Wells, A. (2009). Emotional Disorders and Metacognition: Innovative Cognitive Therapy. Wiley.
39. World Health Organization, 2008. The Global Burden of Disease: 2004 Update.

Aims and objective

• To study Cognitive Reactivity and Meta-cognition in patients with First Episode Major Depressive Disorder, Recurrent Major Depressive Disord,er and healthy control and to make comparisons among them.
• To explore the relationship between Cognitive Reactivity and Meta-cognition in patients with First Episode Major Depressive Disorder and Recurrent Major Depressive Disorder, if any.

Study design

It will be a cross-sectional and non-interventional study in a clinical population in a tertiary care hospital setting.

Method

In this study, all newly registered and old patients who are currently symptomatic, attending Adult Psychiatry OPD, KGMU, and have been diagnosed with First Episode Major Depressive Disorder or Recurrent Major Depressive Disorder by the consultant in-charge will be screened for inclusion in the study. Patients willing to give informed consent will be screened using Mini International Neuropsychiatric Interview (M.I.N.I. 7.0.2) to rule out co-morbid psychiatric disorders.

If the patient is eligible for the study, their socio-demographic data, family, and clinical history will be recorded on the semi-structured proforma. Beck Depression Inventory-II (BDI-II) will be administered to assess the current level of severity of depression in the symptomatic patients.

Healthy volunteers will be taken up in the control group from the community (The researcher’s neighborhood and informants accompanying the patient attending the Adult Psychiatry OPD in KGMU, Lucknow). Those who shall provide written informed consent and fulfilling the criteria will form the study sample. Global Health Questionnaire-12 (GHQ-12) will be administered on participants in the healthy group and they shall be matched on age, sex, and education. Questionnaires of Cognitive Reactivity (Leiden Index of Depression Sensitivity- Revised), Meta-cognition (Meta-cognition Questionnaire-30), Cognitive Coping (Emotion Regulation Questionnaire), and Beliefs about Rumination (Positive Beliefs about Rumination Scale and Negative Beliefs about Rumination Scale) shall be administered on both the symptomatic groups (First Episode Major Depressive Disorder and Recurrent Major Depressive Disorder) and the healthy group. Administration of questionnaires will be clinician-assisted as and when required. The obtained data will be statistically analyzed and interpreted with the help of the computer-based statistical tool SPSS (24 versions).

Intervention

Setting

Psychiatry Department - Clinical Psychology Unit (Department of Psychiatry, K.G.M.U, Lucknow, U.P.)

Inclusion and exclusion criteria for the study group (First Episode Major Depressive Disorder And Recurrent Major Depressive Disorder**)

Inclusion Criteria:

• Patients with a diagnosis of First Episode Major Depressive Disorder or Recurrent Major Depressive Disorder according to DSM 5.
• Patients willing to give written informed consent.
• Adults (≥18 to 60 years age)
• Patients having score ≥14 on BDI-II.
• Not receiving any psychological treatment for their current depressive episode**

Exclusion Criteria:

• Patients with any other co-morbid psychiatric disorder.
• Patients with suicidal intent and those diagnosed with severe depression with psychotic symptoms.
• Patients with a physical disability or condition requiring priority medical management.
• Patients who are unable to comprehend the questionnaires or are unable to co-operate for the interview.

Inclusion and exclusion criteria for healthy control group

Inclusion Criteria:

• Adults(≥18 to 60 years age)
• Participants willing to volunteer and give written informed consent.

Exclusion Criteria:

• Presence of any psychiatric disorder (GHQ-12 score ≥3)
• Participants who are unable to comprehend the questionnaires or are unable to co-operate for the interview.

The sample size for primary outcomes

The sample size was estimated to be 40 in each of the two clinical groups (Patients with First Episode Major Depressive Disorder and Recurrent Major Depressive Disorder) and 40 healthy control group participants (determined using weighted prevalence rate for current experience of 2.68% from National Mental Health Survey 2015-2016) using the following formulae:

n = Zα/22 ­*p*(1-p) / MOE2

• where, Zα/22 is the critical value of the Normal distribution at α/2 (for a confidence level of 95%, α is 0.05 and the critical value is 1.96),
• p is the sample proportion [prevalence value is 0.0268 (2.68%)]
• MOE is the margin of error (value is 0.05),

However, because of brevity of time the investigator will strive to obtain a minimum sample of 30 patients in each of the two clinical groups (Patients with First Episode Major Depressive Disorder and Recurrent Major Depressive Disorder) and 30 healthy control group participants. Patients and participants over and above minimum shall be in included in the two clinical groups and healthy control group if time permits the investigator.