The key to understanding why these symptoms show themselves as they do lies in the chemical manipulations caused in the brain when a person is taking an SSRI.
The term itself — ‘Selective Serotonin Re-uptake Inhibitors’ — is a roundabout way of saying these drugs inhibit the natural recycling of serotonin. In simpler terms, it is helpful to think of SSRIs as running defense on the natural cyclical flow of serotonin between nerve endings.
In a normal nervous system serotonin in the brain is sent from the “sending” nerve ending to a “receiving” nerve ending. The locus of this exchange is the synapse — the no-man’s land that exists between sending and receiving nerves. The “Sender” releases serotonin which enters the synapse, there to be absorbed into the nerve ending of the “Receiver.” Whatever serotonin is not absorbed by the Receiver gets flushed back into the Sender to be recycled and eventually re-released, making for a lively give-and-take between the Sender and the Receiver. When SSRIs are introduced they change the terms of this dance. The Senders still send and the Receivers still receive. But those random bits of serotonin that don’t get initially absorbed are blocked from being recycled into the Senders and forced back into the Receiver, thus the denotation “serotonin re-uptake inhibitor.” (This 30-second video shows the re-uptake inhibiting action of SSRIs):
The logic of this blockage is this: Studies that arose during the 1950s, when brain chemistry science was in its formative stage, happened upon the notion that the lack of serotonin in the brain directly affects depression, psychotic behavior, and anxiety. Thus, the optimal way to treat depression, according to this theory, is to increase serotonin levels in the brain. Hence, the development and rise of SSRIs and their subsequent exponential dissemination. (By 2008, antidepressants were the third-most-common prescription drug taken in America.) The theory about the role of serotonin in the depressed person’s brain has been challenged more recently and new studies have come out contradicting it.
But this new information is of little help to the millions whose brains have been altered by SSRIs and who remain bound to them, in many cases, against their wills.
As noted, SSRIs increase serotonin in the brain by forcing molecules back into the Receiving nerve ending that otherwise should have been reabsorbed by the Sending nerve ending. As a result, the brain is experiencing more serotonin impulses on the Receiving nerve, which enables the patient to feel better for a while. But this effect is temporary.
When the drug is preventing the serotonin from being recycled, it means two things:
- for a time, the Receiver is over-stimulated by forced serotonin, while,
- the Sender is gradually becoming depleted because of the lack of recycling.
The serotonin becomes deficient in the Sender, which begins to short circuit some of the Receivers waiting to receive. SSRIs sabotage the natural recycling effect between nerves, altering the connection between the Sending / Receiving neurons at the synapsis, disabling the re-uptake pump (a pore) that flushes the serotonin back into the Sender be recycled.
Because the Senders become depleted and thus stop sending, further depleting the number of receptor sites, this results in the commonly-called “poop-out” syndrome, necessitating an increase in the dosage of the SSRI in order to maintain the positive plus-serotonin effect. “There are fewer receptor sites [so] you’re getting depleted, you’re running on empty on serotonin. All those drugs ‘poop out’ and stop working after a month or so. So then you have to raise the dose,” says physician Dr. Gary Kohls.
In essence, the serotonin-sending function actually becomes depleted because of the very medication intended to increase it. Because of the inevitable depletion of the Senders and Receivers, these drugs stop working effectively after a time. “SSRIs increase serotonin only on the synapse level, and that is temporary, altering the brain at least long term and maybe permanently in some cases,” says Kohls, adding, “with a lot of damage being done in the meantime.”