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