47 replies to this topic

[unregistered_user]

Update: Before deciding to take smaller doses I wanted to try one more large/attack dose. I took about 3.04g piracetam in one dose with 1.25g of Choline at 3:15pm. I’ll report back with the effects of this larger does.

[unregistered_user]

Well that test was a total flop. About 30 minutes after dosing I crawled into bed and slept for 3 hours. The night before I slept 10+ hours so I wasn't exhausted...the piracetam at such a high dose just knocked me right out. Looks like I'll be sticking to 800mg-1g per dose from now on. At least I experimented like this on my day off but damn, that consumed the prime hours of my day.

Edited by semi-retarded-individual, 09 June 2010 - 12:05 AM.

[dilenja]

SRI, Hope the recalibration is treating you well and you're back on your feet today!

As far as glutamate is concerned with I-ADD, One hypothesis is that I-ADD is 'associated with' a type of dysfunction of the NMDA receptors (which are potentiated by glutamate), whereby sustained excessive activity of glutamate at NMDA receptors leads to downregulation of D2 and possibly D4 subtypes of dopamine receptors and correlates with increased D1 activity. It is alleged that this imbalance purportedly causes a 'fundemental disconnect' of the Prefrontal Cortex, which would no doubt be the predominant cause of I-ADD executive dysfunction.

Interestingly a study (http://www.ncbi.nlm....3?dopt=Abstract) comparing Methylphenidate (Ritalin) and Atomoxatine (Straterra) demonstrated that after 16 weeks of treatment, Striatal glutamate levels decreased in individuals using both Ritalin and Straterra, but that Prefrontal glutamate levels decreased only in the group using Straterra. Although the sample group was prohibitively small (n=4), this is of interest since Straterra's MOA is believed to be primarily within the Prefrontal cortex, and since Ritalin's is (Dose Dependantly) believed to primarily impact the striatum. Incidentally, ancedotal reports suggest Ritalin has not generally been successful at standard dosages in treating I-ADD, as it has been in ADHD. Furthermore, researchers observed elevated resting glutamate in the striatum and prefrontal cortex of Dopamine D4 receptor knockout mice, implying that decreased dopamine D4 receptor expression increases extracellular glutamate and also alters its regulation. Other research also suggests that D4 in the prefrontal cortex can mediate cognitive and also striatal motor processes - lending further validity to D4 receptors as a theurapeutic target.

This is not to say that glutamate itself is directly to blame for I-ADD, but that rather it is a disruption of the mechanisms regulating glutamate likely to be at fault, of which many different mechanisms play a part. As there is an obvious relationship between NMDA activity and executive dysfunction, it would stand to reason that glutaminergic substances, and inded anything impacting NMDA activity should be carefully weighed and considered prior to incorporation within one's regimen for treating I-ADD.

Since increased glutamate activity would be more likely to exacerbate excessive activity at dysfunctional NMDA receptors than not, I would personally think that the Amino Acid L-Glutamine and 'unnecessary' precursors would not likely to be of theurapeutic use for I-ADD, and if anything would be more likely to do more harm than good.

[stablemind]

Hows piracetam working for you lately?

[stablemind]

SRI, Hope the recalibration is treating you well and you're back on your feet today!

As far as glutamate is concerned with I-ADD, One hypothesis is that I-ADD is 'associated with' a type of dysfunction of the NMDA receptors (which are potentiated by glutamate), whereby sustained excessive activity of glutamate at NMDA receptors leads to downregulation of D2 and possibly D4 subtypes of dopamine receptors and correlates with increased D1 activity. It is alleged that this imbalance purportedly causes a 'fundemental disconnect' of the Prefrontal Cortex, which would no doubt be the predominant cause of I-ADD executive dysfunction.

Interestingly a study (http://www.ncbi.nlm....3?dopt=Abstract) comparing Methylphenidate (Ritalin) and Atomoxatine (Straterra) demonstrated that after 16 weeks of treatment, Striatal glutamate levels decreased in individuals using both Ritalin and Straterra, but that Prefrontal glutamate levels decreased only in the group using Straterra. Although the sample group was prohibitively small (n=4), this is of interest since Straterra's MOA is believed to be primarily within the Prefrontal cortex, and since Ritalin's is (Dose Dependantly) believed to primarily impact the striatum. Incidentally, ancedotal reports suggest Ritalin has not generally been successful at standard dosages in treating I-ADD, as it has been in ADHD. Furthermore, researchers observed elevated resting glutamate in the striatum and prefrontal cortex of Dopamine D4 receptor knockout mice, implying that decreased dopamine D4 receptor expression increases extracellular glutamate and also alters its regulation. Other research also suggests that D4 in the prefrontal cortex can mediate cognitive and also striatal motor processes - lending further validity to D4 receptors as a theurapeutic target.

