Whats the difference between a mood stabilizer and an SSRI

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What do each of them do to brain chemistry and what effects do they have? And how does a professional decide which one would be best suited for someone?

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Anonymous 0 Comments

Mood stabilizers and SSRIs are used for different things. Even though an SSRI sounds like it should be considered a stabilizer because it helps depression, which is bad for your mood, Doctors use the terms a little different than we do as normal people. A mood stabilizer is what a physician would use is for an acute episode where your mood is not stable in any direction. If you are depressed your mood is stable, it is depressed but it isn’t changing. Someone who is having a psychotic episode or is experiencing a manic episode will have a mood that is in flux. Using something like haloperidol helps the brain steady itself within hours for pills and minutes for an injection. Someone who is having an acute episode can go from barely lucid to being able to communicate with their doctors when treated with a stabilizer. SSRIs just don’t do that.

Surprisingly, a lot psychiatric medications are not well understood from the mechanism of action standpoint, so when you look up haloperidol it says “it is thought to block D2 receptors in the brain…” Similarly, with SSRIs, they block serotonin from being absorbed by neurons thereby increasing serotonin activity. This is based on the monoamine hypothesis. This might be totally right, but so far conclusive proof of the posited mechanisms of action are lacking.

Anonymous 0 Comments

Mood stabilizers are for the treatment of a different set of illnesses vs SSRIs, which are specifically antidepressants.

Mood stabilizers, like lithium, act to “level out” mood and brain activity. Exactly how they work is not yet proven. Some, like lithium, appear to slow down some neurochemical processes, which is theorized to result in a levelled out mood by, metaphorically, putting the brakes on. Others work in different ways, e.g. “antipsychotics” are designed to treat psychosis, the inability to distinguish what is real from what is not.

An SSRI is a “selective serotonin reuptake inhibitor”. We call them “selective” because they mostly affect serotonin only, as opposed to having more than minor effects on dopamine or norepinephrine. “Serotonin reuptake” is something neural cells do, where they absorb serotonin floating around in the synaptic cleft, storing it away (or breaking it down) rather than letting it be used. SSRIs reduce the rate at which serotonin reuptake occurs, hence, they inhibit it. Theory is that insufficient serotonin leads to a failure of the brain to properly respond to the stimuli it receives, causing feelings in general (but especially positive feelings) to be muted or deadened.

The purpose of mood stabilizers is to help folks with bipolar disorder, psychosis, or other *disrupted* mental states gain a healthier, normalized mental state. SSRIs are one specific class of antidepressant/anti-anxiety medication, designed to restore normal neurotransmitter function. Both types of drug affect neurotransmitters, though usually very different ones, and a psychiatrist would determine which medication(s) to prescribe based on careful medical examination and diagnosis of the relevant issues. E.g., a person can have both bipolar disorder and depression and anxiety, meaning that they might need both a mood stabilizer *and* an SSRI. Or maybe they don’t need the SSRI, because treating the bipolar disorder may address the underlying issues contributing to their depression and anxiety. Etc.

Anonymous 0 Comments

The honest answer is we don’t know. 

There’s a good reason for this. We can analyze urine and even blood but what we need to be able to do is monitor neurotransmitters in real time. The problem with this is it’s dangerous. Normally folks can volunteer for dangerous procedures but anyone volunteering to put probes in their  brain might not understand the risk enough to consent. 

So until we can do that, most of these drugs are pure guesswork. The clinical trials reveal as much – sometimes they’re more effective than placebo, sometimes not. The only common link for effective medication studied appears to be adjuvant therapy, leading many to believe the therapy is actually doing the heavy lifting.