438 replies to this topic

[nito]

so ur sayng that the smartpowders sold by mike could be toxic and fake? : /

[brain]

double post, please delete.

Edited by brain, 19 January 2010 - 01:04 AM.

[brain]

some research:

Glutamate and Depression: Clinical and Preclinical Studies

The past decade has seen a steady accumulation of evidence supporting a role for the excitatory amino acid (EAA) neurotransmitter, glutamate, and its receptors in depression and antidepressant activity. To date, evidence has emerged indicating that N-methyl-d-aspartate (NMDA) receptor antagonists, group I metabotropic glutamate receptor (mGluR(1) and mGluR(5)) antagonists, as well as positive modulators of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors have antidepressant-like activity in a variety of preclinical models. Moreover, antidepressant-like activity can be produced not only by drugs modulating the glutamatergic synapse, but also by agents that affect subcellular signaling systems linked to EAA receptors (e.g., nitric oxide synthase). In view of the extensive colocalization of EAA and monoamine markers in nuclei such as the locus coeruleus and dorsal raphe, it is likely that an intimate relationship exists between regulation of monoaminergic and EAA neurotransmission and antidepressant effects. Further, there is also evidence implicating disturbances in glutamate metabolism, NMDA, and mGluR(1,5) receptors in depression and suicidality. Finally, recent data indicate that a single intravenous dose of an NMDA receptor antagonist is sufficient to produce sustained relief from depressive symptoms. Taken together with the proposed role of neurotrophic factors in the neuroplastic responses to stressors and antidepressant treatments, these findings represent exciting and novel avenues to both understand depressive symptomatology and develop more effective antidepressants.

aside from any actual excitotoxicity, excess glutamate activity, this study seems to suggest, lowers mood and increases depression. I'm not sure, but wouldn't we probably know by now if piracetam had this kind of neurotoxicity? everything we've seen in the literature so far, despite some of our own subjective malaise, seems to suggest the opposite. maybe it's possible that piracetam is increasing glutamate to a degree which is deleterious without actually causing any excitotoxicity, or that it has an innate means of compensating for this.

from: https://www.neurorel...e.php?issue=352

Studies examining patients with major depressive disorders have also found a higher ratio of excitatory to inhibitory amino acids. Anxiety models have successfully used glutamate antagonists suggesting a similar excitatory:inhibitory neurotransmitter imbalance in these patients. Research in this area continues.

....These findings parallel observations that theanine, an ingredient in the above mentioned products, acts as a glutamate antagonist and thereby reduces excitatory neurotransmission. Studies have found that theanine will decrease the extent of excitotoxic brain damage following neurological injury in models of ischemic stroke.

...nother amino acid that has been found to modulate the balance of excitatory and inhibitory neurotransmitter activity is taurine. A number of TAAT products contain taurine: TravaCor, GABAMax, CeroLox, and PrevAmine. Taurine interacts with the GABA receptor and potentiates its function and therefore reduces excitatory neurotransmission. Therefore, taurine affects the inhibitory/excitatory balance by enhancing GABA and does not directly affect glutamate.

Maintaining a proper balance between excitatory and inhibitory neurotransmitters is a primary element in optimizing neurotransmission and maintaining brain function while minimizing excitotoxicity.

interesting stuff, here (http://www.jpp.krako...15_article.html):

The results show that NR1 mRNA, the main NMDA glutamate receptor subunit, is present in the cortex and medulla of rat adrenal gland, while specific mRNAs coding for NR2A and NR2B failed to be detected in adrenal tissue.

...Glutamate receptors in the adrenal medulla have been associated with catecholamine release (6—8). In vitro experiments on isolated adrenals and cultured chromaffine cells have shown that NMDA have the highest potency amongst glutamate receptor agonists used to stimulate catecholamine secretion under basal conditions (7, 8). The role of NMDA receptors has been supported also by in vivo pharmacological studies under both control and stress conditions, showing that manipulation of NMDA receptors is sufficient to inhibit catecholamine response to a stress stimulus (6, 9). Potential significance of NMDA receptors localized in the adrenal cortex is unclear.

....Glutamate acting on local adrenal receptors could origin either from hypothetical glutamatergic innervation of adrenal medulla or from the pool of circulating amino acids (23, 24). Thus, the glutamate, its analogues, food additives and drugs (designed to interact with glutamate receptors in the brain) may exert their action directly on the adrenal gland. The adrenals together with other peripheral organs expressing glutamate receptors could represent potential peripheral targets for neurotransmitter mediated excitotoxicity, food toxicity and should be considered in the therapy (24).

The increase of NR1 gene expression in response to stress could lead to formation of new receptors, which may modulate the sensitivity of adrenal tissue to subsequent stress stimulus or to circulating levels of excitatory amino acids. Though the molecular mechanisms are not known, observed stress-induced rise in NR1 subunit gene expression seems to represent an important factor by which stress exerts long-term effects on adrenal function.

