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MDMA Recovery (Stories & Support - 4)

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Well my two cents is (applying specifically to those who have trouble sleeping with their LTC) lowered testosterone and the symptoms of it can happen with sleep deprivation and insomnia, as well as depression. So it's possible that antipsychotics that can treat the aforementioned sleep/depression issues could restore testosterone, although lower testosterone has been seen in schizophrenics chronically treated with antipsychotics (although a lower rate of hormonal issues with Zyprexa compared to Risperidone).

But it seems to me like antipsychotics would mainly be something to try after SSRIs don't work.

What's been well studied and observed in MDD patients is higher stress hormones, which have been linked to actually causing MDD and have led the way for animal models of depression (neurogenic hypothesis of depression), and they are developing drugs to block these stress hormones (CRF antagonists). But antipsychotics do help decrease cortisol as well (https://www.ncbi.nlm.nih.gov/m/pubmed/27112637/) although they are not without their risks.

"Our findings suggest that haloperidol can directly regulate the hypothalamic-pituitary-adrenal (HPA) axis and immune system through a pharmacological action via D2 receptor antagonism. Finally, our data suggest that the increased hippocampal resting cerebral bloodflow is a manifestation of the reduction in IL-6 and cortisol which follows the administration of haloperidol."
 
https://www.ncbi.nlm.nih.gov/m/pubmed/17617388/
https://www.ncbi.nlm.nih.gov/m/pubmed/21689105/
https://www.ncbi.nlm.nih.gov/pubmed/17022948

I found this three studies (there are much more) about Curcumin and it's effects on Neuroplasticity, Neurogenesis, the Serotonin-System, HPA-Axis regulation, etc.
It seems like Curcumin could actually reverse the effects of chronic stress, this, and some other very powerful effects like cancer inhibition, anti-inflammatory effects, and much more.
Cotcha, I would be happy if you could tell me/us your opinion on curcurmin, because I'm very interested to hear your statement.
 
There seems to be some relationship between 5HT2A and tinnitus as well. Many people with tinnitus (not drug induced) report a decrease in tinnitus when using MDMA..... And a lot of people report Mirtazapine (potent 5HT2A blocker) is the the only AD that is known to not make tinnitus worse. Now I'm not sure what the connection is, but it appears there is.
 
Not sure if this is relevant but some years ago my dad had a really annoying tinnitus episode for about one month, mostly induced by extreme chronic stress. In this time his eye pressure was too high either. But after the stress got less, the eye pressure normalized and the tinnitus completely disappeared. So it could also be stress or anxiety related.

Stress and anxiety actually impair the whole brain chemistry, so there could be some cross factors between these those two and the problems directly induced by MDMA.
 
The issue with curcumin is getting it into the CNS - you probably need liposomal formulations to get high enough quantities into the brain. I would try Longvida, UCLA's formulation, if you have the dough. P-glycoprotein inhibitors can probably help in the mean time but careful combining that with other meds like SSRIs.

Careful not to get too much curcumin into your system.
 
5-HT2A activators (psychedelics) are often known to make tinnitus worse as well.

Not that mirtazapine is selective for 5-HT2A by any means.
 
Yeah it's a dirty drug, but a mild one. I'm in week 3 from ending it and haven't experienced anything too crazy. Yeah all I was saying is that over on the tinnitus forum people say that taking MDMA eliminated their tinnitus while they where high

I agree with the anxiety thing....mine took a noticeable spike a couple months ago when I had a sleepless night and got stressed about it.
 
Could it be possible that the reduced cognitive function, slowness of motorics and all those effects be because MDMA disturbs the normal release of Neurotransmitters in the whole brain? And if a brain cell is activated, it releases neurotransmitters. We actually never use all of our brain cells, and these we use more often are those who fully recover, but the one's that we use rarely, like in extreme situations or difficult cognitive situations, recovery slower because they aren't used so often?
It would in some way explain why (in my case) it's so difficult to make fast and accurate movements or react properly and fast enough in extreme situations or situations where I need to react very fast.
 
Cotcha Yankinov said:
The issue with curcumin is getting it into the CNS - you probably need liposomal formulations to get high enough quantities into the brain. I would try Longvida, UCLA's formulation, if you have the dough. P-glycoprotein inhibitors can probably help in the mean time but careful combining that with other meds like SSRIs.

Careful not to get too much curcumin into your system.
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Hm…I somewhere heard Curcumin is very lipophilic and so should easily pass the blood-brain barrier. Do you know more specific details about it? (p.m. if so)
 
Very low water solubility is actually one reason for the low bioavailability. Anyways, studies have shown high oral doses produce minimal plasma levels and the plasma levels aren't sustained at all "No curcumin was detected in the serum of subjects administered 500, 1,000, 2,000, 4,000, 6,000 or 8,000 mg. Low levels of curcumin were detected in two subjects administered 10,000 or 12,000 mg." - https://www.ncbi.nlm.nih.gov/m/pubmed/16545122/

As I recall, liposomal formulations were shown to greatly increase bioavailability and plasma concentrations.
 
