StateOfRegret

I tried it 3 times, I believe, twice at 500mg and once at 1000mg (well, 2 500mg-doses a few hours apart). I can't rule out placebo, but it semed to help somewhat with anxiety. It didn't do anything for "brain fog", however, and actually seemed to make my vision slightly blurry (a big drawback for me, as I find it hard enough to focus as is). I'd be willing to try it again, however. On the day where I took 1000mg I had some nausea after taking the second 500mg dose. I can't rule out the possibility that this was due to my horrible diet, however

All people start without degrees That being said, Einstein went to a Swiss polytechnic university and obtained exceptional grades in mathematics and physics on his entrance exam. He was no amateur and received education in his field. Which "theory on time" are you referring to? His special and general theories of relativity both deal with time, and how time is measured in different frames of reference. Both have been confirmed to a very high level of accuracy, and underpin much modern technology.

Interesting. Thanks for the update :-) I've read about buspirone on SocialAnxietySupport. It seems that it is generally well-tolerated but, for most people, not very effective. There are exceptions, however :-)

Thanks, WuWei, sorry to hear about the generic fiasco. I'm not depressed, but they (the doctors) often prescribe SSRIs for anxiety as well, so I like to educate myself about them, in case I'm ever offered SSRIs

Exciting! I'll go buy smokes as well, just to give my F5-button a rest!

It's not speed, I'm willing to bet :-P That said, amphetamine doesn't really have a smell, any smell must be due to production impurities. Edit: Didn't you say you were going to do an "allergy test" of ~1mg or so?

You added it here: http://hppdonline.com/index.php?/topic/2230-what-do-you-do-in-a-day/?p=17459. It's bit confusing, when two threads have so similar names

WuWei: Is Lexapro doing anything, HPPD-wise (worsening visuals, affecting brain fog etc)? Sorry if you've already answered this question in another thread.

Is HPPD really that exceedingly rare? I find it hard to believe! Is there a flaw in their research methodology?

Thanks for sharing! The amnesic and hypnotic effects is my biggest "issue" with benzodiazepines (that and their tendency to cause dependence and withdrawals in the long run), since I'll mostly be using them for stressful situations at university such as teaching, presentations and days where my HPPD and associated anxiety is worse, for whatever reason. But being on the verge of falling asleep or forgetting things is, unfortunately, pretty unacceptable in those situations. Oxazepam has had very few of those side-effects for me (I do not know why this is) while alprazolam is almost useless for me, since it doesn't relieve my anxiety very effectively and makes me very, very drowsy. I've even experienced worsened HPPD symptoms on alprazolam to the point that I was relieved when it stopped working!

Sam93: Ah, yes, pyrazolam! I've been meaning to look into that. How was your experience with it? I'm guessing that it does not share etizolam's tendency to induce little tolerance and physical dependence?

Somewhat off topic: A very interesting model of nerve signal conduction (the Soliton Model) is being developed at the Niels Bohr Institute of Theoretical Physics (where I study) which proposes that nerve signals are actually propagating density pulses associated with (as I understand it) some sort of phase transition. This model seemingly solves numerous problems with the "electrical" model of signal conduction and explains the (previously poorly understood) mechanism of action of numerous anesthetics.

I'm very sensitive to sleep "disturbances" as well. Today I took a nap in the afternoon, just over an hour, and woke up with visual distortions greatly amplified feeling very brainfoggy.

And conversely, I suffer from anxiety but not DP/DR (sure, some detachment due to brain fog at times, but not DP/DR).

It is extremely anxiogenic for me as well. I used to drink large amounts of coffee every day before being struck with HPPD, but not anymore.

My train of thought was this: Imagine for a moment that etizolam has no affinity for non-benzodiazepine receptors. We know that different aspects of benzodiazepine activity is mediated through different receptor subtypes. If etizolam exhibits an effect profile which is different from largely non-selective agonists, then it must be selective, by one mechanism or another. Whether it is ''tissue-selective'' (my own word... i.e. binds to benzodiazepine receptors in certain areas of the body) or subtype-selective is not so clear. Perhaps my reasoning is flawed? The fact that etizolam seems to have some monoaminergic effects as well complicates the situation, needless to say! Off topic (wrt propranolol: Yes, this is my second day of low-dosing (5mg). It seems to be pretty efficient at lessening anxiety spikes. It doesn't do anything for baseline anxiety, but simply knowing that I'm not going to panic is somewhat comforting.)

I'll probably respond to your post little-by-little (feeling a little low on energy at the moment - I'm trying out the beta blocker propranolol (for "mini-panic attacks"), something I'm likely to start a topic about at some point ). Dynamic binding affinity; Are you talking about dose-dependent changes in affinity? I must admit that this is not something that I'm familiar with - what would be the mechanism? :-)

My HPPD developed slowly over the course of years, but the two experiences that made it much, much worse were not all that bad, mentally. The first one was a blatant overdose of some mislabeled hallucinogenic chemical, which, while physically very uncomfortable (so much so that we went to the ER) was not a "bad trip" as such. No feelings of impending doom. Lots of nervousness, of course, since the bodily symptoms felt legitimately dangerous, but I managed to "keep it together", anxiety-wise. The second experience was vaporizing a synthetic cannabinoid (UR-144). I was somewhat anxious during the experience, but not extremely so. I was still able to have a mostly good time. Then, upon waḱing the next morning, I wasn't having such a good time any more...

