1565 replies to this topic

[Isochroma]

Sunifiram is - like the racetams but more powerfully - a potentiator - of the cholinergic receptor-system and maybe others.

"These compounds, although not showing affinity in binding studies for the most important central receptors or channels, are able to prevent amnesia induced by modulation of several neurotransmission systems."

It is neither an antagonist nor an agonist at any of the known receptors - also like the racetams.

The key to getting better receptor response is neither antagonists nor agonists - the brain up or downregulates to compensate - but restoring the speed, sensitivity and density of them. Piracetam for example causes an increase of up to 30% in the density of muscarinic acetylcholinergic receptors in addition to its other effects. This increase in receptor density only occurs when the existing density is substandard due to aging or damage and does not occur in young brains.

Aging and damage cause both a decrease in receptor numbers (density) and a decrease in per-receptor sensitivity along with other changes such as decreased available energy (ATP) and loss of membrane fluidity, however - the key thing to remember is that aging and damage do not alter the negative-loop feedback systems in proportion to the functionality losses in the systems that they regulate. That means that the brain will compensate to keep perceived signal strengths and speeds constant despite the losses that aging and damage cause. Thus, the brain's own lack of perception of its losses means that it will tend to sabotage efforts to compensate by external means if those means attempt to push or pull against its natural regulatory tendencies.

Those negative-feedback loops have their own ideas about what's optimal - or what was optimal, but they don't keep up with the times. They are the guardians - the ultimate gatekeepers that issue the rules.

A more sophisticated approach is to sabotage - bias - the regulatory sytems themselves instead of the systems they regulate, but that approach too has its problems. First it is simply more difficult, and second it still does not correct for the fundamentally decreased functionalities of the systems being regulated, so restoration of original ligand densities or increase above original values has by itself negative side-effects even if the agent(s) used to affect such a change themselves have no side-effects.

The only solution to this conundrum is to restore the original functionality, thus normalizing the ratio of function to negative-feedback inhibition that was preset by genetics at birth.

The racetams and some other molecules can by unknown and known means partially correct these deficiencies, making alteration of the regulatory systems unnecessary because those systems are already evolutionarily precalibrated for the correct values - assuming the organism was healthy to start with. If that is not the case then other treament(s) may be required or it may not be possible to achieve complete or even partial restoration.

Some individuals have by genetics at birth incorrect regulatory values and for them alternatives will be necessary. Paradoxically, for those with genetically inborn excessive activity, aging and damage itself can decrease that activity and thus the manic type may as they get older and/or more damaged lose or experience a decrease in such activity, leading them to believe that their brain health is improving when it is actually in decline. Paradoxically, racetams and other therapeutics that restore original functionality may bring back their old 'problems', but are still valuable therapeutics.

Restoring the youthful function may for these individuals mean the need to treat inherent problems that have become masked by the rust of aging/damage. They may mistake the positive therapeutic effects of functional restoration as negative if their original function was biased towards excessive stimulation and thus quit the agents instead of investigating further the cause. I have seen many cases on this forum and others of precisely this phenomenon, though it is not common.

For example, in my case I have a genetic bias toward light sleeping and awakening many times in the night. On first taking Piracetam I noticed it took longer to get to sleep at night, however I realized that I was sleeping better and this compensated for the decreased sleep hours. However, due to aging after starting Piracetam I no longer notice this effect but still notice far improved sleep quality and better total restoration by morning.

However, someone with one or more stronger genetic biases may not be able to reach a suitable balance without further corrective actions. Luckily I am not one of them.

Edited by Isochroma-Reborn, 02 April 2013 - 06:52 AM.

[mait]

Very very good article for AMPA - dopamine connection from one of the Bluelight.ru discussions: http://www.jneurosci...0/12/4480.full.

