Psychological Depression Research Paper

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Depression is a common psychiatric disorder that places a great burden on society. Major depressive disorder (MDD) is defined by the American Psychiatric Association as characterized by dysphoric mood and/or loss of interest or pleasure in all or nearly all activities, plus at least four other symptoms (i.e., sleep problems, appetite disturbance, fatigue, psychomotor agitation or retardation, feelings of worthlessness or guilt, difficulty concentrating or making decisions, recurrent thoughts of death or suicide), that occur during most of the day, nearly every day, for at least two weeks and with significant impairment in social or occupational functioning. Dysthymic disorder (DD) lasts at least two years in adults (and at least one year in children and adolescents). It is defined by similar, although fewer, symptoms (i.e., depressed mood and at least two of the following: appetite problems, sleep disturbance, fatigue, low self-esteem, concentration difficulties, hopelessness).

Subtypes of MDD include atypical depression (characterized by weight gain and an increase in sleep and appetite), melancholic depression (characterized by pervasive loss of interest or pleasure, or lack of mood reactivity, and at least three of the following: distinct quality of mood, mood worse in the morning, terminal insomnia, psychomotor disturbance, significant appetite decrease or weight loss, excessive guilt) and cyclical depression (e.g., seasonal affective disorder).

Bipolar disorder is characterized by dramatic swings from depressive to manic episodes (e.g., elevated, expansive, or irritable mood) that last at least one week (four days for hypomania), or any duration if hospitalized, during which individuals experience at least three of the following symptoms (four, if mood is only irritable): inflated self-esteem, decreased need for sleep, pressured speech, racing thoughts, distractibility, increased goal-directed activity, or risky behaviors. These symptoms occur most of the day, nearly every day, with clinically significant impairment.

Depression also falls on a continuum of severity from sad mood to diagnosed depressive disorders. The subjective state of sadness by itself is not necessarily pathological, but when it occurs simultaneously with other symptoms it is referred to as a symptom complex or syndrome. A clinical syndrome is considered a distinct disorder when it has a specific course, outcome, etiology, and treatment response.

Epidemiology

In the United States, lifetime prevalence rates are 20.8 percent for any mood disorder; 16.6 percent for MDD; 2.5 percent for DD; and 3.9 percent for Bipolar. Lifetime prevalence rates of MDD differ by gender, with 21.3 percent reported for women and 12.7 percent for men; by age, with 0.3–2.5 percent reported for children, 15–20 percent for adolescents, and 10.6 percent for older adults; and by nation, with 1.5 percent reported in Nagasaki, Japan, and 27.3 percent in Santiago, Chile. In a given year in the United States, the incidence of MDD is 3.0 per 1,000 and the incidence of any mood disorder is 9.5 percent.

Depression is recurrent and often chronic. Median MDD durations range from 19 to 22 weeks in adults across multiple episodes, and mean durations range from 26 to 36 weeks in children and adolescents. Remission is defined as no longer meeting full criteria for a depressive episode. If another “episode” develops before two months pass with only minimal symptoms, it is considered a relapse (for predictors of relapse see Keller et al. 1983); if more than two months have elapsed, it is considered a recurrence (for predictors of recurrence see Keller and Bolland 1998).

Etiology

The etiology of depression involves the complex interplay of genetic, biological, personality, cognitive, interpersonal, and environmental factors. Kenneth Kendler’s developmental model of MDD in women has identified an internalizing pathway (including neuroticism and early-onset anxiety disorders), an externalizing pathway (focusing on the role of conduct disorder and substance misuse), and an adversity pathway (e.g., disturbed family environment, childhood sexual abuse, parental loss), all of which might be anchored in genetic risk.

