A response to a question about genetic polymorphisms and SSRI’s. My answer: Excellent question. This question has not been asked in this manner previously. So thank you for asking it 🙂
First an explanation of SSRIs. The selective serotonin reuptake inhibitor prevents some of the reuptake of serotonin at the synapse. As is my usual wont, here is a story. There are no videos, unless u want me to make one 🙂
Neurotransmitters do exactly that, transmit neural impulses across the synapse (the synaptic cleft). So when an impulse comes down requiring serotonin, this neurotransmitter is released from the vesicles (warehouse) and carries the information to a receptor on the other side of the synapse (presynaptic to post synaptic). The impulse continues its course to wherever it is going next. The serotonin that occupied the receptor now pops off the receptor and does one of three things. It hangs around with its buddies or it is broken down by MAO (don’t get nervous…other enzymes too!) Or it will be reabsorbed for reuse. (accurate clinically if not scientifically)
The action of serotonin is directly related to the amount of this neurotransmitter within the synapse. As such, when in normal circumstances, the amount of serotonin in the vesicles drops and thereby there is less serotonin in the synapse, symptoms do occur. The development of the serotonin reuptake inhibitor prevents some of the serotonin from being reabsorbed thereby increasing the serotonin at the synapse.
As you may imagine this may help for perhaps 10 years until the vesicles are bereft of serotonin and thereby the synapse has very little serotonin. Then there is very little serotonin to reuptake and the medicine seems to fail.
The SSRI works at the synapse and doesn’t affect the pathways over much the pathways takes place mostly in the axons of the nerves and deal mostly with how neurotransmitters are created and how they are broken down. Some of the action takes place in the synapse but I am unsure how or if polymorphisms will affect the total amount of serotonin in the presence of an SSRI. I tried to find a good graphic for you which is below.
In actual practice, the utilization of amino acid therapy in support of the serotonin pathway and the appropriate cofactors and the eradication of inflammatory problems which would cause the tryptophan to be pulled into an alternate pathway to create quinolinic acid (a bad thing) is the best methodology to deal with this issue on a clinical basis.
Hope I answered your question. Dr. Jess