These data indicate that regulation of the state of phosphorylation of GluR1 represents a probable mechanism for control of AMPA receptor currents by dopamine and psychostimulants. Results from a previous study involving a Ser⁸⁴⁵-Ala mutation of GluR1 indicated that phosphorylation of GluR1 at Ser⁸⁴⁵ was required to potentiate peak currents carried by homomeric GluR1 receptors (Roche et al., 1996). In addition, PKA agonists reversed synaptic depression of AMPA currents in hippocampal slices by increasing phosphorylation at Ser⁸⁴⁵ (Kameyama et al., 1998; Lee et al., 1998). Taken together, these data suggest that dopamine-induced, PKA-mediated, phosphorylation of Ser⁸⁴⁵ in slices and in vivo is likely to enhance glutamatergic transmission through AMPA receptors.

The data further suggest that dopamine and D1 agonists regulate AMPA receptor currents through the selective phosphorylation of Ser⁸⁴⁵. The proportion of GluR1 subunits phosphorylated at Ser⁸³¹ is greatly increased by activation of PKC (Fig. 1 B) or CaMKII signaling pathways (our unpublished observations), suggesting that both Ser⁸⁴⁵ and Ser⁸³¹ can serve to mediate neurotransmitter-specific effects on AMPA receptors.

The present results show that the regulation of AMPA receptor current through phosphorylation is likely to be a rapid, acute, and dramatic response to neostriatal dopamine release by psychostimulant drugs. The enhancement of AMPA receptor currents by these drugs represents an attractive mechanism by which glutamate receptors and their signaling pathways might be recruited to mediate a variety of effects, such as increased immediate early gene (IEG) expression (Konradi et al., 1996), which may eventually lead to sensitization. In support of this idea, AMPA or NMDA receptor antagonists block amphetamine-induced IEG expression (Konradi et al., 1996) and prevent the development of behavioral sensitization to amphetamine (Karler et al., 1989; Wolf, 1998).

Maybe just maybe this helps to explain why many of the first reports of sunifiram usage described it in comparable manner to amphetamine. Maybe the pro-cognitive and pro-concentration effects of amphetamine are the results of increased AMPA-energic activity and maybe some of the negative effects of amphetamine usage are also mediated via this pathway. My initial hooray "I want to try this compound" feeling has somewhat cooled now.

Edited by mait, 02 April 2013 - 01:50 PM.

[Isochroma]

Your assumptions do not apply to Sunifiram.

As has already been found, this molecule and racetams work in different ways than amphetamine and have no affinity for such receptors.

You are making a mistake, please re-read my post and others who have experienced it.

Also, try it for yourself before prejudging it.

[mait]

Your assumptions do not apply to Sunifiram.

As has already been found, this molecule and racetams work in different ways than amphetamine and have no affinity for such receptors.

You are making a mistake, please re-read my post and others who have experienced it.

Also, try it for yourself before prejudging it.

I am not just prejudging this pharmacological agent. I am just posting some questions I have came across while searching about Sunifiram in order to make up my mind whether to try it or not. Here are few very good posts about it from Bluelight.ru (http://www.bluelight...logy-discussion):

I think in the presence of an orthosteric agonist, an AMPAkine would make for increased neurotoxicity. I am however, talking in the context of excitotoxins, such as AMPA or domoic acid (of amnesic shellfish poisoning fame)

AMPAkines have varying modes of action, some increase ion current flux intensity, and some stabilise open channel gating, also there are varying degrees of selectivity for flip vs flop receptor isoforms (which determines selectivity for Ca++ vs Na+ permeability).

They do, on the whole, appear to induce BDNF release, which is likely to be neuroprotective, from reports out there they don't appear to cause much behavioural alteration in lab animals whilst under the influence, just performance enhancement, rather than motor stereotypy etc as seen with stimulants.

There doesn't seem to be excitotoxicty, the safety profile seems fairly decent. Although one, farampator (one of the CX series) impaired episodic memory, I believe this was whilst the drug was acting, though.

Piracetam and Aniracetam are both AMPAr positive modulators, acting at different binding sites, there are quite a lot of allosteric binding sites possible at different AMPAr subtypes. Both show quite excellent tox profiles.

like anything else, there is the question of affinity and efficacy.