There is extensive evidence showing a link between stressful life events and the onset and maintenance of depression in both children and adults, although there is considerable variability in how different individuals respond to the same stressful event. Diathesis-stress theories focus on interactions among individual vulnerabilities and life stressors. Stress “activates a diathesis, transforming the potential of predisposition into the presence of psychopathology” (Monroe and Simons 1991, p. 406). A wide range of genetic and psychosocial vulnerability factors have been identified with regard to depression. Avshalom Caspi and colleagues (2003), and others, have shown one such gene-environment interaction: a functional polymorphism in the promoter region of the serotonin transporter gene that moderates the influence of stressful life events on depression.

It is not clear how much variance in depression can be attributed to genetic factors. Twin studies conducted by Patrick Sullivan, Michael Neale, and Kenneth Kendler in 2000 found that 31 to 42 percent of the variance in liability to depression was explained by additive genetic effects, 58 to 67 percent by individual specific environmental effects, and a negligible 0 to 5 percent by shared environmental effects. In contrast, adoption studies have typically reported negligible genetic effects and evidence of small but significant shared environment effects.

A number of biological processes have been implicated in depressive disorders. As outlined by Michael Thase, Ripu Jindal, and Robert Howland in 2002, depressed individuals show neuroendocrine dysregulation in the form of abnormal hypothalamic-pituitary-adrenal (HPA) axis response to stress, hyposecretion of growth hormone (GH) in response to pharmacologic challenge, and neurochemical dysregulation, particularly in the serotoninergic and dopaminergic systems. Studies have also found that abnormal functioning of the prefrontal cortexlimbic-striatal regions, reduced prefrontal volume, and hippocampal abnormalities are associated with depression (see Davidson et al. 2002).

Personality, defined as an individual’s characteristic pattern of thinking, feeling, behaving, and relating to others, has long been linked with depression, and it may moderate the effect of stress on depression. The personality trait of negative emotionality (NE), defined as the propensity to experience negative emotions (e.g., anxiety, fear, sadness, anger), has been particularly associated with depression. Related constructs include negative affectivity and neuroticism.

Cognitive models of depression assert that individuals who have negative beliefs about themselves, the world, and their future, and who have a tendency to make global, stable, and internal attributions for negative events, are more likely to become depressed when confronted with stressors than are individuals without such negative beliefs. Evidence consistent with the cognitive-stress interaction has not been found prior to late childhood or early adolescence around the time when children are developing abstract reasoning and formal operational thought.

Interpersonal vulnerability to depression is characterized by impaired social skills, interpersonal dependency, and social inhibition. The relation between interpersonal difficulties and depression is most likely reciprocal and transactional. Some depressed individuals engage in excessive reassurance-seeking from others concerning their worth and lovability. This behavior may provoke frustration and irritation in others, thereby eroding social support and generating increased stress. The centrality of social ties in relation to depression has received considerable empirical support, and such ties may play a role in gender differences in the rates of depression that begin to emerge during adolescence.

Intervention

Pharmacotherapy is the most common approach to the treatment of depressive disorders. Meta-analyses of randomized controlled studies indicate that serotonin and noradrenaline re-uptake inhibitors (SNRIs) demonstrate superior efficacy over selective serotonin re-uptake inhibitors (SSRIs), which in turn present with different side-effect profiles and superior general tolerability compared to tricyclic antidepressants (TCAs). In depressed youth, fluoxetine, an SSRI, has been found to perform significantly better than a placebo. Patients with bipolar disorder are frequently treated with mood stabilizers such as lithium, valproate (Depakote), or lamotrigine (Lamictal).

Cognitive-behavioral therapy (CBT) is one of the most effective psychosocial treatments for depression. In CBT, individuals are taught to modify negative thought patterns, realistically evaluate the accuracy of their beliefs, and develop problem-solving and coping skills (see Beck et al. 1979). In a 1999 mega-analysis of data from several treatment studies, Robert DeRubeis and colleagues found that cognitive therapy was as effective as medications in the treatment of more severely depressed adult patients. Although medications can be quite effective in reducing acute symptoms of depression, they do not reduce the risk of subsequent depressive episodes once their use is discontinued. In contrast, cognitive therapy has been shown to have an enduring effect following successful treatment. In adolescents, a large clinical trial yielded favorable results for CBT compared to supportive or family therapy (see Brent et al. 1997). The Treatment for Adolescents with Depression Study (TADS 2004) found that at the 12week assessment CBT alone did not fare as well as medications (fluoxetine) alone or medications in combination with CBT. However, the difference between CBT and medications alone was no longer present by the 18-week assessment.

