Major Depressive Disorder

Definition and common characteristics of Major Depressive Disorder

A major depressive disorder is diagnosed if there has occurred one or more “major depressive episodes” (Diagnostic and Statistical Manual, 4th Edition, of the American Psychiatric Association, DSM-IV).

In order to understand and or diagnose a major depressive disorder, it is necessary to first discuss the concepts of depression and major depressive episode.

Depression is a debilitating emotional problem distinct from normal sadness has long been recognized. In fact, depression of the clinical type was described in surprisingly accurate detail by Hippocrates over 2000 years ago.

How specifically does the modern mental health profession distinguish between a period of normal sadness and what is now called a major depressive episode?

According to the DSM-IV, three factors must be considered: intensity, duration, and context.

Intensity

Many professionals believe that depressed mood occurs on a continuum of severity from normal sadness to severe. According to the DSM-IV, in order for a period of sadness to qualify as a major depressive episode the intensity of sadness must be such as to result in symptoms such as reduced pleasure in activities that used to be pleasurable, weight and sleep disturbance, changes in level of physical activity, fatigue, feelings of worthlessness, reduced ability to concentrate and make decisions, or continuing preoccupation with death or thoughts of suicide.

Duration

Another question that arises is how long must such symptoms exist to constitute a major depressive episode. The DSM-IV requires that the above symptoms must be present most of the day, nearly every day, for a period of at least two weeks.

Context

The DSM-IV states that the period of sadness should not be called a major depressive episode if the person has suffered a severe loss e.g. if one’s mate has died and the grieving does not continue past two months or if the grieving does not include extreme features such as suicidal thoughts or attempts.

Even with the availability of specific criteria to distinguish ordinary sadness from major depressive episode, distinguishing the two is still difficult since the process involves clinical judgment which is subjective.

At present there is no objective scientific test for clinical depression, that is no blood test or brain scan can positively identify depression. Finally even if one could objectively determine the existence of the various criteria, the criteria themselves are again based on clinical judgment and speculation and therefore are open to the criticism as being rather arbitrary.

Prevalence of Major Depressive Disorder

The lifetime prevalence for major depressive disorder was found to be 16.6% in a large US epidemiological study (Kessler 2005) making it, by far, the most prevalent of the mood disorders.

It was followed in decreasing prevalence by bipolar disorder (combined types I and II) at 3.9%, and dysthymia at just 2.5%.

Indeed major depressive disorder is the most common psychiatric condition of the 20 disorders survey by Kessler et al followed by alcohol abuse at 13.2%, and specific phobia at 12.5%.

However even this high rate of lifetime prevalence does not adequately convey the massive numbers of people who come to mental health professionals suffering from depression (Patten, 2008).

Although the epidemiological survey by Kessler et al (2005) did not examine whether major depressive disorder has remained constant over time, two other studies, one in Scandinavia (Andersen et al, 2011) and one in Australia (Goldney et al, 2010) have found evidence that the current prevalence of major depressive disorder has been increasing over time (e.g. from 6.8% in 1998 to 10.3% in 2008 in Australia).

Etiology (Causes)

There is research evidence supporting each of the following as possible causes of depression or as factors influencing the development of depression:

  • Developmental trauma (complex PTSD, codependency).
  • Loss of something or some person of great personal significance to us e.g. a loved one
  • Lack of or reduced frequency of pleasant events and experiences e.g. a healthy sex life
  • Lack of positive interpersonal relationships, especially intimate ones, interpersonal difficulties
  • Genetic factors
  • Feelings of failure e.g. unemployment, failure to attain life goals
  • Chronic mild stress or acute severe stress or trauma
  • Habitual negative or maladaptive patterns of thoughts, perceptions, feelings, and behaviour.
  • Social exclusion, stigmatization, or discrimination perhaps as a result of a mental or physical handicap or a physical disfigurement
  • Loss of social status
  • Sexual and/or reproductive difficulties

The above list is just a few of the postulated causes of depression. Moreover recent research has suggested that more than one of these possible factors may be involved and that they can often work in an interactive way.

For example there can be an interaction between genes and environmental factors where genes exert a causal effect on whether the environmental factor will influence risk, or an interaction between environmental factors and genes where environmental factors exert a causal effect on (modify) how effective genes are in influencing us.

This is a newly considered type of interaction called epigenetics. Epigenetics adds a new layer of complexity to picture of the causation of clinical depression.

The conclusion is that the causes of depression are generally so complex and variable that for any given person who is clinically depressed it is difficult in most cases to state definitely what caused the condition.

Treatments for Major Depressive Disorder

Because of the complexity of causation described above it is logical that a variety of treatment interventions may be effective in treating depression.