Thanks for reading it :-) I can see a few statements in the article which could be misinterpreted if one were very sloppy, especially the part where they speak of selectivity towards BZ receptors in the cerebellum as opposed to those in the spinal cord. In fact, the way I read the article, there is some indication that etizolam induces much less motor impairment at effective doses. Look: "Abecarnil did not induce any impairment of the motor performance of mice in the traction test up to 100 mg/kg, p.o. (Fig. 6). On the other hand, the tested BZs impaired the motor performance, giving rise to the ED50 value of 20 mg/kg, p.o. for etizolam, 9.1 mg/kg, p.o. for diazepam and 8.4 mg/kg, p.o. for clotiazepam" The ED50 is the dose which induces a given effect (here; motor impairment) in 50% of the population. We see that more etizolam, compared to diazepam, is required (in mice) to induce motor impairment. This is quite significant, seeing as how etizolam is clearly a much more potent anxiolytic than diazepam, meaning that it would presumably induce very little motor incoordination at therapeutic dosages. Not that I ever personally found this to be a big problem at therapeutic dosages of benzodiazepines, anyway, but it seems indicative of selectivity. Yeah, I probably should update the wiki article. A shame it has already been quoted so many places on the web. Also, note how the quote begins "Similar to other benzodiazepines...", implying that etizolam is a benzodiazepine.

It is? I can access it just fine - that's strange. Thanks! Only do it if/when you feel like it, mate I'm at a friend's place - he's asleep by now, and I'm studying benzodiazepine receptors on a chocolate high I probably should be getting home... edit: On a slightly related note, it is a shame that abecarnil is so hepatoxic. It seems like such a perfect candidate for a non-sedating, non-hypnotic anxiolytic. It is apparently a highly selective benzodiazepine agonist exhibiting much less potential for physical dependence and withdrawal symptoms. In fact there are several candidates for HPPD-friendly benzo work-alikes. Ideally, the way I see it, we would have a benzo that is non-sedating and non-hypnotic while retaining anxiolytic and anti-convulsant activity (clonazepam is generally accepted as a good anti-convulsant benzodiazepine, I would think that this is part of the reason why it is the preferred benzodiazepine for many HPPD sufferers).

(unimportant rambling) I apologize for spamming this thread somewhat, but novel, selective benzodiazepine agonists are highly interesting to me. Though I don't have a regular benzo habit - I try to keep it to approximately once per week, and I've never exceeded the equivalent of 10mg diazepam at any one time. I have, however, found them indispensable for stressful situations such as teaching and family get-togethers as my anxiety and feelings of "dissociation" spike in these situations. (end unimportant rambling) From reading the Etizolam Experiences thread over at drugs-forum (and a similar thread at a Danish board) I've noticed that experiences differ widely with regards to the degree of sedation and hypnotic action of etizolam, though there seems to be a consensus that it is strongly anxiolytic. There seems to be some disagreement with regards to development of tolerance as well, with some users reporting requiring a quick escalation in dose. Another point of disagreement is the degree of selectivity of etizolam. Wikipedia states: "Similar to other benzodiazepines, etizolam binds unselectively to benzodiazepine receptor subtypes." However, the reference for this claim is the following article: Pharmacological characterization of the novel anxiolytic beta-carboline abecarnil in rodents and primates. Upon skimming this article I'm unable to find any justification for the statement - if anyone else feels like looking through it I would be much obliged :-) I'm very skeptical about such a statement until I see some actual receptor affinities, since complete non-selectivity is, to my knowledge, highly unusual. This would, as far as I understand, mean that the equilibrium constant for the formation (or dissociation) of etizolam+receptor complex had to be the same for all receptor subtypes, which I find find highly improbable from a purely steric point of view, so to say. I may be wrong, however, since I have not studied pharmacology! Sam93: Do you have a reference for your claim of α2 selectivity? I'd be very interested in collecting some sound pharmacological data on etizolam (and perhaps other benzodiazepine agonists), with the assistance of anyone who wants to chime in :-)

I had a negative experience with l-theanine of queasiness and heightened anxiety. But this was in combination with benzodiazepines (Oxazepam) and it was shortly after my HPPD had become bad, so I figured that it was mostly an anxiety reaction related to ingesting the theanine without knowing how it would affect me. I have not tried theanine since, but I plan to at some point.

On a slightly related note (sorry for derailing the thread slightly), I've stumbled upon what seems to be the holy grail of benzodiazepine pharmacodynamics, an article named An Updated Unified Pharmacophore Model of the Benzodiazepine Binding Site on ɣ-Aminobutyric Acida Receptors: Correlation with Comparative Models. I was able to download the full-text article with my university library account. To moderators: I'm unsure if I'm allowed to share it here per the forum rules. If not, please delete the following link. An Updated Unified Pharmacophore Model of the Benzodiazepine Binding Site on ɣ-Aminobutyric Acida Receptors: Correlation with Comparative Models It would seem that some concentrated structure/activity analysis could lead to novel selective benzodiazepine agonists with less side-effects (I'd say that hypnotic action and memory impairment are clearly undesired side-effects in an anxiolytic or anticonvulsant medication! :-) )

Have you seen any thorough reports of etizolam withdrawal (or lack thereof). Most I've seen were from relatively short-term use and thus fairly inconclusive. I don't wish to get into a habit of using benzodiazepines (or analogues) on a daily basis, but it's always nice to as much as possible about the compounds one ingests (even if just as a means of convincing oneself not to over-indulge). Personally I find that oxazepam is quite useful as an occasional anxiolytic (however the onset of action is impractically long, more than an hour) while alprazolam is of almost no use for me. I can feel anxious on alprazolam while being sedated and lethargic. As far as I know, this is quite uncommon(?). Oxazepam seems to relieve my visual symptoms a little, while alprazolam does absolutely nothing in this regard. Next on my list to try are etizolam and clonazepam, in that order.

Ah, it's is so good to see that you're acquiring some Coluracetam after all. I'll be awaiting your verdict in excitement :-)