Interpersonal psychotherapy (IPT) for depression addresses problems associated with role transitions, grief, interpersonal deficits, and interpersonal disputes. In studies with depressed adults, IPT has performed better than treatment as usually provided in the clinic, or placebo, although not better than cognitive therapy or tricyclic antidepressant medications with and without IPT (see Shulberg et al. 1996). An adaptation of IPT for use with depressed adolescents has been found to be efficacious (see Mufson et al. 1999).

Studies aimed at preventing depression have shown positive, albeit modest, effects. Universal prevention programs, which target all members of a population, have not been found to be as effective as selective programs targeting individuals at risk or indicated programs targeting individuals who are already showing symptoms but do not have the full disorder. Although evidence is growing that depression can be prevented, the effects have tended to be relatively short-lived. Future research needs to develop and test interventions that have more enduring preventive effects. It is also important to identify who is most likely to benefit from which type of intervention, as well as the mechanisms through which such programs work.

Bibliography:

  1. Beck, Aaron T., Augustus J. Rush, Brian F. Shaw, and Gary Emery. 1979. Cognitive Therapy of Depression. New York: Guilford.
  2. Brent, D. A., et al. 1997. A Clinical Psychotherapy Trial for Adolescent Depression Comparing Cognitive, Family, and Supportive Treatments. Archives of General Psychiatry 54: 877–885.
  3. Caspi, A., et al. 2003. Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene. Science 301: 386–389.
  4. DeRubeis, R. J., L. A. Gelfand, T. Z. Tang, and A. D. Simons. 1999. Medication versus Cognitive Behavior Therapy for Severely Depressed Outpatients: Mega-Analysis of Four Randomized Comparisons. American Journal of Psychiatry 156: 1007–1013.
  5. Keller, M. B., and R. J. Bolland. 1998. Implications of Failing to Achieve Successful Long-Term Maintenance Treatment of Recurrent Unipolar Major Depression. Biological Psychiatry 44 (5): 348–360.
  6. Keller, M. B., P. W. Lavori, C. E. Lewis, and G. L. Klerman. Predictors of Relapse in Major Depressive Disorder. Journal of the American Medical Association 250 (24): 3299–3304.
  7. Monroe, S. M., and A. D. Simons. 1991. Diathesis-Stress Theories in the Context of Life Stress Research: Implications for the Depressive Disorders. Psychological Bulletin 110 (3): 406–425.
  8. Mufson, L., M. M. Weissman, D. Moreau, and R. Garfinkel. 1999. Efficacy of Interpersonal Psychotherapy for Depressed Adolescents. Archives of General Psychiatry 56 (6): 573–579.
  9. Sullivan, Patrick, Michael Neale, and Kenneth Kendler. 2000. Genetic Epidemiology of Major Depression: Review and Meta-Analysis. American Journal of Psychiatry 157: 1552–1562.
  10. Thase, Michael E., Ripu Jindal, and Robert. H. Howland. 2002. Biological Aspects of Depression. In Handbook of Depression, Ian H. Gotlib and Constance L. Hammen, 192–218. New York: Guilford.
  11. Treatment for Adolescents with Depression Study (TADS) Team. 2004. Fluoxetine, Cognitive-Behavioral Therapy, and Their Combination for Adolescents with Depression: Treatment for Adolescents with Depression Study (TADS) Randomized Controlled Trial. Journal of the American Medical Association 292 (7): 807–820.

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