onedayillsailagain

So, apparently there's a retailer carrying 7,8-DHF: http://tht.co/7.8-Dihydroxyflavone.html at $22/g (which ain't bad). I can't vouch for their legitimacy though; they seemed to pop up out of nowhere (specifically, when LC user yadayada mentioned them in several LC threads). There's a Reddit discussion on their legitimacy going on here. Their CoA (FWIW I suppose) can be found here. As for the group buy; judging from the last update, it should be received by the coordinator within a week. So, with a bit of luck, I'll have it soon.

Interesting BPC. Still, other anxiolytic (neuro)peptides seem superior, in that they lack sedative effects. As for your question: To be honest, I have yet to contact my supplier for a quotation for Emapunil.. I presume, judging from the lack of it being in stock anywhere, that it will require custom synthesis, which is substantially more expensive. But, I'll ask some people, and see what they come up with.

There are several reports of Minocycline-induced DP.. Conversely, there are one or two stating it helped DP. Interesting. I'd still think D-Cycloserine would be better though. By the way; I happened to mention NewMind in a Reddit post, and how they never replied to my e-mail about D-Cycloserine, and they replied. Just in case you guys were considering it.

Great that you're doing better! It is interesting that an Meclizine improved your situation, as it is an anti-cholinergic - like several alkaloids in Datura. But, it is also an anti-histamine, interestingly. Perhaps it's helping some allergic response that was exacerbating your condition. Or, the vestibular effects may be implicated indeed. I recently acquired Sudden Sensorineural Hearing Loss, and have had vertigo ever since, and the whole ordeal has significantly exacerbated my symptoms as well. I might look in to this; I was considering betahistine myself, as it lacks anti-cholinergic properties and causes vasodialotion locally in the inner ear, as well as being an anti-vertigo agent. Regardless of the cause of your improvement, it happened, which is what is most important. Here's to hoping it sustains and gets progressively better! All the best, Odisa.

Sorry; I was in a hurry and didn't see it was Syntheso who posted. My bad! BPC: I would look in to D-serine or Sarcosine as NMDAR co-agonists; those mega-doses of glycine make me nauseous, and I'm not one to get nauseous fast. Plus it's sweet, with a disturbing twist. Preferably D-serine, as it is a full agonist. About Eglumegad: The reduction of intracellular cAMP is quite interesting, as this would mean less CREB activation, which could exert beneficial effects on Dynorphin levels. (If I recall correctly; haven't spent too much time looking into those pathways). As for the reduction of dopamine levels: whether that would be beneficial or detrimental, would be dependant on the localization I suppose. It's interesting that a glutamatergic agonist is neuroprotective, rather than excitotoxic. I'm not sure how beneficial the reduction of glutamate would be.. I mean it does seem to be the working theory currently for DP (considering the Lamotrigine stuff), but I can't say I completely agree with this view. Nonetheless, still interesting.

Highly interesting BPC! I've known of Eglumegad for a while, but somehow failed to notice this. Anyway, I'm late for a bus, I'll reply in detail when I get back

http://www.nature.com/npp/journal/v25/n4/full/1395707a.html I'd suggest reading the entire article. Though Coluracetam didn't quite seem to cut it, I do see potential for selective Muscarinic agents, possibly particularly for the M1 subunit. Xanomeline is one such agent that activates M1, although it's non-selective, moreover also antagonizes M5, and also has a high drop-out rate due to adverse events. Unfortunately, most other muscarinic agents are either not centrally active, or are antagonists. I still have to look in to Vedaclidine, which may or may not be centrally active; this is not clear from an initial glance. To be fair, however, other subtypes still warrant investigation.

I concur with mikezero and brake.

Hey Andrew, just wanted to ask: what are your thoughts on Suni after you've tried it? I'm considering trying Unifiram myself. Hope you're doing well, Odisa

Very good that this is moving forward; thanks David! Unfortunately I currently can't commit to helping out as much as I would like, but I will of course be donating. Hopefully I can join in later in terms of more hands-on approaches... better late than never

Was looking in to Metadoxine (a 5-HT2B antagonist) and came across this: http://www.ncbi.nlm.nih.gov/pubmed/18337424

Seems so. I don't know much about that to be honest, but I am very interested in the endophinergic mechanisms they observed. I'll see if I can get the full article one of these days.

http://link.springer.com/article/10.1023%2FA%3A1009571806136

Worth a shot indeed. I must warn though: if you're going to try this at home, be absolutely sure that you know what you're doing. TUS is also used to kill neuronal tissue.