ADubbs said:
over on the tinnitus forum people say that taking MDMA eliminated their tinnitus while they where high
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Interesting, although just to play devils advocate, that could be noise induced hearing loss related tinnitus (or did they specifiy the tinnitus came out of nowhere?) and/or maybe getting high just takes their mind off of it and then those "tinnitus circuits" start to calm down. I mean for most people, taking MDMA is an incredibly enjoyable experience, and you tend to leave the world behind.
 
Amml said:
We actually never use all of our brain cells, and these we use more often are those who fully recover, but the one's that we use rarely, like in extreme situations or difficult cognitive situations, recovery slower because they aren't used so often?
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The general principle of this might hold true (in terms of things that are used less get weaker, and things that get used more get stronger and recover) but we do at least tend to use all of our brain cells, the old "we only use 10% of our brains" thing is kinda old I guess. Maybe only 10% of our circuitry at any given time, but different circuits that do different tasks can still be routed through the same brain cells.

But a lot of our brain cell's interactions with each other are much more specific than "off" or "on", a brain cell probably has to receive certain input in a certain context to give certain output (and there are different ways that downstream cell can then choose to respond and pass on a certain signal or not to respond to that signal), even though all those same brain cells are being activated and used in different scenarios, they can do different things depending on how they are used.

So you might say that the circuits (as opposed to specific brain cells) we use are strengthened while the ones we don't use are weakened. Although there are of course exceptions, or at least they appear to be exceptions at first glance, for example exposure therapy for phobias/PTSD/anxiety. Having somebody purposefully be around something that really stresses them out doesn't actually strengthen their stress response when done properly (when their fear isn't reinforced) - each time they do the exposure their self reported stress levels are lower and lower.

Once they realize that their irritational fear of red cars doesn't make sense and that being around a red car isn't going to hurt them, the circuits that say mentally "oh my god it's a red car I'm going to die" start to get used less and then they weaken. So the "the car is not going to hurt me" circuits get strengthened and then they can oppose the "the car is going to hurt me" circuits.

But if the red car became alive and ran them over then the exercise would have had the opposite effect on them, even though both of those reactions to those two different scenarios could be mediated by the same brain cells. Hope this made some sense!
 
Cotcha Yankinov said:
Very low water solubility is actually one reason for the low bioavailability. Anyways, studies have shown high oral doses produce minimal plasma levels and the plasma levels aren't sustained at all "No curcumin was detected in the serum of subjects administered 500, 1,000, 2,000, 4,000, 6,000 or 8,000 mg. Low levels of curcumin were detected in two subjects administered 10,000 or 12,000 mg." - https://www.ncbi.nlm.nih.gov/m/pubmed/16545122/

As I recall, liposomal formulations were shown to greatly increase bioavailability and plasma concentrations.
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Yes, I already heard that pure curcurmin is actually none adsorbed and read nearly everything about adsorption factors and so on. The only thing I was surprised was the note you have mentioned about the amount of curcumin that passes the blood brain barrier. Liposomal formulations show a way higher adsorption of curcumin and have strong effects on people with joint pain or general inflammation. And the levels of curcumin metabolits in their blood are high too if it's taken as liposomal formulation. So did you mean that it is possible that it still wouldn't get a lot of it in the brain because of this glycoprotein transporter, or does this only count for the adsorption in the gut?
 
Cotcha Yankinov said:
The general principle of this might hold true (in terms of things that are used less get weaker, and things that get used more get stronger and recover) but we do at least tend to use all of our brain cells, the old "we only use 10% of our brains" thing is kinda old I guess. Maybe only 10% of our circuitry at any given time, but different circuits that do different tasks can still be routed through the same brain cells.

But a lot of our brain cell's interactions with each other are much more specific than "off" or "on", a brain cell probably has to receive certain input in a certain context to give certain output (and there are different ways that downstream cell can then choose to respond and pass on a certain signal or not to respond to that signal), even though all those same brain cells are being activated and used in different scenarios, they can do different things depending on how they are used.

So you might say that the circuits (as opposed to specific brain cells) we use are strengthened while the ones we don't use are weakened. Although there are of course exceptions, or at least they appear to be exceptions at first glance, for example exposure therapy for phobias/PTSD/anxiety. Having somebody purposefully be around something that really stresses them out doesn't actually strengthen their stress response when done properly (when their fear isn't reinforced) - each time they do the exposure their self reported stress levels are lower and lower.

Once they realize that their irritational fear of red cars doesn't make sense and that being around a red car isn't going to hurt them, the circuits that say mentally "oh my god it's a red car I'm going to die" start to get used less and then they weaken. So the "the car is not going to hurt me" circuits get strengthened and then they can oppose the "the car is going to hurt me" circuits.

