Selective serotonin reuptake inhibitor Guide, Meaning , Facts, Information and Description
Selective serotonin reuptake inhibitors (SSRIs) are a class of antidepressants. They act within the brain to increase the amount of the neurotransmitter, serotonin (5-hydroxytryptamine or 5-HT), in the synaptic gap by inhibiting its re-uptake. One notable characteristic of SSRIs is that, unlike other classes of antidepressants, SSRIs were rationally designed drugs. Instead of being discovered by accident, SSRIs were specifically designed while considering the biological causes of depression. SSRIs are frequently prescribed for anxiety disorders, obsessive-compulsive disorder, and eating disorders. Though not specifically indicated by the manufacturers, they are also sometimes prescribed to treat Irritable Bowel Syndrome.SSRIs are not thought to be strictly addictive, but discontinuing their use is known to produce both somatic and psychological withdrawal symptoms, a phenomenon known as "SSRI discontinuation syndrome" (Tamam & Ozpoyraz, 2002). Their effectiveness does not appear to be higher than tricyclic antidepressants, which were the most commonly used class of antidepressants before the development SSRIs. However, SSRIs have the important advantage that their toxic dose is high, and, therefore, they are much more difficult to use as a means to commit suicide. Further, they have less or milder side effects.
Many drugs in this class are familiar through advertising, including
- fluoxetine (trade name: Prozac®, Fontex®, Seromex®, Seronil®, Sarafem®)
- paroxetine (trade name: Paxil®, Seroxat®, Optipar®, Aropax®, Paroxat®)
- sertraline (trade name: Zoloft®)
- escitalopram oxalate (trade name: Lexapro®, Cipralex®)
- citalopram (trade name: Celexa®, Cipramil®, Emocal®, Sepram®)
- fluvoxamine maleate (trade name: Luvox®, Faverin®)
- Duloxetine (trade name: Cymbalta®)
Depression has been linked to a lack of stimulation of the recipient neuron at a synapse. To stimulate the recipient cell, SSRIs inhibit the reuptake of serotonin. As a result, the serotonin stays in the synaptic gap longer than it normally would, and has the chance to be recognized again (and again) by the receptors of the recipient cell, which can finally be stimulated that way.
Why not give serotonin directly? First, serotonin ingested orally will not cross the blood-brain barrier, and therefore won't have an effect on brain functions. Second, pure serotonin would turn on every synapse it reaches, whereas SSRIs only enhance a signal that is already present, but too weak to come through.
SSRIs are described as 'selective' because they affect only the reuptake pumps responsible for serotonin, as opposed to earlier antidepressants, which affect other monoamine neurotransmitters as well. Because of this, SSRIs lack some of the side effects of the more general drugs.
Serotonin is made from tryptophan, an amino acid. If depression is caused by lack of serotonin, rather than insensitivity to it, SSRIs alone will not work well, whereas supplementing with tryptophan will. In 1989 the FDA made tryptophan available by prescription only in response to an outbreak of eosinophilia-myalgia syndrome caused by impure L-tryptophan supplements sold over-the-counter. Some critics have suggested that this appears to have been done to make money for the manufacturers of SSRIs.
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Some say that the supposed biological causes of depression, which SSRIs were designed for, have never in fact been proven scientifically. They claim that there is no scientific evidence for the existence of the disorders that SSRIs are designed to treat, or that they are based on a chemical imbalance of the brain, or that SSRIs effectively handle this chemical imbalance.
Allen J. Frances, professor of psychiatry at Duke University Medical Center writes: "psychiatry’s claim that mental illnesses are brain diseases... is not true. There are no objective diagnostic tests to confirm or disconfirm the diagnosis of depression... There is no blood or other biological test to ascertain the presence or absence of a mental illness, as there is for most bodily diseases. If such a test were developed... then the condition would cease to be a mental illness and would be classified, instead, as a symptom of a bodily disease."
The mode of action of these antidepressant drugs on their direct target, the serotonin transport protein, and possible regulatory mechanisms with respect to long-term alleviation of depression, although having been investigated both neurobiologically and clinically over the last years, are not yet understood.
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