Medication Action in Shyness and Social
Anxiety - Information
Social Anxiety Shyness Info
The action mechanism of the medications used in Shyness and Social Phobia / Social Anxiety is controversial. There is some unity in the explanations of the hypothetical antidepressants action mechanisms. That being so, I will offer a few considerations on them.
After reading the article on Neuro
Approach of Shyness and Social Anxiety Disorder, one can deduct what happens with the use of the medications:
– If the medication acts where the defect is, it will be effective; otherwise, it will be ineffective.
– Any type of the medications mentioned in another article can act on more than one of these defects, without our knowing it.
– The association of medications makes it possible to reach the highest number of defective sites.
Neurotransmitters, Depressions, Phobias
Serotonin, noradrenaline – These two substances appear as neurotransmitters in synapses in the brain regions involved with the state of alertness. It is possible that other neurotransmitters also play a role in the process, but the strongest evidence points to these two. In reality, serotonin is at the core of the HYPOTHESES most diffused in several emotional and behavioral disorders. Examples:
– in the depressions, it would be decreased in the synaptic
– in the phobias, it would be equally decreased in the synaptic spaces.
Serotonin Re-uptake Pump –
This pompous name does not refer to any driving engine or any intake turbine. It simply refers to pores in the
proximal neuron membrane that allow the selective passage of serotonin from the synaptic space to its interior . These pores are important in regulating the serotonin level in the synaptic space. Some unknown mechanism determines the serotonin flow back to the proximal neuron's interior .
Some substances WOULD ACT to preclude or to reduce this return or re-uptake, which would raise the serotonin levels in the synaptic spaces in certain brain regions. The result would be the correction of distortions in the message sent by the chemical signal to the distal neuron. These substances would then be useful in cases of depressions and phobias.
Noradrenalin – The mechanisms of production, regulation, action, and metabolization of noradrenalin in the synapses are poorly known. Nevertheless, it is accepted that its action time on the distal neuron, as well as the amount of available synaptic space, is important to the correct or incorrect conduction of the signal. In this manner, the inhibition of its reabsorption or the prolongation of its action time could modulate its effects on the synapses.
It is worth highlighting that noradrenalin is also produced by the suprarenal gland to act in other parts of the organism and generate various other effects.
There is evidence that serotonin and noradrenalin act in an integrated manner in the brain.
As I said above, it is possible that other neurotransmitters are involved in conducting these stimuli, but, at present, the evidence points to serotonin and noradrenaline. You can imagine that if the neuron produces other neurotransmitters, there are other re-uptake pumps and selective pores .
Social Anxiety Disorder Medications Information
The drugs most often used for Social Anxiety Disorder are antidepressants, anxiolytics, and beta-blockers. Antidepressants are first line medications. In the second line are the ansiolitics and beta-blockers.
Antidepressants – Antidepressants are in three main groups:
* The so-called "modern" antidepressants.
* The monoamine oxidase inhibitors (MAOI).
* The tricyclics.
The so-called "modern" antidepressants constituted, for example, by sertralin, fluoxetin, paroxetin, and venlafaxine, WOULD INHIBIT the serotonin re-uptake. And that will enhance the amount in the synapse. Citalopran WOULD STIMULATE the receptors in the distal neuron, and that will enhance their "sensitivity" to the neurotransmiters.
The monoamine oxidase inhibitors (MAOI) would inhibit an enzyme called monoamine oxidase. This enzyme deactivates noradrenaline as soon as the
signal reaches the distal neuron. The inhibition of this enzyme would produce an increase of noradrenaline in the space or some extension of its action time , correcting eventual distortions in the message.
The tricyclics WOULD ENHANCE the serotonin and noradrenaline activity. That is a vague explanation: we don't know what "to enhance the activity" is.
Others, like mirtazipine, would increase the sensitivity of some serotonin and noradrenalin receptors while, at the same time , blocking others. Reboxetine already would inhibit the reuptake of noradrenalin, conciliating action similar to IMAO, without the risks that these present.
The use of the antidepressants would correct the distorted perception of threat in risk-free locations or situations.
Antidepressants Associations –
A few psychiatrists use combinations of certain antidepressants for patients with depression and Social Anxiety. In addition to being dangerous, that practice does not have sufficient controlled research to point to.
WARNING! Serotonin reuptakes or any other antidepressant cannot be associated with monoamine oxidase inhibitors.
The most frequently used are the benzodiazepines. Their action mechanisms are even more mysterious than those reported for antidepressants. It seems that, used in isolation, they do not yield satisfactory results.
However, Alprazolan is used alone by many psychiatrists. That drug was the first to produce good results in the essays on Panic Disorder many years ago. Although the anxiety attacks in Social Anxiety have different basis from that of the Panic Disorder, Alprazolan is the medication of choice among many psychiatrists.
Beta-Blockers – They block the beta-adrenergic receptors , i. e., they block some receptors on the distal neurons that are activated by noradrenaline. They seem to act indirectly, that is, to reduce the intensity of the attacks by reduction of peripheral symptoms, such as by slowing down the heart, sweating, and tremors .
The hypotheses about neurotransmitters action indicate that associations of active principles acting on the serotonin reuptake pumps and in the receptors (distal neurons) reach most people suffering from these woes. However, we cannot associate MAOI with other antidepressants.
In this article, verbs were purposely used in the conditional form because we are dealing with hypotheses. The synaptic space is so small that it is impossible, with current tools, to be certain, for instance, that a given neurotransmitter decreases. On the other hand, molecular biology has not advanced enough to identify defects in the proximal and distal neurons. With respect to this, advances in knowledge of the mechanisms of actions of neurotransmitters, principally those of serotonin and noradrenalin, and the genes that control its production and transportation, open the way for the synthesis of new drugs.
However, clinical practice and experiments have demonstrated that many anti-depressant substances are useful in eliminating or in relieving the anxiety attack symptoms in Social Phobia / Social Anxiety and in severe Shyness.
In other articles, we will examine these active principles in further detail.
Updated December, 2005;
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