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eros
Posted Mar 12, 2002 10:53 AM
Why Some Antidepressants Work, While Others Don’t—Part 2 of 4
The most frustrating thing about antidepressant treatment is finding the correct medication or combination of medications. It’s hard enough searching by trial an error, but you also have the dreaded wait of 6-8 weeks before you know of its full benefit.
Doctors are faced with guessing which drug will work. These are educated guesses at best. Experienced doctors know how to narrow it down quickly, once they see how you’re responding. In part 3 I will go in more detail how this is done.
Antidepressants (except MAOI’s) work by blocking what is known as “reuptake.” Nerve cells in the brain do not touch each other. There is a space, known as the synaptic cleft that separates these cells. When one nerve cell is stimulated, it will release a chemical known as a neurotransmitter. These transmitters travel across the space and attach themselves to the adjacent nerve cell. Once enough of the transmitters are attached, the adjacent cell then fires, creating a domino effect.
People who suffer from depression, for some reason, haven’t enough of the neurotransmitters for cells to fire as rapidly as they should. Part of the problem is that when the cell of origin fires, and releases its neurotransmitters, some travel across while others are sucked back into the cell of origin. This is what is referred to as reuptake. The role of an antidepressant is to block and prevent the neurotransmitters from being reabsorbed into the original cell, allowing the transmitters to attach to the adjacent cell as they should.
Sound simple? So why don’t they all work? A neurotransmitter (on a molecular level) is shaped like a puzzle piece. The neurotransmitter attaches itself to the cell by fitting itself into a receptor site, shaped as its compliment. The molecule of an antidepressant is shaped like a puzzle piece as well and competes for the reuptake receptors, by fitting itself into the receptor site, blocking it. Unfortunately, everyone’s receptor sites may vary in shape. Therefore, if the antidepressant molecule doesn’t fit well, reuptake isn’t sufficiently blocked, and the antidepressant is ineffective for that particular individual.
The molecules of the various antidepressants are shaped differently. Proper treatment requires the antidepressant molecule fit snugly in the reuptake receptor site of the patient. Currently, we have no way of knowing in advance, which antidepressant will be effective. Thus we have trial and error. Currently, scientists are doing gene studies and have found that DNA tests have predictive value. In other words, a persons DNA sample will be able to tell the doctor which antidepressant will be the most effective. The DNA sample will also let the doctor know if you have a paradoxical reaction to antidepressants (becoming more depressed and suicidal). You may not see this test on the market for another two or three years, but this will cut down on the trial and error, achieving remission much faster.
More to come. Next FYI post will focus on how experienced doctors methodically select the proper antidepressant through the trial and error process.
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