The way the ligand gates the channel dictates more the behaviour than potency.

A good example would be barbiturates vs benzos at GABAa allosteric sites. Benzos increase the efficacy of GABA, as do barbs, but while the benzos increase frequency of channel opening, whilst the barbs cause the channel open time to lengthen, resulting in increased current flux per opening, rather than more openings with average current passing. The body can compensate for an overly large dose of a benzo by releasing less GABA, but with the way barbs gate the channel, it can do far, far less about it, explaining the increased toxicity of barbs over benzos (and why whilst tolerance can build to the high or sedation, the LD-50 doesn't rise, as it does with say, an opiate, where a user can eventually build up such a monster monkey on his back that grams of H a day can be survived)

Incidentally, barbs are AMPA antagonists in addition to their GABAergic effects, unusual mode of doing it too, by getting into the ion channel, then stabilizing the receptor in an agonist-bound, desensitized state, sort of locking itself in there (the AMPA receptors structure is formed of subunit tetramers, and closes around the ligand like the shell of a bivalve mollusc)

Synergy between those AMPAkines that increase channel open frequency, and those that increase open times will be possible, most likely, the two effects seeing as they are occuring seperatly of each other in different ligands, suggests that seperate binding sites mediate the two effects.

A further action that some AMPAkines produce, is that they inhibit desensitization of the receptor, normally AMPARs desensitize very quickly on agonist binding of glutamate (although some exogenous direct agonists have very different desensitization kinetics) which allows for more efficient signalling before the receptor desensitizes.

However, weather its a good thing, may be another matter entirely. As has been stated, glutamatergic overactivation is dangerous, producing excitotoxicity. It looks like most AMPAkines are pretty safe, and don't appear to be excitotoxins, but its important to be careful. Combining one that increases channel open frequency, with one that gates the channel in a manner analogous to barbs at GABAaRs would of course produce a synergistic effect, weather or not its safe or not, I do not know. But the parallel between benzos and barbs should be born in mind, the body has mechanisms where excess glutamate can be very rapidly removed* but if the channel is forced to remain open whilst there is already excess stimulation, or a greater threshold of glutamatergic activity going on, I think there would be a greater potential for toxicity than either mode of action alone.

Also to remember, is that an allosteric modulator binds at a seperate site than the neurotransmitter agonist, in the case of the AMPAr, there are four sites per receptor that bind glutamate, a direct agonist will activate the receptor and cause influx of calcium, sodium and potassium, way too much Ca++, as there is a fine threshold and balance between enough, somewhat better, and extra crispy, which is why there is needed such an efficient, rapid removal system.

The body can't do that in the case of a direct agonist, reducing the level of glutamate released is going to have minimal effect at best,when a potent, artificial agonist gets in there and starts toasting neurons, but in the case of an allosteric positive modulator, the chance to reduce the effect, seeing as how PAMs have no effects on their own, unless the actual orthosteric agonist is bound, then quick lessening of released glutamate should be acheivable.

The Q/I editing site determines permeability to Ca++ or to Na and K, its present in the GluR2 subunit, and the presence of arginine, rather than glutamine at that position in the receptor protein results in vastly decreased capacity to conduct Ca++, and leaves it permeable to sodium and potassium. The latter, in GluR2 subunity expressing AMPARs is by a vast majority, the form expressed the brain.

Not so sure about flip vs flop, but there are a whole crapload of developmental changes during gestation and childhood, restructuring and adapting, pruning off the trash etc, and IIRC there is a switch betwen the two at some point, I think, if I remember properly that in adults its mostly flop-isoform that is present, if not nearly exclusively, but I don't know to what extent, and how it affects practical functioning of the AMPAr-mediated glutamatergic system.

Sunifiram poses few but still important unknown factors for me. So its worth to discuss and speculate on the possible negative side effects of this agent.

Edited by mait, 02 April 2013 - 04:42 PM.

