I've yet to see a single confirmed instance of xylazine, fentanyl or nitazenes being in tianeptine. I don't doubt at all that it induces respiratory depression, almost every opioid I'm aware of does.
Perhaps tianeptine isn't like almost every other opioid you're aware of.
Tianeptine reduces morphine antinociceptive tolerance and physical dependence
Tianeptine prevents respiratory depression without affecting analgesic effect of opiates in conscious rats
The issues re: respiratory depression and wtf exactly is going on are unresolved.
Tianeptine is an atypical tricyclic atypical antidepressant and cognitive enhancer that produces neuroplastic changes and modulates noradrenergic, dopaminergic, and AMPAR glutamatergic pathways [
Citation59,
Citation60]. As mentioned above, AMPARs play a crucial role in maintaining respiratory rhythmogenesis and inspiratory drive through their excitatory activity within the brainstem respiratory networks. These molecular actions prompted an animal study on the ability of tianeptine to reverse morphine-induced respiratory depression with positive results [
Citation61]. However, a series of experiments in humans failed to show any efficacy of tianeptine in reversal of alfentanil-induced respiratory depression (following oral tianeptine) or remifentanil-induced respiratory depression (in response to intravenous tianeptine) [
Citation62]. In fact, it was observed that tianeptine enhanced remifentanil-induced respiratory depression, possibly related to the induction of sedation or to its (weak) μ-opioid receptor mechanism agnostic activity [
Citation63]. Interestingly, the animal data suggest that the sequence of tianeptine administration might affect its ability to reverse opioid-induced respiratory depression [
Citation61]. It seems that the presence of tianeptine in the brainstem preemptively prevents the development of opioid-induced respiratory depression, as observed in animal studies [
Citation61], while administration after an established opioid-related respiratory depression is not effective as observed in humans [
Citation62]. Apparently, the sequence of events initiated by the opioid is not reversed by tianeptine."
"In summary, we discussed three drug classes with absence of efficacy in reversing opioid-induced respiratory depression. While dissimilar in the mechanism of action, animal studies suggest that the common cause for the lack of sufficient drug availability within the brainstem respiratory networks might be responsible for the lack of efficacy. Additionally, lack of receptor selectivity may be involved in the many serotonin-receptor agonists that have been studied."
The initial research on it wasn't FALSIFIED, lol, and it isn't an SSRI. What do you mean to "get it passed as an SSRI"? That isn't how drugs get approved, lol. Why are you just making sh1t up? Drugs get approved based on their efficacy for a given indication and when they've demonstrated safety, etc. It doesn't matter what the mechanism of action is! Why would it? What matters is what happens when its given to people! And they didn't give anyone GRAMS of it in the studies, because they were looking to treat them, not poison them.
It does the opposite. I know lots of people will claim that the enhancement of serotonin reuptake is bullsh*t, but I'd like them to explain why it's a potent anti-asthmatic, then. What's its mechanism of action? They didn't pull that out of their asses. I'm not saying that it necessarily is a reuptake enhancer, but I've been into this stuff since like around the year 2000, and the whole outlook of professionals (at least in the publications I've read) changed when it became a drug of abuse. It's reprehensible. It is a safe and effective antidepressant. No one knows how it works--still.
Lol, fraud. Did it ever occur to you that it has multiple enantiomers? I haven't looked, but I'll bet if you can find an animal study of the different enantiomers, you might see things differently.
They had no reason to LOOK for mu agonist activity. They were targeting depression, and the doses people take to get high are orders of magnitude higher than the antidepressant dose! For depression, it is effective at 12.5mg three times a day! David Pearce (at biopsychiatry.com) has a page he's maintained for decades with links to journal articles about tianeptine. It is so bloody disgusting what the media has done to that drug--because of all of the people it could help.
Take several orders of magnitude more than the therapeutic dose of your SSRI/SNRI and see how it goes. Nobody's talking about that, though, because it doesn't make you feel good. It's ridiculous.
You know you actually can read about its development. You don't have to guess what they were thinking. And it is a tricyclic, yes, but if you look at the structure, you'll see that it's radically different than most of them! BTW, if people took as much of a TCA as they took of tianeptine relative to the therapeutic dose, they'd probably die.
Where's the panic over loperamide, a cardiotoxic opioid?
Under normal circumstances, loperamide has minimal systemic absorption due to extensive first-pass metabolism and limited permeability across the intestinal mucosa. However, in the presence of severe gastrointestinal inflammation, compromised mucosal integrity may enhance loperamide’s central...
www.cureus.com
People pay attention when it gets you high, and then characterize a given drug completely differently. If citalopram got you high, everyone would know about cases like these:
Acute respiratory distress syndrome, metabolic acidosis, and respiratory acidosis associated with citalopram overdose
Hawa Edriss MDa, Marie Pfarr BAb
Correspondence to Hawa Edriss MD
Email:
[email protected]
SWRCCC : 2014;2.(5):24-28
doi: 10.12746/swrccc2014.0205.058
