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Your Antidepressant May Not Work If You Keep Doing This One Thing

People use social comparison to measure their self-worth. Social comparison has been in existence since time immemorial, and it is as ancient as mankind. This practice of self-evaluation is good for self-improvement, but on the other hand, experience has shown that most times, it usually resulted in making people lack faith in themselves than believing in their abilities. This feeling can lead to depression.

However, new research has revealed that antidepressant drugs don’t work for all health issues in a depressed person.

Studies from psychopharmacologists brought out the knowledge that different patients have a peculiar way of responding to antidepressant drugs when it’s been administered to them. It is unfathomable, however, how a patient out of 5 can get positive results from the first antidepressant that would be administered to him or her.

The answer to this nagging question has been unraveled, and we believe it is dependable. Scientists recently carried out research on this subject and the reason some antidepressant drugs work effectively against depression in some patients but ineffective against the same sickness in others.

Marianne Müller was the leader of the research team which came from the Institue of Psychiatric Medicine in Germany. The outcome of their study was titled Typical Genes Found In Man and Animal: Genetic Link To Receptors of Antidepressant And The Function of Glucocorticoid As A Sensitive Receptors. Marianne went ahead to publish the paper in late December.

The high point of the research was the support from other seasoned and world-class foreign researchers who joined the project from Miami University, Harvard University, and Emory University, amongst others.

Historically, the 1950s saw the emergence of antidepressants because that was when their productions became widespread. Antidepressants have since then been endorsed for depression treatment and prevention.

There are many brands of antidepressants, and some of the most commonly used ones are being listed below;

1. Selective Serotonin Reuptake Inhibitors (SSRIs)

Examples are:

– Citalopram (Celexa),

– Escitalopram (Lexapro),

– Fluvoxamine (Luvox),

– Paroxetine (Brisdelle, Paxil).

2. Serotonin and Noradrenaline Reuptake Inhibitors (SNRIs)

Examples are:

– Duloxetine (Cymbalta),

– Venlafaxine (Effexor),

– Desvenlafaxine (Pristiq, Khedezla).

3. Serotonin Antagonist and Reuptake Inhibitor (SARIs)

Examples are:

– Nefazodone (Serzone),

– Trazodone (Desyrel).

4. Monoamine Oxidase Inhibitors (MAOIs)

Examples are:

– Selegiline (Emsam),

– Isocarboxazid (Marplan),

– Phenelzine (Nardil).

5. Tetracyclics

– Amoxapine (Asendin),

– Maprotiline (Ludiomil),

– Mirtazapine (Remeron).

It might be difficult to determine whether you are a responder or nonresponder but read on to learn more.

Marianne and her companions took time to study the antecedent for molecular setup found in antidepressants and their potency. The team built a special tool which made them to easily pinpoint the signs of molecules and pointers to the reason behind responding and non-responding behavior in mice to certain antidepressant drugs.

The stress-prone glucocorticoid receptor was disclosed to be very crucial to the efficacy of depression healing, Marianne research team on mouse and human study declare. Furthermore, the team was able to recognize the peculiar bioprinters and biological signs which could be used to disclose the traits of responders and nonresponders to a certain brand of antidepressants in human.

According to the researchers, there is a suspicion that using mice as case study could lead to discoveries that would point at the possibility of liking the same process in mice to that of human beings when they take antidepressant medications if reality should be considered. Marianne wanted more credible results, and that made her invite other experts from Emory University who are specialists in human diseases.

This research project of the hybrid study was broken down by Tania Carrillo-Roa who works with the same psychiatric clinic. She explained the method used by the group to find the answer to the question of responders and non-responders.

She said that they got the outcome which indicated that there is a group of genes that are linked to the power of reactions to antidepressants in the mice and the researchers from Emory University compared this phenomenon to that of humans who are admitted into their Institution in Atlanta. Molecular marks that are related to antidepressant reactions in the animal could determine the effects of medications on antidepressant treatment in the convalescent, says the research author. More studies showed that glucocorticoid is a vital element in rectifying and maintaining the system of stress hormone system, and it is believed that this element will be instrumental in antidepressant medication.

Marianne and her colleagues used this study to give hope on this matter of a bright future. The main function of the sensitivity of glucocorticoid receptor could produce more efficient antidepressant recommendations for depressed patients if the individual’s biosigns and biological pointers are to be relied on.

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