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NYTimes Article that Highlights Opioids as Antidepressants. Feeling not so alone.

Shkspear

Greenlighter
Joined
Aug 10, 2016
Messages
5
Hi all,

Long time lurker here. Most of what I have learned about harm reduction I have learned from this site. First post but I wanted to share something I saw on the internet today, by chance. If this isn't the right forum, mea culpa and feel free to move it.

Today I read Are Opioids the Next Antidepressant over on the New York Times' site and it really spoke to me. I am a recovering RX addict who's story is typical: Lost relationships, lost money, etc. But I always said to my therapist I never "got high" from Opiates. They simply made me function normally. I didn't feel depressed, or unmotivated. I never "nodded" from them. In fact, 120MG of my DoC would pep me up quite a bit. In the spirit of HR, I *never* recommend anyone ever self-medicate without the consultation of a medical professional, of course. Just my story.

Of course I'm clean now and back to being depressed.

It's interesting as we read the research out there how these drugs are being re-examined. It certainly lends credence to why tianeptine (found to act on the mu and delta receptors) has been touted as such an effective AD.

Kind of made me feel not so alone about it.

Anyway, thanks for your information over the years. I look forward to contributing to this community as you have contributed to me.

- Shks
 
I can understand opoids for immediate suicidality etc. but I think the point of an antidepressant is to induce long term changes that the subject will receive benefit from even when the drug is gone (increases in neurogenesis and neuroplasticity for example).

Ketamine would my choice for immediate suicidality though.
 
Very fair point. I will say it was always more of an acute solution than one that was sustainable, for sure. And hey, it never ends well.
 
It can take an acute solution to get you to the point where more long term things like outlook changes or therapy etc. can take hold so it's not like acute solutions are pointless - I'm sure they have their place.
 
I've tried many antidepressants and none of them ever had any real noticeable effect.

I found opiates work very well, but only lasts for a bout a month or two, opiods work much better.

Tramadol and suboxone are very different in that I found that I could continuously benefit from their antidepressant effects lasting the longest as use continued.

I'm pretty sure I read somewhere that Suboxone is getting trials for antidepressant use and that's terrible because nothing is worth an opiate/opiod addiction.
 
I've tried many antidepressants and none of them ever had any real noticeable effect.

I found opiates work very well, but only lasts for a bout a month or two, opiods work much better.

Tramadol and suboxone are very different in that I found that I could continuously benefit from their antidepressant effects lasting the longest as use continued.

I'm pretty sure I read somewhere that Suboxone is getting trials for antidepressant use and that's terrible because nothing is worth an opiate/opiod addiction.

Yeah tramadol works great as an antidepressant, it the only SNRI/SSRI I would go on.
 
I've tried many antidepressants and none of them ever had any real noticeable effect.

I found opiates work very well, but only lasts for a bout a month or two, opiods work much better.

This.

As I thought of the difference between opiates and opioids after publishing this post, I have to agree. Tianeptine (never recommended in daily, high dosage!) acts on the receptors but is not a traditional opiate and people report a lot of success with it because of it's Mu and Delta activity. It's not necessary to take it at the 100mg+ range to get that activity but many chase a rush.

I found a fabulously interesting post (that I have to find the source of) where someone said they take 1/4 of a Hydrocodone/APAP 4-5 times per month for depression.

But I do have to agree with you David, as an addict myself, I can't say I would want it forced upon the masses. The trouble isn't the opiate itself. The trouble is the dopamine inducing pleasure center (hedonistic tone, etc.) that as humans we typically say: More! Must have more!

And sadly this is why your average 40 year old soccer mom/dad could break their hand then travel down a long road of addiction that may never end.

Good replies, all. I was always curious what experienced Bluelighters thought of this.
 
As others have mentioned, one's immediate thought is that opioids don't sound like sustainable option for anything, but then you think of the kappa receptor and the long-term effects of Salvia or Iboga (reverse tolerance and addiction treatment, respectively) spring to mind. There are plenty of anecdotal reports of their use as antidepressants, and they have the 'bang' one expects would be needed for them to be one-time or occasional treatments.

