Depression is one of the most common and expensive of all psychiatric disorders. Nearly one in four women, along with one in six men, experience depression during their lifetime and up to 65% experience recurrent episodes of the disorder (Slavich & Irwin, 2014). Consequently, many people with depression never receive diagnosis or treatment. This leaves nearly 30%–35% of adults reaching remission by using current therapeutic approaches and leaving over two thirds of the disease burden intact (Slavich & Irwin, 2014). These variables contribute to substantial social and economic drain. Accordingly, depression has been projected to be the fourth leading cause of overall disease burden, along with the chief cause of nonfatal disease burden internationally.
Carlson (2014) states that the therapeutic effect of noradrenergic and serotonergic agonists and the depressant effect of reserpine, a monoaminergic antagonist, suggest the monoamine hypothesis of depression. This hypothesis suggest that depression is caused by insufficient activity of monoaminergic neurons (Carlson, 2014). However, although SSRIs have an instant effect on serotonergic transmission in the brain, they do not relieve the symptoms of depression for several weeks. This, therefore, disproves the monoamine hypothesis. Additionally, evidence suggests that a region of the prefrontal cortex serves as a focal point in a network of brain regions that are involved in the regulation of mood. Therapeutic treatments for depression, including deep brain stimulation, transcranial brain stimulation, vagus nerve stimulation, and treatment with SSRIs or SNRIs, decrease the activation of the prefrontal cortex (Carlson, 2014). This decreased activation may ease the symptoms of depression by reducing the activation within the amygdala. Consequently, stressful events suppress hippocampal neurogenesis, and antidepressant treatments increase neurogenesis. Therefore, the effects of antidepressant treatments are abolished by suppression of neurogenesis.
Behavioral and cognitive-behavioral approaches have been found to be effective for both the treatment of unipolar depression and the prevention of future depressive episodes (Wedding, 2013). Wedding (2013) states that additional approaches are effective for treating depression, including interpersonal psychotherapy, short term psychodynamic psychotherapy, nondirective supportive psychotherapy, and couples’ therapy. Convincingly, the effects of cognitive behavioral therapy on depression is modest, and psychological treatments are more likely to be used in combination to medication treatment rather than on their own.
Conclusively, depression is appearing in many forms, and often can be comorbid with other mental illness. Careful consideration is given to the delineation of normal sadness and grief from a major depressive episode. Majorly depressed individuals typically feel unworthy and have strong feelings of guilt. An individual who suffers from a major affective disorder, such as depression, holds a considerable risk of death by suicide (Carlson, 2014). Treatment for depression should be personalized through professional cultural competence, continued education, and patience. Popular forms of Cognitive Behavioral Therapy have been stated to show progression, along with medication, to aid those who suffer with depression. Depression shows no bias to those of different culture, ethnic group, or parental raising. Depression can affect anyone and should be dealt with professionally.
Carlson, N. R. (2014). Foundations of behavioral neuroscience (9th ed.). Boston, MA: Pearson.
Slavich, G. M., & Irwin, M. R. (2014). From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. Psychological Bulletin, 140(3), 774-815. doi:10.1037/a0035302
Wedding, D. (2013). Current Psychotherapies, 10th Edition [VitalSource Bookshelf version]. Retrieved from https://bookshelf.vitalsource.com/books/9781285821085