[alecnevsky]

I don't think I'll ever use adderall or ritalin just because I'm afraid of messing with reward pathways. But, does sunifiram compare to any of the previously mentioned stims or maybe phenylpiracetam?

No. I did twice normal dose of PP yesterday to be sure. I am starting to think PP is only good for stamina and not for subtleties of any kind, whether in sports or in academics. Sunifiram seems like much more "organic" energy.

[alecnevsky]

I just benchmarked memory on Sunifiram and saw consistent improvement in all memory tests on cambridge science. I noticed less errors and less deviations below last highest score (which may be of interest to adhd.) So I am thinking that this is at least as good as aniracetam and likely better.


Dosage was 5-6mg twice in 5hrs.

Edited by alecnevsky, 02 April 2013 - 10:04 PM.

[renfr]

What about an IQ test? Are your reasoning and logics much better than baseline?

[matthewebbert]

Anyone knows how this compares to noopept?

[alecnevsky]

What about an IQ test? Are your reasoning and logics much better than baseline?

I didn't do any other tests than memory b/c the main effect shown in the research papers was 150-200% ACh release.

Also keep in mind that most of those tests are either WM or short-term.

Edited by alecnevsky, 02 April 2013 - 11:16 PM.

[MizTen]

I don't think I'll ever use adderall or ritalin just because I'm afraid of messing with reward pathways. But, does sunifiram compare to any of the previously mentioned stims or maybe phenylpiracetam?

... Sunifiram seems like much more "organic" energy.

That's a good description of how it feels. I really don't see much similarity to pharmaceutical stimulants.

[MizTen]

This is day 8 for me. I took 12mg in the late morning. I had planned to stop yesterday, but instead stopped other noots, and have only had one cup of coffee. Although the smooth happy ease has faded, there are many effects remaining and I am also learning how best to use sunifiram in the future. I may use it until I am fully off coffee, which will probably be another few days.

• One of the things that I was able to do when the sunifiram was affecting me more strongly is do some fairly deep emotional processing, something that my perceived stress level (before sunifiram) prevented me from doing. Just having some of the mental clutter and distraction of anxiety removed, in addition to making the present moment much more enjoyable, made it possible to think, see, and thus conclude a little differently. So I am better than I was before. Much better, I have less baggage because I was able to solve some difficult dilemmas that I've had for years.
• Meditation is more sustained and effective than normal.
• The stimulant effect is still around, not as strongly, it was never invasive even when it was pretty strong. Now it's just energy and I can easily direct myself through what I need to do without procrastinating.
• Sensory enhancement, though not apparent all the time, is still in the background and will fully resurface when I'm receptive. During a quiet period today I was looking at a painting I've had for years and the colors and shapes just started popping out, the picture took on a beautiful golden glow, super-saturated colors, higher contrast, the HDR effect. I saw much, much more in that picture than I'd ever seen before and I also saw it very sharply and clearly, as if I'd had a several diopter improvement in my eyesight. I have monovision normally, which means no real depth perception. I am an artist, ha ha!
• I can eat just fine, no aversion, but also no hunger.
• I am sleeping fine, though I do use melatonin, theanine, etc.before bed. Just have to take the sunifiram early enough.
• Social activities are a little harder today, but there also wasn't as much fun stuff, and a lot of very difficult things instead.
• I notice my writing is a bit more scattered than normal, but I rarely write this much because I usually worry how it comes off.
• Now (after sunifiram) when I need to regain emotional clarity, I can easily reach a state of deep peace and gratitude, despite some of the crap that gets thrown my way. Usually when challenged, I have to work very hard to regain my emotional balance and come up with a better perspective. In the past that could take me days.
• It's a stimulant and an anxilotic. A sensory enhancer and a relational booster, which quite a lot of tasks for one chemical, considering there doesn't seem to be an real burnout. Oh, its also a multi-tasking aid, and that also in a big way for me.
• This is potentiated by exercise, by certain foods, caffein, meditation, sensory stimulus, outdoor activities, and social activities. Supplements maybe also. Sulbutiamine amplifies the sunifiram.