In fact there are probably more treatments available for depression than any other disorder although the effectiveness of some of them is hotly debated. Even the supposed superiority of "evidence-based treatments" over "treatment as usual" has been questioned (Wampold et al, 2011).

Some of the more popular treatment approaches are summarized below:

  • Cognitive Behavioural Therapy (CBT). Currently one of the most generally used approaches is the CBT approach as developed by Aaron Beck and others. The CBT aims to modify thinking, feeling or behaviour in such a way as to reduce depression.

    One of the most important of these CBT techniques is cognitive restructuring in which the therapist helps the client to develop more adaptive beliefs and self-talk to replace the maladaptive ones which have contributed to the causation of the depression.
  • Pharmacotherapy. This is probably the most prevalent type of treatment offered to those with depression and usually involves the use of antidepressant medications such as the well known drug Prozac. For a recent reviews of the use of pharmacological agents in major depression, see Menchetti et al, 2011; Schmidt et al, 2011).

    However, after decades of drug use and research, there is still considerable controversy over the pharmacological approach with some debating whether the therapeutic effect of the medication is significantly greater than that due to a placebo effect. Excellent video from 60 minutes on antidepressants and the placebo effect.

    In the UK antidepressants are no longer used as the first line treatment for mild to moderate depression.
  • Physical exercise. There is now abundant and excellent research showing that an appropriate program of exercise is as beneficial as antidepressants for most persons with depression. However the severely depressed as well as some less depressed persons may not follow such an exercise program.

    It is to be noted that there is research evidence supporting the idea that neurogenesis is involved in depression and other affect disturbances (Petrik et al, 2012).

    Neurogenesis is the formation of new neurons through the cell division of specialized progenitor cells. Both exercise and antidepressants induce neurogenesis in certain brain regions e.g. the hippocampus.
  • Holistic, blended psychotherapy. Because of the many possible causes of depression, including stress in general (Markou, & Cryan, 2012), some therapists use a holistic blended approach.

    Because of the frequent occurrence of childhood trauma in the childhood history of those with depression, another approach which is utilized is the codependent approach (Mellody, 1989).

    This codependence approach is holistic and can be thought of as involving three components, usually in the following sequence:
    1. awareness of the childhood trauma
    2. emotional acceptance and working through of the real life losses and suffering caused by the childhood trauma. The focus is on emotions.
    3. finally an action phase in which the CBT approach can be applied.

References

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders. (4th ed.) Washington, DC: Author.

Andersen, I., Thielen, K., Bech, P., Nygaard, E., & Diderichsen, F. (2011). Increasing prevalence of depression from 2000 to 2006. Scandinavian Journal of Public Health, Vol 39(8), 857-863.

Petrik, D., Lagace, D. C., & Eisch, A. J. (2012). The neurogenesis hypothesis of affective and anxiety disorders: Are we mistaking the scaffolding for the building? Neuropharmacology, 62(1), 21-34
Goldney, R. D., Eckert, K. A., Hawthorne, G. & Taylor, A. W. (2010). Changes in the prevalence of major depression in an Australian community sample between 1998 and 2008. Australian and New Zealand Journal of Psychiatry, Vol 44(10), 901-910.

Kessler, Ronald C., Berglund, Patricia, Demler, Olga, Jin, Robert, Merikangas, K. R., Walters, Ellen E., (2005). Lifetime Prevalence and Age-of-Onset Distributions of DSM-IV Disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry, Vol. 62(6), 593-602.

Markou, A., & Cryan, J. F. (2012). Stress, anxiety and depression: Toward new treatment strategies. Neuropharmacology, 62(1), 1-2.

Mellody, Pia. (1989). Facing Codependence. San Francisco: Harper.

Menchetti, M., Casini, F., Versari, M., Bortolotti, B., Nespeca, C., & Berardi, D. (2011). Pharmacological treatment of depression in primary care. An updated literature review (2000–2009). 8(4), 234-242.

Patten, S. B. (2008). Major depression prevalence is very high, but the syndrome is a poor proxy for community populations' clinical treatment needs. The Canadian Journal of Psychiatry / La Revue canadienne de psychiatrie, 53(7), 411-419.

Schmidt, H. D., Shelton, R. C., & Duman, R. S. (2011). Functional biomarkers of depression: Diagnosis, treatment, and pathophysiology. Neuropsychopharmacology, 36(12), 2375-2394. doi:10.1038/npp.2011.151

Wampold, B. E., Budge, S. L., Laska, K. M., Del Re, A. C., Baardseth, T. P., Flűckiger, C., . . . Gunn, W. (2011). Evidence-based treatments for depression and anxiety versus treatment-as-usual: A meta-analysis of direct comparisons. Clinical Psychology Review, 31(8), 1304-1312.