Fluoxetine, Citalopram, Escitalopram (Efficacy)

More and more frequently, evidences are obtained demonstrating that genetic polymorphisms in certain genes are related to a good response to certain antidepressants. Genetic polymorphisms in enzymes called cytochromes (CYP2D6, CYP2C19, CYP2C9, etc) are associated with better or worse metabolism, tolerability and development of adverse effects in a large number of antidepressants on the market. However, the discovery of genetic variations in other genes with different actions, such as the ABCB1 transporter gene, the COMT gene, the MAOA gene, the serotonin transport genes (5-HTTR) and the monoamine receptors (5-HT2A and 5-HT1A) among others, are providing increasingly clear evidences that the variability in the response to certain antidepressants between patients is linked to different genetic variants present in these genes that differ between individuals. Genetic variants (or polymorphisms) in these genes can modulate the response to antidepressants.

In this technical report we study some variants of these genes that affect the response of fluoxetine, citalopram, escitalopram but that may also affect the response of other antidepressants, both SSRIs and non-SSRIs, such as mirtazapine, paroxetine and fluvoxamine.

Both fluoxetine, citalopram and escitalopram (the three drugs on which this technical report focuses) are antidepressants of the family of selective serotonin reuptake inhibitors (SSRIs) and are prescribed for depressive disorders, generalized anxiety and worry or excessive tension. Their commercial names are the following: Fluoxetine (Adofen®, Luramon®, Prozac®, Reneuron®), Citalopram (Calton®, Citalvir®, Prisdal®, Relapaz®, Seregra®, Seropram®), Escitalopram (Cipralex®, Escilan®, Escimylan®, Esertia®, Heipram ®, Lexapro ®).

Genes analyzed

5-HT2A HTR1A HTR2A MAOA

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