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 reuptake. One notable characteristic of is that, unlike other classes of antidepressants, SSRIs were rationally designed drugs.

Instead of being discovered by accident, Selective serotonin reuptake inhibitors 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.

Selective serotonin reuptake inhibitors are not addictive in the strict sense of the word (i.e. animals given free access to the drug do not active seek it out and do not seek to increase the dose), but suddenly discontinuing their use is known to produce both somatic and psychological withdrawal symptoms, a phenomenon known as "SSRI discontinuation syndrome" (Tamam & Ozpoyraz, 2002). Compared to the withdrawal symptoms of such drugs as opiates, alcohol or cocaine, these are slight.

Their effectiveness does not appear to be higher than tricyclic antidepressants, which were the most commonly used class of antidepressants before the development of Selective serotonin reuptake inhibitors.

However, Selective serotonin reuptake inhibitors 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 fewer or milder side effects.

How SSRIs works
In the brain, information is passed between two neurons (nerve cells) via a synapse, a small gap between the cells. The neuron that sends the information releases neurotransmitters (with serotonin among them) into that gap.

The neurotransmitters are then recognized by receptors on the surface of the recipient cell, which upon this stimulation, in turn, relays the signal.

About 10% of the neurotransmitters are lost in this process, the other 90% are released from the receptors and taken up again by monoamine transporters in the sending cell (thus reuptake).

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 Selective serotonin reuptake inhibitors 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, Selective serotonin reuptake inhibitors 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.

As the production error responsible for the contamination would have been easily correctable, some critics have suggested that this appears to have been done to make money for the manufacturers of Selective serotonin reuptake inhibitors.

Criticism of SSRIs
SSRIs have been the focus of much controversy. Some feel that Selective serotonin reuptake inhibitors are prescribed by overzealous doctors or psychiatrists in cases where their use is only marginally indicated.

According to this argument, societal pressures have created a precedent for the pursuit of "normal" mental or emotional functioning by chemical means versus a more holistic approach (diet, exercise, sleep, stress reduction, etc).

Furthermore, in late 2004 was much media attention given to a proposed link between SSRI use and juvenile suicide.

For this reason, the use of Selective serotonin reuptake inhibitors in pediatric cases of depression is now recognized by the FDA as warranting a cautionary statement to the parents of children who may be prescribed SSRIs by a family doctor.

While people can benefit from antidepressants or painkillers, they might develop an addiction to prescription medication if they take them without strict following their doctor’s orders about dosage and frequency.

Effect not well understood
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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