Depression

Cad said:

Everyone I know that has tried them has ended up with serious sexual side effects, numb emotions, etc. Serious inability to orgasm, not caring about sex anymore, etc..

Obviously do what you gotta do if you're suicidal but not being able to have a satisfying sex life would cause depression just by itself.

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Some of it is med-dependent. Zoloft and Paxil are particularly infamous for ED and sexual side effects. Wellbutrin often increases libido, though it's in the atypical antidepressant class; it's not a SSRI or SNRI.

I agree with Izo that they make sense in certain situations, and they should basically always be done in conjunction with talk therapy (and there should probably be monotherapy with just talk therapy before ADs are even considered).

The problems in the US are:

• People just stay on them forever instead of using them to get through the worst of the depression and then working with their provider to taper
• In the 90s, they were basically handed out like candy without any serious discussion about the emotional blunting and sexual side effects that can occur with them. Providers didn't talk to people nearly enough (still often is the case, although it seems like providers may be talking about that a bit more in the wake of Perdue Pharma and the opiate blowback).
• Historically, health plans did not have very good coverage for psych
• Very difficult to get into any form of talk therapy due to a shortage of providers
• When you can get in, a lot of the talk therapy nowadays is neo-Freudian "trauma-informed therapy" (i.e. bullshit) where the therapist is spending time trying to dredge up issues from your childhood rather than working with you in the here and now to develop healthier patterns of thinking. Not saying that there isn't a subset of people who can benefit from going back to their past to see what they can find, but this is the minority, IMO. A lot of the trauma-informed shit doesn't really feel catered to solving problems, just to drag things out as long as it can to extract more money from the patient and the health plans.
• Talk therapy has a certain subjective element to it where both the therapist and patient need to "click." Sometimes a therapist may be very competent, but they just aren't a good fit for specific individuals, which further increases the frustration on the part of the patient when they need to look for another provider.

ToeMissile said:

There's a good bit of overlap in anxiety & depression, so I can see how decreasing anxiety could also reduce depression.

During my Holiday Inn stay, I did some reading:

https://www.perplexity.ai/search/what-is-the-relationship-betwe-EjIij7LaRsKZBU7XmBAtgw#23

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I like to look at what the drugs actually do rather than what conditions doctors say are "indicated." Buspar is a selective serotonin agonist (means it stimulates certain serotonin receptors) and a selective dopamine receptor antagonist (calms down or de-stimulates some dopamine receptors). What serotonin and dopamine do is way beyond anything I'm about to type out, but I'd start in the pharmacodynamics section of a drug you're looking at:

Buspirone acts as a partial agonist of the serotonin 5-HT1A receptor with high affinity.[3][38] It is a partial agonist of both presynaptic 5-HT1A receptors, which are inhibitory autoreceptors, and postsynaptic 5-HT1A receptors.[3] It is thought that the main effects of buspirone are mediated via its interaction with the presynaptic 5-HT1A receptor, thus reducing the firing of serotonin-producing neurons.[3] Buspirone also seems to have lower affinities for the serotonin 5-HT2A, 5-HT2B, 5-HT2C, 5-HT6, 5-HT7 receptors where it probably acts as an antagonist.[37]

In addition to binding to serotonin receptors, buspirone is an antagonist of the dopamine D2 receptor with weak affinity.[3][38] It preferentially blocks inhibitory presynaptic D2 autoreceptors, and antagonizes postsynaptic D2 receptors only at higher doses.[3] In accordance, buspirone has been found to increase dopaminergic neurotransmission in the nigrostriatal pathway at low doses, whereas at higher doses, postsynaptic D2 receptors are blocked and antidopaminergic effects such as hypoactivity and reduced stereotypy, though notably not catalepsy, are observed in animals.[3] Buspirone has also been found to bind with much higher affinity to the dopamine D3 and D4 receptors, where it is similarly an antagonist.[45]

And then go do research and figure out what those particular serotonin receptors do and the dopamine ones do. "In general" serotonin is more tied to mood, stimulating serotonin receptors elevates mood and makes emotional things seem more intense. Dopamine is more tied to motivation, taking action, and reward system. This is VASTLY oversimplifying, but you get the idea.

SSRI's by contrast try to elevate your circulating serotonin levels (body naturally makes serotonin, a neurotransmitter, in certain amounts; a serotonin agonist sits in the serotonin receptors and stimulates them - a serotonin agonist could be considered fake serotonin that is activating the receptor in a different way than natural serotonin) by preventing the body from re-absorbing serotonin as it usually does, thus elevating the circulating levels. This "should" elevate your mood and probably does temporarily, but the body down-regulates serotonin receptors in response to elevated serotonin levels:


Which is probably why the effects level off after a while and you're just left with bullshit side effects.

I'm not sure anybody really knows why serotonin effects mood, but it does, and we know what these drugs do even if we don't exactly know why.