Salvia and Iboga may not produce these effects via the kappa receptor, and even if they do it's not quite what the NYT had in mind, but hey, they're still opioid agonists.
 
Ibogaine anti addictive action might be due to a3b4 nicotinic receptor antagonism.

It is a promiscuous beast isn't it?

Well, Salvinorin A is pretty specific for the kappa receptor, and it seems plausible that any anti-depressant effects it has are a result of a homeostatic reduction in those receptors after its use. The reverse tolerance would have to have another mechanism, else we're in trouble and dynorphin would start licking its lips - depression all over again.
 
I've tried many antidepressants and none of them ever had any real noticeable effect.

I found opiates work very well, but only lasts for a bout a month or two, opiods work much better.

Tramadol and suboxone are very different in that I found that I could continuously benefit from their antidepressant effects lasting the longest as use continued.

I'm pretty sure I read somewhere that Suboxone is getting trials for antidepressant use and that's terrible because nothing is worth an opiate/opiod addiction.
Not all the studies are being conducted with buprenorphine alone...some are in combination with a mu antagonist, so the resulting treatment functions as a selective kappa antagonist.

An antidepressant based on standalone buprenorphine would make patients dependent, but not addicted. There is a huge difference. Obviously many people can, and do, live productive lives while dependent on buprenorphine.
 
Ibogaine anti addictive action might be due to a3b4 nicotinic receptor antagonism.

http://www.pubfacts.com/detail/1190...trategy-to-reduce-opioid-and-stimulant-self-a
Recent evidence of Ibogaine antiaddiction points strongly towards the involvement of its metabolite NorIbogaine its first pass metabolite rather than the parent: cf this recent paper (but caution! this company is promoting Nor-Ibogaine for OP/$tim dTox so they have vested interest. But the evidence look pretty strong). Noribogaine rather than Ibogaine is responsible for the antiAddictive effect.
Unlike IBG, norIbogaine is a strong kappa agonist but not a sigma or a nicotinic antagonists (2 targets suspected of involvement in IBG anti-depressant and anti-addiction effect). Same with dextromethorphan (DXM and its O-desmethyl metabolite DXO and its anti-addiction . I f I remember there were a thread earlier on that. Here is abstract of Mash paper:
Oral noribogaine shows high brain uptake and anti-withdrawal effects not associated with place preference in rodentsMash DC1, Ameer B2, Prou D2, Howes JF2, Maillet EL3. J Psychopharmacol. 2016 Jul;30(7):688-97. doi: 10.1177/0269881116641331. Epub 2016 Apr 4 http://www.ncbi.nlm.nih.gov/pubmed/27044509

[h=3]Abstract[/h]This study investigated the effects of noribogaine, the principal metabolite of the drug ibogaine, on substance-related disorders. In the first experiment, mice chronically treated with morphine were subjected to naloxone-precipitated withdrawal two hours after oral administration of noribogaine. Oral noribogaine dose dependently decreased the global opiate withdrawal score by up to 88% of vehicle control with an ED50 of 13 mg/kg. In the second experiment, blood and brain levels of noribogaine showed a high brain penetration and a brain/blood ratio of 7±1 across all doses tested. In a third experiment, rats given oral noribogaine up to 100 mg/kg were tested for abuse liability using a standard biased conditioned place paradigm. Noribogaine-treated rats did not display place preference, suggesting that noribogaine is not perceived as a hedonic stimulus in rodents. Retrospective review of published studies assessing the efficacy of ibogaine on morphine withdrawal shows that the most likely cause of the discrepancies in the literature is the different routes of administration and time of testing following ibogaine administration. These results suggest that the metabolite noribogaine rather than the parent compound mediates the effects of ibogaine on blocking naloxone-precipitated withdrawal. Noribogaine may hold promise as a non-addicting alternative to standard opiate replacement therapies to transition patients to opiate abstinence.

© The Author(s) 2016.
 
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