I have a feeling after I've washed out for a while that some of the most "sunny" effects may return. I consider this for myself to be a fairly powerful nootropic.

Some of the commentary and information, especially from Isochroma and Allethrin, really struck some chords. Though I am not much of a detail person when it comes to "proving" science for others, some of their conclusions were very similar to my speculations and theories.

This lasts in one form or another, more that 4 hours. I seem to be able to rekindle quite a few of the effects many hours later with the above mentioned potentiators.

I do not feel and am not acting manic. But I do think the brain needs some time out to consolidate and process the new stuff that sunifiram reveals, and possibly the healing that its experienced. It's probably not good to take any of the nootropics all the time. Give your brain a chance to work unaided at a higher level.

Edited by MizTen, 03 April 2013 - 03:14 AM.

[Isochroma]

Excellent report once again and thanks!

Your input is greatly appreciated and helps to allay the unfounded fears of other forum members - ones who perhaps are wary of Sunifiram's unknown effects and justly so considering the awful effects of many drugs - stimulants especially. Since they are working on only a simplified receptor-ligand paradigm, they - like the scientists - can't wrap their braincells around why it works [the dreaded Mechanism(s) of Action] and so they keep returning to the same tired old explanations that just don't work for these remarkable molecules. Like methed-out lab rats chasing their tails in circles.

I note that your report is the first to mention how Sunifiram combines with other drugs - Caffeine and Sulbutiamine in particular. I will be sure to remember it when compiling reports for the experiences page.

[Q did it!]

I am finding very similar effects noted by MizTin. The "sunny" effect does ware off after the first few dosages but the stimulation remains. It stacks very will Coluracetam and other recetams. Will be testing it with Noopept soon.

[Isochroma]

Excellent!

I am checking my tracking many times a day in great anticipation of dosing experimentation

[tritium]

I revieced mine yesterday and started today. First I took 11mg at 8am. About 30-40 minutes in, I start to feel a tingling or slight thumping pressure on the left side of my brain. Soon this goes away and I start to feel somewhat euphoric and happy. As I was walking to class, I notice many random things in the landscape that I have never noticed for years. I also noticed that random ideas seem to come more often. I have yet to test how it effects memory.

Around 12:30, when the sunshine feeling starts to fade, I made the dumb mistake of taking another 5mg. After this I seem to get really depressed for no apparent stimulus. Tomorrow I'll try a much smaller dose and see if the effects are better.

One negative effect is that it seemed to make me a lot less sociable and more introverted. However, I have a speculation that it may just be doing a lot of healing/rewiring, which may make my cognition go down temoprarily until the things are fixed. This also happened when I started Piracetam after several alcohol binges.

One other thing to keep in mind is that it may effect you very differently than me, since there is a possibility that I may have high functioning Autism. Maybe this isn't what I need, since I read that these types of people don't need more LTP, but rather more LTD. Their signal to noise ratio in terms of EPSP seems to tilt more towards noise.

Edited by tritium, 03 April 2013 - 05:27 AM.

[Allethrin]

Blah I'm starting to feel some burnout/downsides to this chemical I think.

There is one significant negative that I have noticed: Sunifiram makes me inclined to stay up later than I should, reading/working on interesting things. I have irresponsibly shifted my sleep schedule the last several days and it feels like it's catching up.

Sunifiram also seems to have a strong impact on my sleep quality. I am able to fall asleep in my normal 1-2 hours after going to bed (my typical sleep onset problems.) Two nights ago, I used the Sleep Cycle iPhone app to graph my sleep depth during the night, after a day that I had taken a solid amount of sunifiram.

It revealed that I dropped into VERY deep sleep quickly after I finally fell asleep. Instead of the normal spiking/falling associated with normal sleep cycles, the 8 hours that I was in bed progressed in a nearly perfect linear pattern from very deep sleep to moderate-depth sleep at the end of the night. The sleep graph was nearly a straight line instead of the normal ups and downs. I have never seen this pattern before. I woke up physically fresh but mentally exhausted, feeling like maybe I had missed out on necessary REM sleep. I had another somewhat abnormal sleep pattern last night.

