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Onemorestep last won the day on May 22

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About Onemorestep

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  1. Good to hear Jbalsa! Let us know how it goes. Does mirtazapine interact with the 5ht2a receptor? For some reason I feel like I heard it did once.
  2. It just isnt available as a prescription. You can buy it on ceretropic I believe. I almost did last October and didn’t for whatever reason.
  3. I’ve been thinking a bit about naltrexone too. Lately I’ve been using DSIP at nights and I notice it makes me feel pretty great. One of the ways it works is my mild opioid antagonism so if that is what I’m responding to then low dose naltrexone might be nice too.
  4. Man I was going to order some of this stuff in October and didn’t get around to it. About a month later I came across something that made me think “holy shit thank god I didn’t take that.” But for the life of me I can’t remember what it was or where I found it. I just remember knowing that I would have had a horrific reaction to it had I tried. If I can remember what it was I’ll post it.... but I’m glad to hear it isn’t doing that to you!! Remember to keep an eye on your liver i beleive you can buy buy this in the USA from ceretropic.
  5. Do they have the same exact MoA? I thought it was just that briv had 20 Times potency for inhibiting sv2a. We don’t know why keppra works for hppd. It might be the sv2a inhibition or it might be something completely else. My experience with researching keppra was that all the research is for epilepsy, and was centered around a few MoA for the drug. It’s possibly that keppra does other things in the brain and the pharma company wasn’t even looking there. In fact, I would say if you are correct that briv has fewer sides but is more powerful, reasoning says it probably has different moas from keppra. That being said, if you try one and it doesn’t work, why not try the other. Racetams are very weird drugs. They’ve been studied, but not enough imo. I would love to see more work done with them to create other compounds for healing.
  6. Perhaps give uridine a shot. You may be right and your hppd isn’t choline based. It could be other neurotransmitters/receptors are out of whack making your current cholinergic functioning uncomfortable. I know my cholinergic receptors aren’t damaged, but my dopamine/glutamate ones are. This makes having normal levels of acetylcholine rather uncomfortable for me. Anhedonia, depressed mood, etc. no fun.
  7. @TheMythos coming off keppra actually made me less intelligent. Fucked my memory back to the state it was pre coluracetam/baclofen therapy. However, I think this is where my brain wants to be. I could increase my memory again through cholinergics but it makes me horribly depressed. aminita is a cholinergic agonist I think? I think you can overdose on it and get cholinergic poisoning. One thing I’ve noticed with hppd is my cholinergic neurons don’t seem to understand homeostasis anymore. They take a very long time to go back to where they are supposed to be. If I take things that boost it, the effect is seemingly permanent for like a year or two before it returns to normal. Idk what that’s about.
  8. @TheMythos did quitting smoking make this worse worse right away? I keep a really steady amount of nicotine (not tobacco) in my system theorizing that the downregulation of those receptors is actually good for my symptoms.... I’m also quite addicted haha. have you ever tried uridine? I’m just curious. It would be interesting to know if that helped or hurt.
  9. It definitely is something probably everyone with hppd has issues with. Hard to have high anxiety without probably having high cortisol haha. my doctors say I’m in range though..... perhaps I’m just used to living with this crap 💩
  10. Not sure about ataxia... funny it’s so close to ataraxia but deff not as nice... i would love love to try topamax but my body responded so poorly to keppra I have a bit too much anxiety about it. Since I don’t know what MoA in keppra caused them, I can’t say whether top won’t do the same. im interested to see if you’ll return to the same state as pre topamax. I know keppra seemed to have benefits for me even after I stopped.
  11. Yea I got mine from getting nbombed too. I also experienced the muscle spasm as one of my symptoms. However, I can say that I was able to regain a significant amount of cognitive function (I could barely speak when I got hppd... it was bad.) time, sobriety, and healthy life experiences will do a lot of good for you. I promise you, if you hang on, it will get better. I’ve been in that dark hole and know it can be difficult to believe that it will, but we are molded in the fires of adversity are we not? In many ways, while I still suffer quite a bit (mostly through damaging my hypothalamus with drugs post acid) this was probably something that needed to happen to me. I’m doing stuff with my life I probably wouldn’t have if I had continued down the path I was on.
  12. I was recently looking into autoimmune stuff as I seem to suffer from several issues relating to my system.... plus my t4 levels came back pretty low. Wonder what this will bring up.
