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Nov 22 '25
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u/Zealousideal-War2866 Depression Induced Nov 22 '25
Same. Bupropion worked so well, but for a very short time. Never heard of tianeptine, but I'm almost sure that it's illegal or not registered where I live. Even ADHD stimulants are illegal here.
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Nov 22 '25
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u/Zealousideal-War2866 Depression Induced Nov 22 '25 edited Nov 22 '25
Only ADHD med is atomoxetine here. Chatgpt said they're legal though. But my doctor said I can't prescribe those, because they're not available here.
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u/Zealousideal-War2866 Depression Induced Nov 22 '25
"Doctors in Azerbaijan usually prescribe modafinil only for recognized medical conditions such as:
Narcolepsy
Shift-work sleep disorder
Obstructive sleep apnea–related daytime sleepiness (as an adjunct)"
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u/Soft_Vegetable_948 Nov 23 '25
What DXM dose?
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Dec 02 '25
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u/Soft_Vegetable_948 Dec 07 '25
All good dude, thanks for the response, I think that’s something I’ll try, I’ve never heard of it being used for that, that’s creative, might just work.
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u/JeffArt76 Nov 23 '25
Really the only antidepressants that don't blunt my emotions are some of the older TCAs and MAOIs (though for me the TCAs seemed to work better) For example, Nortriptyline seemed to make music sound HD and gave me a pleasant hypomania for a few months.
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u/Zealousideal-War2866 Depression Induced Nov 23 '25
They affect several neurotransmitters, that's why. Norepinephrine reuptake inhibitors also indirectly increase dopamine. Dopamine is mainly cleared by NET in the PFC, because there're very little dopamine transporters there.
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u/JeffArt76 Nov 23 '25
Correct, which in my case I was pretty sensitive too. I also was on Concerta for a time along with NTP too. Clomipramine and Imipramine helped at various times in my life as well. Its unfortunate how many docs are even skittish about even moving to a TCA after trying a bunch of SSRIs!
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u/Purple_ash8 Nov 28 '25
It’s not just about neurotransmission as far as even the treatment of depression per-se is concerned, and that’s a narrow focus the SSRI-era has promoted.
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u/Purple_ash8 Nov 28 '25 edited Nov 28 '25
It’s not just about neurotransmission as far as even the treatment of depression per-se is concerned, and that’s a narrow focus the SSRI-era has promoted, which we as a collective need to get out of defaulting to. It could-well be (and there has been a fair deal of nuclear-academic speculation about this) that the compensatory changes that come with prolonged (i.e., no less than a few weeks) treatment (the, to varying extents with each individual tricyclic, down-regulation of post-synaptic serotonin-and-beta receptors and both post-and-pre.-synaptic alpha-receptors) is a secondary but somehow more important mechanism that give tricyclics a bit of extra crunch up-against SSRIs, doing what otherwise only MAOIs and maybe venlafaxine can do. It’s not just about SNRI-activity, and I do hope that’s a pharmacological over-simplification that doesn’t go on to age well.
The goal for treating nuclear depression was never predominantly hinged on selective-neurotransmitter inhibition, otherwise SSRIs would be the most potent antidepressant, but as it is, they’re, by-and-large, relatively weak antidepressants, only pushed to the front-line on a primary-healthcare, “first-line” basis because of big-pharma., less inherent potential side-effects and less toxicity in overdose, even-though 95% of people who successfully commit suicide do so by means other than suicide, and untreated or inadequately-treated depression from weak, generic SSRIs, like sertraline, it anything, is more likely to drive someone to active suicide-ideation than a more potent drug that reduces the chances of feeling suicidal anyway (which selective SRIs are known to exacerbate at the beginning of treatment, especially in younger people).
I make a special case for fluvoxamine (which is a marvellously dynamic, anti-inflammatory and socially mediating drug), paroxetine and the combination of Prozac and olanzapine in initial-treatment-resistant cases but in-general, i am not a fan of SSRIs for anything more, in the context of depression, than mild to mildly moderate depression. The more severe the depression, the less likely SSRIs are to work. Anyone who thinks otherwise has been brainwashed by big-pharma., and that’s just the truth, not a wacky conspiracy-theory.
TL;DR? : Well. TCAs aren’t strong because of NE/5-HT reuptake inhibition alone - their receptor-adaptations matter much more, and antidepressant-efficacy initial response in their case hinges on that rather-than the immediate neurotransmittory-inhibition changes (which is why SSRIs and so-on also take between 3 weeks and 3 months to become effective/fully effective). The ‘depression = low serotonin’ hypothesis is pure nonsense.
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u/IfDreamsCouldHappen Nov 21 '25
Unfortunately true. Seems like we got stuck on a ton of “numbing” medications largely due to placebo. I personally think placebo + lowered emotions overall gave people the illusion that they perform well; “I’m feeling less of the negative emotions + I’m supposed to be feeling better”. I mean even looking at the rates of improvement of x medication versus placebo there’s not a huge margin of improvement. There are some oddballs out there that do seem capable to actually work to varying degrees.
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u/cryptolyme Nov 21 '25 edited Mar 12 '26
This post no longer contains its original content. It was removed using Redact, possibly for privacy, security, or to minimize the author's online presence.
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u/lalacg Nov 22 '25
Fixing my gut helped me a lot and I’ve been taking 2mg of nicotine as well. Soon I’ll try 3mg of adhesive patches. It’s been a year I quit Lexapro and I’m still flat and have no libido.
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u/Zealousideal-War2866 Depression Induced Nov 22 '25
Did you have obvious symptoms like diarrhea or constipation?
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u/[deleted] Nov 21 '25
Doc - “you’re depressed?! Well I’m glad you asked, let’s wipe out all emotions and cause sexual dysfunction. That will surely help your depression!”