Depressive disorders have been with mankind since the beginning of recorded history. In the Bible, King David, as well as Job, suffered from this affliction. Hippocrates referred to depression as melancholia, which literally means black bile. Black bile, along with blood, phlegm, and yellow bile were the four humors (fluids) that described the basic medical physiology theory of that time.
Depression, also referred to as clinical depression, has been portrayed in literature and the arts for hundreds of years, but what do we mean today when we refer to a depressive disorder? In the 19th century, depression was seen as an inherited weakness of temperament. In the first half of the 20th century, Freud linked the development of depression to guilt and conflict. John Cheever, the author and a modern sufferer of depressive disorder, wrote of conflict and experiences with his parents as influencing his development of depression.
In the 1950s and '60s, depression was divided into two types, endogenous and neurotic. Endogenous means that the depression comes from within the body, perhaps of genetic origin, or comes out of nowhere. Neurotic or reactive depression has a clear environmental precipitating factor, such as the death of a spouse, or other significant loss, such as the loss of a job. In the 1970s and '80s, the focus of attention shifted from the cause of depression to its effects on the afflicted people.
Causes of Depression:
Some types of depression run in families, indicating that a biological vulnerability to depression can be inherited. This seems to be the case, especially with bipolar disorder. Families in which members of each generation develop bipolar disorder have been studied. The investigators found that those with the illness have a somewhat different genetic makeup than those who do not become ill. However, the reverse is not true. That is, not everybody with the genetic makeup that causes vulnerability to bipolar disorder will develop the illness. Apparently, additional factors, possibly a stressful environment, are involved in its onset and protective factors are involved in its prevention.
Major depression also seems to occur in generation after generation in some families, although not as strongly as in bipolar I or II. Indeed, major depression can also occur in people who have no family history of depression.
Treatment for Depression:
Antidepressant medications: Selective serotonin reuptake inhibitors (SSRIs) are medications that increase the amount of the neurochemical serotonin in the brain. (Remember that brain serotonin levels are often low in depression.) As their name implies, the SSRIs work by selectively inhibiting (blocking) serotonin reuptake in the brain. This block occurs at the synapse, the place where brain cells (neurons) are connected to each other. Serotonin is one of the chemicals in the brain that carries messages across these connections (synapses) from one neuron to another.
Dual-action antidepressants: The biochemical reality is that all classes of medications that treat depression (MAOIs, SSRIs, TCAs, and atypical antidepressants) have some effect on both norepinephrine and serotonin, as well as on other neurotransmitters. However, the various medications affect the different neurotransmitters in varying degrees.
Some of the newer antidepressant drugs, however, appear to have particularly robust effects on both the norepinephrine and serotonin systems. These medications seem to be very promising, especially for the more severe and chronic cases of depression. (Psychiatrists, rather than family practitioners, see such cases most frequently.) Venlafaxine (Effexor) and duloxetine (Cymbalta) are two of these dual-action compounds.
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Treating Depression
Atypical antidepressants are so named because they work in a variety of ways. Thus, atypical antidepressants are not TCAs, SSRIs, or SNRIs, but they are effective in treating depression for many people nonetheless. More specifically, they increase the level of certain neurochemicals in the brain synapses (where nerves communicate with each other). Examples of atypical antidepressants include nefazodone (Serzone), trazodone (Desyrel), and bupropion (Wellbutrin).
Monoamine oxidase inhibitors (MAOIs) are the earliest developed antidepressants. Examples of MAOIs include phenelzine (Nardil) and tranylcypromine (Parnate). MAOIs elevate the levels of neurochemicals in the brain synapses by inhibiting monoamine oxidase. Monoamine oxidase is the main enzyme that breaks down neurochemicals, such as norepinephrine. When monoamine oxidase is inhibited, the norepinephrine is not broken down and, therefore, the amount of norepinephrine in the brain is increased.
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