I was just checking to see whether there were any new articles on HPPD. Aside from some entheogen paper claiming HPPD is synonymous to flashbacks (which was also a 2014 paper.. sigh), this is what I could find: Objective: An unusual side effect of hallucinogen use is the appearance of hallucinogen persisting perception disorder (HPPD). Despite high rates of prior hallucinogen use among individuals with schizophrenia, there is insufficient data on the clinical characteristics of individuals suffering from co-occurring schizophrenia and HPPD. Methods: Twenty-six hospitalized patients with schizophrenia and prior LSD use (12 with HPPD and 14 without HPPD), were recruited. Participants were clinically assessed using validated tools and details regarding hospitalizations were retrieved from their medical records. Those patients who also had HPPD completed a questionnaire addressing HPPD-associated perceptual disturbances. Results: Participants were mostly male (n = 22, 84.6%) and had an average age of 32.3 (SD = 7.67). Nearly half (n = 12, 46.2%) met criteria for HPPD. No significant differences were found in sociodemographic and clinical characteristics (including response to anti-psychotic medications and adverse effects) between the groups. Nine individuals (75%) in the schizophrenia and HPPD group reported the ability to identify specific precursory cues for the appearance of the HPPD-associated perceptual distortions, and 8 (67%) reported the ability to distinguish HPPD perceptual disturbances from those associated with their psychotic disorder. Conclusions: Very little is known about the co-occurrence of schizophrenia and HPPD, or the clinical implications associated with it. Further research is needed to understand the clinical impact of this comorbidity. source I'll try to get the full article later.

Nope, right handed. How many of you have simian lines?

I came across SciOpen Research Group (SRG), and thought: "Awesome!". They now have an IndieGoGo campaign to raise funds for microscopic tissue analysis to assess the effects of J147; a potent neurotrophic Curcumin derivative that's orally active. They are a self-proclaimed "Guerilla Biotech" research group. I'll just post the video, so you can see for yourself: Bridging the "Valley of Death": Introduction to SRG: https://www.youtube.com/watch?fv=4x4efcbRRWg Now their main focus is ALS, however this is just their first project. They are interested in any neurogdegenerative disorders. Now I'm not saying they'll be interested in HPPD, or if they can even do something for it, but I just wanted to post this as I found it an inspiring example. Perhaps, if they are successful, more initiatives such as this will take off, and somewhere along the line HPPD may become a focus of research as well? Or, whatever fruits such endeavours bear, may be applicable to us. Either way, I found it post worthy.

Interesting.. Who made this sub-forum? Anyhow, I was playing with the idea of making a new HPPD website to be honest, but haven't been doing that great lately, so I've been procrastinating. One awesome thing I came across, is the Discourse forum software. Interestingly, the schizophrenia forum already uses it. It's in Beta and requires some tinkering, runs on Ruby so won't be compatible with your average web-hosting (works good on Digital Ocean running Ubuntu). But it's so much better than any forum software I've seen to date. Also, it's completely free for non-profits, unless you want them to set it up for you.

I'd suggest trying some CBD, if you have the pocket for it. So far CanChew seems to be legit, whereas CibDex made me stoned.

Hi Doreen, I was just wondering: is there a deadline for the survey? Thank you, Odisa

https://www.youtube.com/watch?v=H7pEBHiDpJQ

Sorry BPC, but I figured this would best suit a new topic, so I moved the posts. Thanks for the vid; pretty interesting stuff.. Though then again it would be limited to seeing black and white. Moreover, I wonder whether the people actually "see" an image in their mind when navigating through space.

Indeed. Discussion of HPPD starts at the last 11:30 minutes (in case you're not interested in 30 mins of stuff we generally already know). What they did not mention is the level of chronicity in that HPPD is generally a 24/7 thing, which I found quite disappointing. Also they failed to mention the detriments of Clonazepam, and it was the only treatment they cited. Ahh well, it's a pop-culture podcast after all.

@BPC, although I don't doubt that would be a highly interesting read, however ultimately I don't see how that could be easily applicable to our condition. I currently have "The Synaptic Self" and "The Principles of Neural Science" that I still need to read too! Also, I'd think that if such things as you describe were possible, one would have to have a pretty good level of cognition. I mean if I had the issues of falling sensation, I doubt I could keep focused enough to retrain with any type of therapy currently; perhaps this is not the case in mild cases of HPPD who could retrain more easily, but then again I'd think perhaps other therapies would be more appropriate in that case. Also; did he describe in detail how to perform the therapies? This is presuming not all/other regions are suffering from deficits in neuro/synapto/myelinogenesis.

Well, as I said I'm not 100% certain, but read through this: I also just did a write up on "Why not to use the CILTEP stack". I also just noticed this: source This indicates that synaptic NMDAR activation increases BDNF expression (good), but also induces CREB activity (see my write-up on why this is unfavorable). Extrasynaptic NMDAR activation causes CREB deactivation which in turn blocks induction of BDNF expression. This, I believe, brings us in a bit of a conundrum where activating synaptic NMDARs would upregulate Dynorphin expression via CREB, thus leading to dissociative symptoms, whereas activating extrasynaptic NMDARs induces the unfavorable blockage of BDNF expression. Solution? Hmm.. TrkB agonism to compensate for extrasynaptic NMDAR activation induced blockage of BDNF expression? However yet again there are conflicting statements; the underlined text indicates a difference in synaptic or extrasynaptic NMDAR activation and the effect on apoptosis, whereas the first quote states that there is not in the case of NR2A. I don't know, I haven't been as meticulous about it as I would like, so perhaps I've made some mistakes/too much assumptions. For example; I'm assuming NR1/NR2A = NR2A, but that may be a receptor coupling of NR1+NR2A that's being referred to, so please take this all with a grain of salt All this conflicting stuff is confusing me, so I'm procrastinating, haha! NMDA receptor function: subunit composition versus spatial distribution. might be enlightening.