An important confounding factor here is that I went to bed much later than my normal bedtime. I felt quite mentally fatigued the following day (and today, as well). I have continued taking sunifiram, just at a somewhat reduced dose. Many of the cognitive benefits have remained, but the mood lift has lessened/disappeared, and the quality of the effect seems to have worsened somewhat. Yesterday I felt like the cognitive space I occupied was somewhere between the calm zenlike focus of pramiracetam, plus the mental stimulation of modafinil, but still quite different from either.

I felt there was a cognitive tradeoff being made. I was extremely attentive and responsive on the moment-to-moment, on the shortest timescales, but it was difficult to think from a more expansive standpoint. I was very unproductive yesterday.

I still retained much of the wit and sharpness of speech, although the overall talkativeness and prosociability declined, compared to the first 2-3 days.

Overall I'm getting the impression that this drug makes me feel like I'm meditating all the time, and this gets to be simply too much to sustain for more than a few days, and my brain gets worn out and wants to rest.

I think in the future it is important for me to be mindful of keeping a good `cognitive diet' and other health habits when taking sunifiram. If increased LTP is fortifying the brain pathways related to what I engage in on a daily basis, then I want to use that opportunity to cultivate habits such as going to bed at a normal hour, adapting to zero caffeine, etc.

One more thing: In future experimentation, to minimize sleep issues I will limit dosing to once daily, upon waking, and keep the dose significantly lower than I have taken this past week (~3-5 mg)

[therein]

I have access to full-text articles on Sunifiram. I can upload them if anyone is interested.

LIST:
Novel nootropic drug sunifiram improves cognitive deficits via CaM kinase II and protein kinase C activation in olfactory bulbectomized mice
Design, synthesis and nootropic activity of new analogues of sunifiram and sapunifiram, two potent cognition-enhancers.
Pharmacological characterization of DM232 (unifiram) and DM235 (sunifiram), new potent cognition enhancers.
Structure-activity relationship studies on unifiram (DM232) and sunifiram (DM235), two novel and potent cognition enhancing drugs.
AMPA-receptor activation is involved in the antiamnesic effect of DM 232 (unifiram) and DM 235 (sunifiram).
DM235 (sunifiram): a novel nootropic with potential as a cognitive enhancer.

[Isochroma]

I need these:

Novel nootropic drug sunifiram improves cognitive deficits via CaM kinase II and protein kinase C activation in olfactory bulbectomized mice
AMPA-receptor activation is involved in the antiamnesic effect of DM 232 (unifiram) and DM 235 (sunifiram)
DM235 (sunifiram): a novel nootropic with potential as a cognitive enhancer

Already have these - links below to full PDFs for everyone:

Design, synthesis and preliminary pharmacological evaluation of new analogues of DM232 (unifiram) and DM235 (sunifiram) as cognition modulators.pdf
Pharmacological Characterization of DM232 (Unifiram) and DM235 (Sunifiram), New Potent Cognition Enhancers.pdf
Structure-activity relationship studies on unifiram (DM232) and sunifiram (DM235), two novel and potent cognition enhancing drugs.pdf

I use SendSpace.com - it works well.

Edited by Isochroma-Reborn, 04 April 2013 - 12:06 AM.

[therein]

I just downloaded the ones you asked for. Do I need to modify anything so that these can't be linked back to me? I'm assuming they aren't doing any watermarking.

[Isochroma]

No.

Just upload the PDFs to SendSpace.

[therein]

Novel nootropic drug sunifiram improves cognitive deficits via CaM kinase II and protein kinase C activation in olfactory bulbectomized mice
http://www.sendspace.com/file/bp2ann

AMPA-receptor activation is involved in the antiamnesic effect of DM 232 (unifiram) and DM 235 (sunifiram)
http://www.sendspace.com/file/ow3jfh

DM235 (sunifiram): a novel nootropic with potential as a cognitive enhancer
http://www.sendspace.com/file/inhc39

[Isochroma]

Good work and thanks from everyone!