But if the red car became alive and ran them over then the exercise would have had the opposite effect on them, even though both of those reactions to those two different scenarios could be mediated by the same brain cells. Hope this made some sense!
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That sounds senseful to me. Maybe this could be an explanation why the most people with depression feel normal again even after the treatment with antidepressants, beside the neurochemical changes. And the reason why mindful meditation works.
But I really think there is a difference between a single anxiety situation and the LTC. For me the main psychological LTC symptom was that total loss of interest in everything, that childish like feeling that everyone has. And I had the feeling the LTC is 100% the opposite of the positive effects you get from MDMA.
In my case, on MDMA I loved to dance really crazy and enjoying nature was the most beautiful thing ever. I liked this things even before, not that hard as on MDMA, but after the MDMA experience it just felt like exactly this things that made my life so beautiful and worth to live, and that were enhanced by MDMA, just felt like they were shut mute.
 
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@Amml

Stuff like that is *exactly* why I am wondering why people say LTC is psychological.

I have NEVER EVER heard of somebody one day completely losing interest in activities randomly from 100--->0%. Only in the case of something drug related have I ever heard of that. And I am not counting trauma etc since that wouldn't be out of nowhere.

Most depression and anxiety disorders are accumulated from a long term period not an instant on/off switch.
 
I imagine that many psychologists looking at this would try to intellectualize this on a phenomenon level - that is to say they want an intuitive explanation like "the self is shutting down and blocking joyful input because it has received too much stimulation" (really random horrible example), but there's probably no way to really understand this intuitively like there is with a person being acutely depressed after a loss of a loved one for example. They miss their loved one, fairly easy to understand although there might be complicating factors like guilt or regret if they didn't leave on a good note or get to talk about something that they meant to, but at least that's intuitively understandable. With LTCs, there's probably something specific (or multiple things) going on at a biological level that have no real purpose, no rhyme or reason to it.

But whatever the abnormal biology is, it can then go on to cause phenomena that it might help to try to think about intuitively. For example, LTC causes a lot bad symptoms, then people worry and ruminate. Some of the same biology that causes the symptoms probably causes biology that's more conducive to rumination and over-thinking as well. We can at least intuitively know that the over-thinking, if present in an LTC sufferer, is bad (and you might have been doing it before as well, just not over-thinking about negative things that stress you) and we can know that the over-thinking is contributing to the LTC or perpetuating it, and therefore we should try to do whatever we can to curb all the over-thinking.
 
Anyone got any guidance on 5 htp use? Should I stick it out? Bought some on Friday as I couldn't stand the stress of the last 5 and a half months of hell. Didn't sleep great on it, but yesterday I felt slightly less depressed, I wasn't ruminating quite so much on suicidal thoughts/thinking I've lost it, but physically felt more anxious and unsteady. Is this normal when starting 5-htp? Didn't take any last night because of it.
 
mf140 said:
Anyone got any guidance on 5 htp use? Should I stick it out? Bought some on Friday as I couldn't stand the stress of the last 5 and a half months of hell. Didn't sleep great on it, but yesterday I felt slightly less depressed, I wasn't ruminating quite so much on suicidal thoughts/thinking I've lost it, but physically felt more anxious and unsteady. Is this normal when starting 5-htp? Didn't take any last night because of it.
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I used 5-HTP in from the 3rd-7th month of LTC. Dosage: about 50mg/3x day
In my case I used st. johns worth the months before so it worked immediately on me. But without any other substances it could take about 1-2 weeks to feel the positive effects, just like in the case of SSRI. Try to not use it more than 2 months, so the normal Serotonin-Synthesis doesn't get too disturbed. And buy capsules with a low 5-HTP content, so you can find your needed dosage more accurate. On good days I only needed 50mg, on some bad days I dosed up to 300mg. And I still don't think that it was such a good idea to take it 4 months long.

In my opinion 5-HTP is more something like a substance that helps very much in short term, but has no positive long term effects, at least in my case.

Read this to get more information about 5-HTP:
http://www.bluelight.org/vb/threads/80280-5-HTP?s=
 
I don't know if you saw my earlier posts but 5 HTP sent me into the depths of hell. Although it worked for the first two hours on it. I'm still in that hell.
 
fnono33 said:
I don't know if you saw my earlier posts but 5 HTP sent me into the depths of hell. Although it worked for the first two hours on it. I'm still in that hell.
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How long are you into LTC? Maybe your brain chemistry is too disturbed by now and this change made it worse. Probably like SSRI don't work for some people too.
And if remember right you once mentioned that a single cup of coffee got you back to point zero. It seems like your brain is very sensitive to substances. Could that be possible? I'm just comparing that, because I have no problems with coffeine and if I take some other substances, even in the worst case it makes the symptoms just a bit stronger.

Cotcha, could this be though HPA-axis disregulation?
 
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