This is not to say that glutamate itself is directly to blame for I-ADD, but that rather it is a disruption of the mechanisms regulating glutamate likely to be at fault, of which many different mechanisms play a part. As there is an obvious relationship between NMDA activity and executive dysfunction, it would stand to reason that glutaminergic substances, and inded anything impacting NMDA activity should be carefully weighed and considered prior to incorporation within one's regimen for treating I-ADD.

Since increased glutamate activity would be more likely to exacerbate excessive activity at dysfunctional NMDA receptors than not, I would personally think that the Amino Acid L-Glutamine and 'unnecessary' precursors would not likely to be of theurapeutic use for I-ADD, and if anything would be more likely to do more harm than good.

Lots of users have noted a nice boost in piracetam's efficacy after glutamine supplementation, and since piracetam improves the efficiency of NMDA receptors shouldn't glutamine supplementation be fine as long as it is combined with piracetam?

[dilenja]

Glutamine, in and of itself is fine, and is found in plentitude in the food sources we consume everyday. Taken by individuals with a properly functioning glutaminergic system I can think of no reason why standalone-glutamine supplementation would pose a particular risk. Also too, glutamine taken with Piracetam should definately provide for an increased response. As to whether Piracetam has the ability to 'normalize' NMDA activity, I believe this is an additional matter completely. From the full-body papers and numerous abstracts I've recently reviewed, I've gathered researchers generally agree that Piracetam increases synaptic glutamate transmission by antagonizing ionic CA+ channel blocking mechanisms (which cause an influx of CA+ into the ion channel triggering neural transmission), but are less clear with respect to how, if, and to what extent Piracetam would exert a regulatory influence limiting the level of CA+ influx allowed into the channel. A number of researchers suggest that such a mechanism should exist, but they then go on to provide very little or no insight as to how such a mechanism would be purported to work. Anecdotal reports of this mechanism also do not provide supporting evidence through literature, and without sufficient and credible evidence that such a mechanism exists I'm unconvinced as to the extent Piracetam can normalize NMDA activity. As a result of this, I suppose I do feel Piracetam usage carries an increased risk for individuals with disorders associated with excessive glutamate activity, with the risk being that Piracetam may not possess a regulatory or modulatory mechanism sufficient enough to prevent the increased CA+ influx from further exacerbating the condition. This is not to say that Piracetam should be contraindained in individuals with the above conditions, but rather that under these conditions especially that treatment could possibly cause more harm than good.

Edited by dilenja, 18 June 2010 - 12:42 AM.

[stablemind]

Glutamine, in and of itself is fine, and is found in plentitude in the food sources we consume everyday. Taken by individuals with a properly functioning glutaminergic system I can think of no reason why standalone-glutamine supplementation would pose a particular risk. Also too, glutamine taken with Piracetam should definately provide for an increased response. As to whether Piracetam has the ability to 'normalize' NMDA activity, I believe this is an additional matter completely. From the full-body papers and numerous abstracts I've recently reviewed, I've gathered researchers generally agree that Piracetam increases synaptic glutamate transmission by antagonizing ionic CA+ channel blocking mechanisms (which cause an influx of CA+ into the ion channel triggering neural transmission), but are less clear with respect to how, if, and to what extent Piracetam would exert a regulatory influence limiting the level of CA+ influx allowed into the channel. A number of researchers suggest that such a mechanism should exist, but they then go on to provide very little or no insight as to how such a mechanism would be purported to work. Anecdotal reports of this mechanism also do not provide supporting evidence through literature, and without sufficient and credible evidence that such a mechanism exists I'm unconvinced as to the extent Piracetam can normalize NMDA activity. As a result of this, I suppose I do feel Piracetam usage carries an increased risk for individuals with disorders associated with excessive glutamate activity, with the risk being that Piracetam may not possess a regulatory or modulatory mechanism sufficient enough to prevent the increased CA+ influx from further exacerbating the condition. This is not to say that Piracetam should be contraindained in individuals with the above conditions, but rather that under these conditions especially that treatment could possibly cause more harm than good.

Back to the drawing boards again then... dexmethylphenidate seems like a better option now.

[unregistered_user]

The benefit of Piracetam is still noticeable but I think it has become more subtle. I read the thread here on microdosing so instead of taking 800mg doses I'll try dosing at 200mg to see what difference, if any, that creates. I've been taking Piracetam and Choline Bitartrate with Rhodiola Rosea for the past week and while I like this combination, I'm not convinced that my NOW Foods Brand of RR is as potent as some of the others might be so I've ordered the RR from New Chapter along with a multi and Jarrow Formula's Ashwagandha. I'll post back after a week or so with some results.

[mattblack UK]

With Rhodiola, I had a great experience the first time I had one. Felt really clear headed and happy. Could really feel it working.
Unfortunately, I have not had the same experience again... its almost like a built a tolerance for it after 1 day!

I have tried ashwaghanda before and experienced no noticable effects. Tried it for about a month and a half.

This maybe just me by the way, I do seem to have a very high tolerance for drugs and herbs. I have tried my girlfriends valium before with no noticable effect!