  13. I’ll have to give this a good read when I have a bit of time. Life is a bit hectic right now with business and preparing for a long trip to Europe. from a very brief skim... this is fascinating stuff. I’ve always thought that acetylcholine plays a pretty major role in hppd but it’s just one piece of a very complex puzzle. Drugs that effect it downstream have helped me in the past... but understanding why is more difficult. ive unfortunately not done a huge amount of research into anticholinergic usage and issues that arise from it. The only thing I think I’ve read is it can cause damage to the basal ganglia. But that might be secondary to other disregulation and effects. I’m not sure... I can’t give you any strong suggestions for things to try. I’m a big advocate of bpc-157 and I know it has some effect on cholinergic signaling at least in the body (eyes).... but that’s kinda something I tell people to try because it’s so holistic and adaptogenic. It seems to correct a lot of different neurotransmitter systems involved in hppd. Don’t know if it will last forever but it certainly made a difference for me. I didn’t read much about it effecting many cholinergic neurons. the interesting part is the combination of hallucinogens, dissasociatives, AND acetylcholine precursors causing a really bad time. Hppd seems to not only disregulate the 5ht2a receptor and keeping one in a “trip” state, but from my personal experience it severely diminished my glutamate receptor functioning and increased AND decreased my acetylcholine levels in different areas. The only thing I’ve found that decreases the acetylcholine is keppra and subsequent withdrawals from it. Seems to be a permanent effect. Why, I have no idea. I do know that people who have withdrawn quickly from drugs like lamictal, keppra, and benzodiazepines have complained about “cognitive issues” that I believe are related to poor acetylcholine functioning as the withdrawal from these drugs seems to have reversed the semi permanent effect of coluracetam on my brain (a high affinity choline uptake enhancer). But this is all speculation. sorry I can’t be of more use right now.
  14. “The impact of agomelatine on glutamate signalling has been examined as this excitatory amino acid neurotransmitter and its receptors play a role in depression and antidepressant activity (Mitchell and Baker, 2010). Drugs with glutamate-based mechanisms are endowed with accelerated onset of activity. Currently, the non-competitive NMDA receptor antagonist ketamine appears an attractive therapeutic agent for treatment-resistant patients with depressive disorder (Machado-Vieira et al., 2009). However, the cognitive and dissociative side effects of ketamine limit its widespread application. The exact implication of glutamate in depression and antidepressant treatment is far from clear because of the many interactions with other neurotransmitter systems, for example through kinase phosphorylation and BDNF synthesis in the case of ketamine (Autry et al., 2011). A number of other drugs [e.g. selective GluN2B receptor (NR2B) antagonists, positive modulators of AMPA receptors, and metabotropic glutamate (mGlu) receptor agonists/antagonists for nomenclature see Alexander et al., 2013a] also exhibit antidepressant-like effects in animal models of depression (Hashimoto, 2011), but no clinical studies demonstrating the effectiveness of these drugs are available. Through a synergistic interaction between its MT1/MT2 and 5-HT2C receptor components, agomelatine modulates glutamate signalling, engaging time-dependent modifications of receptors and transporters in circumscribed regions involved in the regulation of mood, circadian rhythms and cognition (Racagni et al., 2011). Thus, the acute administration of agomelatine (40 mg·kg−1 i.p.) abolishes the restraint stress-induced increase in extracellular glutamate efflux in limbic structures such as the basolateral and central nuclei of the amygdala and the hippocampus (Reagan et al., 2012). As previously found with other antidepressants (Bonanno et al., 2005), chronic administration of agomelatine (40 mg·kg−1, i.p., for 21 days) significantly reduced endogenous release of glutamate from hippocampal synaptosomes and decreased the accumulation of SNARE (soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor) complex, a key molecular effector of vesicle docking, priming and fusion at presynaptic membranes (Milanese et al., 2013). Long-term administration of antidepressants elicits adaptive changes in the functional status of mGlu receptors (Paul and Skolnick, 2003; Palucha and Pilc, 2007). This is also the case of chronic agomelatine, which normalizes glutamate release and the expression of mGlu2/3 and mGlu5 receptor mRNAs in the hippocampus of rats subjected to prenatal restraint stress (Morley-Fletcher et al., 2011; Marrocco et al., 2014). Further, chronic agomelatine treatment modulates the expression of mGlu receptor mRNA in a time- and region-dependent manner (Varcoe et al., 2009). For example, agomelatine increases the evening expression of mGlu1, mGlu4, mGlu6 and mGlu8 receptors in the frontal cortex, while some transcripts can be over-expressed in the morning (mGlu7) and at night (mGlu8). Other time-dependent changes are induced by agomelatine, for example in the SCN (where mGlu7 receptor levels increased at night and decreased during subjective day). Those changes in the timing of glutamate receptors could be conveyed by rhythmicity of certain CLOCKgene's transcription factors (Varcoe et al., 2009).” Fascinating. This is something I’d like to look into.
  15. It’s never a bad thing to rule out. To me, this reads easily similar to experiences I’ve had with similar medications though. I’ve personally never experienced a positive placebo effect and find it hard to wrap my head around. One would think I would have, since I never do any kind of blind study on myself (always research as much as I can). Probably my strong negative mindset 😂