My analysis of all three PDFs concludes that none of them contain any overt or covert security features, copyright restrictions or watermarks.

Two more studies that I have in abstract but not full PDF - maybe you can get them - here are the abstracts:

Design, synthesis and nootropic activity of new analogues of sunifiram and sapunifiram, two potent cognition-enhancers

Synthesis and biological evaluation of 3,7-diazabicyclo[4.3.0]nonan-8-ones as potential nootropic and analgesic drugs

Edited by Isochroma-Reborn, 04 April 2013 - 12:38 AM.

[therein]

You're welcome. Let me know if you need any other documents. I seem to have access to all the full-text articles on PubMed, ScienceDirect, Mendeley and some more.

Design, synthesis and nootropic activity of new analogues of sunifiram and sapunifiram, two potent cognition-enhancers
http://www.sendspace.com/file/dqyjj4

Synthesis and biological evaluation of 3,7-diazabicyclo[4.3.0]nonan-8-ones as potential nootropic and analgesic drugs
http://www.sendspace.com/file/rkhpha

[Isochroma]

Thanks again!

I think that's it for the studies relating to DM232/235.

[Introspecta]

Does anyone think this could possibly be a drug that should be used occasionally? Or say use it 4 days on 3 days off or should it be used daily? I know something like Phenylpiracetam is best used occasionally I wonder if this may be the same. I know with Piracetam after about a month of heavy dosing I get a little burnt out from it.

Does Sunifiram tax the adrenals the sane way Piracetam does?

Edited by joelski28, 04 April 2013 - 08:44 PM.

[Isochroma]

Edited by Isochroma-Reborn, 04 April 2013 - 10:19 PM.

[manic_racetam]

Haven't noticed much on my first day. 6mg twice today. Tomorrow I'll try it first thing in the morning and see if anything is more apparent. So far nothing that can set it apart from placebo.

[Isochroma]

Arrived today at 10:50a!

Dosed 11mg on top of usual 5g Piracetam just now at 10:57a.

[Isochroma]

Now for the debriefing.

At 11:42a I noticed while sweeping the floor that my palms were warm and sweaty.

At about the same time I noticed a slight physical discoordination and what seemed to be a slowing of mind.

At about 11:45a I moved on to sweeping the ceramic-tiled part of the floor. They are octagons tiled with squares.

Then the unexplained surfaced: I was feeling the texture of the tiles through the broom handle - it never happened before.

I continued sweeping for some time as I usually do in the mornings. The house is dark and there is not much noticeable whilst doing the dungeonesque chores. The cat's disgorged enteric contents on the floor didn't look much brighter than its usual shade of hardboiled egg-yolk yellow.

After the hour of morning chores I returned to my brighter daylit room and removed my glasses to sit at the computer. I glanced at the glasses as I was about to put them down - the carpet in this room is dark blue-green - and I saw the reflected lights and under it the dark blue-green, so very dark like a swamp.

The utter shinyness and smoothness of the glass startled me. It was so beautifully smooth, so absolutely shiny, gazing into a transparent solid smoothness; a liquid smooth pool. Then I realized that the perfectly shiny smoothness was so beautiful because inside me is now all shiny and smooth like the glass. My mind.

There is a silence there, some utter calmness, it is not like any other racetam.

I sat down and put on the desktop background - a scene of blue and white abandoned sea and sandy islet in the southern islands of Japan. The colours startled me in a way I have not been startled like for a long time if ever.

The black text is different somehow too - sharper and smoother too.

Overall visual dynamic range in chroma seems to have increased by about 20% while luma range by only about 10%.

Edited by Isochroma-Reborn, 05 April 2013 - 07:34 PM.

[emckai]

After traveling the United States, my package will finally be delivered today!

https://tools.usps.c...201080505737419

It's absolutely ridiculous how my package went from Arizona to Colorado to California and back to Nevada..... =_=