[mattblack UK]

With Rhodiola, I had a great experience the first time I had one. Felt really clear headed and happy. Could really feel it working.
Unfortunately, I have not had the same experience again... its almost like a built a tolerance for it after 1 day!

I have tried ashwaghanda before and experienced no noticable effects. Tried it for about a month and a half.

This maybe just me by the way, I do seem to have a very high tolerance for drugs and herbs. I have tried my girlfriends valium before with no noticable effect!

[JChief]

semi-retarded-individual, care to report your current feelings on piracetam? I experience effects very similar to you. Sleep, mood, etc. Great thread though.

Edited by JChief, 10 November 2011 - 01:01 PM.

[Erstwhile]

Rhodiola had awesome effects for me at first but it seems I built a tolerance for its nootropic effects after the first week. This seems to be in line with many users' experiences with RR.

Whenever I feel a cold coming on though, I pop a couple of RR capsules and it seems to prevent me from actually falling ill. Not sure if this is some kind of placebo effect but if it isn't then I suppose the adaptogenic effects of RR still works.

[unregistered_user]

semi-retarded-individual, care to report your current feelings on piracetam? I experience effects very similar to you. Sleep, mood, etc. Great thread though.

Piracetam is tricky (at least for me) because I have had a difficult time zeroing in on what I feel is the most efficacious dose for me. I've gone heavy (as much as 10g per serving) and I've attempted micro-dosing (sub 200mg). I tend to find that right around 1g or less produces the most desirable results.

I'm currently taking multiple supplements: deprenyl, l-phenylalanine, l-theanine, 5-htp, 10g of fish oil, piracetam and a multi-vitamin. Lately I feel in this particular lineup piracetam hasn't been particularly helpful but then again, this is a fairly new stack that I'm still deciding on.

I feel that right now, I'm at a point where I could take or leave piracetam. I don't swear by it and in fact, most times I am hard-pressed to even qualify its benefit. I still notice enhanced saturation after most uses but after having tried piracetam in varying doses and combined with various supplements, I feel the initial magic has all but worn off.

Since I don't believe it to be a detriment to me to continue taking a standard, maintenance dose of around 800mg-1g per day, I will continue using it until it runs out.

[JChief]

Thanks for your input. For me I believe that piracetam just makes me more confident since it allows me to be more articulate and improves my communication skills. The sleep enhancement and increased perception of color and sound are welcome as well. It is useful on the job and in my social life. It improves my mood in some way. Nothing like a euphoria but a positive mindset. When combined with cannabis it certainly combines well in addition to the anxiolytic properties which is nice too. It's very practical and I view it as another multivitamin for a sharper mind. It enhances creativity as well. Noopept has been wonderful as well in combination.

[unregistered_user]

Thanks for your input. For me I believe that piracetam just makes me more confident since it allows me to be more articulate and improves my communication skills. The sleep enhancement and increased perception of color and sound are welcome as well. It is useful on the job and in my social life. It improves my mood in some way. Nothing like a euphoria but a positive mindset. When combined with cannabis it certainly combines well in addition to the anxiolytic properties which is nice too. It's very practical and I view it as another multivitamin for a sharper mind. It enhances creativity as well. Noopept has been wonderful as well in combination.

You're welcome. To be honest, I'm a little scared to try it with pot. My psyche is teetering on a razor's edge when I'm high (at least that's how I sometimes feel) so I'm not sure if piracetam would make that better or worse.

It's possible I've just become accustomed to my slightly more optimized state of mind and am discounting piracetam's role in that. Hard to say really!

[simone_no1]

Hi all, I'm interested to hear your experiences, as PI types, of concerta Vs amphatamines. I have seen numerous anecdotal reports - including the mention by Dilenja above - that concerta works less well than amphetamines for PI. I was recently diagnosed with PI and am taking concerta with moderate success - but wonder if MAS would be better for me. There are only a handful of studies that address this directly, and they are slightly contradictory. However, my overall view is that any substantial effects of drug type on subtypes would have been documented if it was a big issue.... Thanks

[sparkk51]

Hi all, I'm interested to hear your experiences, as PI types, of concerta Vs amphatamines. I have seen numerous anecdotal reports - including the mention by Dilenja above - that concerta works less well than amphetamines for PI. I was recently diagnosed with PI and am taking concerta with moderate success - but wonder if MAS would be better for me. There are only a handful of studies that address this directly, and they are slightly contradictory. However, my overall view is that any substantial effects of drug type on subtypes would have been documented if it was a big issue.... Thanks

 

To further this, what about dexmethylphenidate vs methylphenidate? For the people who have experienced both, are there any noticeable side effects that go away when you switch from methylphenidate to dexmethylphenidate?

[MichaelFocus22]

To Semi-Retarded individual, if you are still here on the forum? Did you find a sustainable solution to ADHD-PI that worked for you? I've yet to find a more comprehensive thread on this other than my own I'm curious to what insights you would have to offer us on the subject. Assuming that you are still here on the forum.