Stimulation of the Amygdala by Glutamate Facilitates Corticotropin-Releasing Factor Release from the Median Eminence and Activation of the Hypothalamic-Pituitary-Adrenal Axis in Stressed Rats

The role of the amygdala in the regulation of hypothalamic release of corticotropin-releasing factor (CRF) was investigated. Microinjection of glutamate (50 nmol) into the amygdala resulted in increased plasma corticosterone in male rats previously subjected to a 14-day unpredictable stressor paradigm (p le 0.05 vs. saline-injected controls). A long-lived increase in corticosterone levels was also observed in rats which were urethane-anesthetized (1.35 g/kg) 3 h prior to glutamate microinjection (p le 0.01 vs. saline-injected controls). These effects on plasma corticosterone were observed despite the presence of high basal levels of corticosterone. Furthermore, microperfusion of glutamate (3-300 µM) into the amygdala of urethane-anesthetized rats resulted in a dose-dependent increase in CRF release from the median eminence, as assessed by in vivo microdialysis (p le 0.025 vs. basal). These results indicate a facilitating role for the amygdala in stress-induced increases in CRF release and subsequent adrenocortical activation.

i think there may be a culmination of factors here which are preventing piracetam from being a sustainable solution for some (if not most). my guesses:

1. acetycholine receptor upregulation leading to reduced monamines, like 5HT and DA, at least in certain areas of the brain. i found that taking deprenyl helped ward off depressive symptoms from piracetam/choline - it may be unrelated, of course.

2. Catecholamine/adrenal burn-out. the interaction piracetam has with the NMDA and glutamate systems is leading to excess release of catecholamines, which has a temporarily stimulating effect, until you basically burn everything out and are left feeling like shit. not unlike the amphetamines. for those of us who may already be susceptible to adrenal fatigue, piracetam might at first appear to be a saving-grace, when reality it's burning off the last of the fuel we have left at a much faster rate, giving the temporary appearance of solving the problem. more research needs to be done to look into the relation between NMDA/glutamate and adrenal hormones, then we could devise a means to try and compensate.

3. glutamate overactivation. there may be a spectrum here, a dose/time response curve. function enhanced to a degree leads to more nonspecific neuronal stimulation, while eventually hitting a peak before beginning to cause negative symptoms/toxicity. magnesium or memantine might be the answer - but then it also might just counteract the piracetam. magnesium, the milder NMDA antagonist of the two, might keep piracetam's NMDA receptor expression in check.


preventing overestimation with magnesium, keeping DA high with deprenyl, and finding a means to supply the adrenals with way more fuel might be an effective way to prevent the poop-out. the latter, burnout, seems like the toughest aspect and the most difficult to try and pull off both effectively and safely. daily tyrosine might help.

Edited by brain, 19 January 2010 - 01:05 AM.

[brain]

from wikipedia:

Progesterone exerts its primary action through the intracellular progesterone receptor although a distinct, membrane bound progesterone receptor has also been postulated.[19][20] Additionally, progesterone is a highly potent antagonist of the mineralocorticoid receptor (MR, the receptor for aldosterone and other mineralocorticosteroids). It prevents MR activation by binding to this receptor with an affinity exceeding even those of aldosterone and other corticosteroids such as cortisol and corticosterone.[21]

Progesterone has a number of physiological effects which are amplified in the presence of estrogen. Estrogen through estrogen receptors upregulates the expression of progesterone receptors.[22] Also, elevated levels of progesterone potently reduce the sodium-retaining activity of aldosterone, resulting in natriuresis and a reduction in extracellular fluid volume. Progesterone withdrawal, on the other hand, is associated with a temporary increase in sodium retention (reduced natriuresis, with an increase in extracellular fluid volume) due to the compensatory increase in aldosterone production which combats the blockade of the mineralocorticoid receptor by the previously elevated level of progesterone.[23]

i always found piracetam made me dehydrated. progesterone, which was my guess at one of the better ways to increase adrenal hormones, actually inhibits aldosterone. so piracetam, with it's ability to increase the presense of related hormones, might inhibit aldosterone through this pathway. mixing a little sodium in with the piracetam might be a wise idea. heres my rough guess at what an effective piracetam adjunction might look like:

tyrosine, 1,000 mg/day
sodium hydrochloride, 1 tsp (?) daily
magnesium citrate, 350 mg/day, possibly morning/night
deprenyl, 5 mg daily
progesterone (not sure about dosage)
3 eggs/day. each egg has 70% RDA of cholesterol, the primary precursor for all adrenal hormones. eat em' with plenty of salt and it's a perfect breakfast to go along with that morning piracetam OJ.
cardio exercise, every day. for the other hormones. i've noticed piracetam reduces the growth of my facial hair.

[acantelopepope]

Nice work, brain! Let's continue this line of research.

In other news, I ordered some piracetam/aniracetam from Cerebral Health--My philosophy is that if all suppliers are sending me piracetam that has the same deleterious effects, it's even more unlikely quality is the issue here.

Again, good job. I feel like we're getting somewhere.

[jackj]

So I got my supply of original piracetam the other day so I thought I would give an update as a possible "non-responder", when I was prior.

My daily intake (prior) was mainly fish oil and sometimes royal jelly (still testing it) and Alcar and ALA. I exercise almost daily and eat well for a late 20's guy.

Seven days ago I started taking the mucuna powder (500mg) in attempt to boost my dopamine. Three days ago I took a daily dose of 5htp along with a complex multi and vitamin C perhaps level it out a bit.

Yesterday I started taking the new source of piracetam (2400mg once and then 1200mg twice a day with food).

So far I have noticed that the almost depressing effects that I was feeling with the other piracetam source are not there (I have not taken any choline yet). I mean I have been feeling pretty sleepy but I think that might be due to the 5htp which I am taking late in the day. I hope to get a decent sleep tonight as havent in the past few days due to other reasons.

Now I know it doesn't rule out one piracetam source as bad but I'm going to give it a week or a few days and switch to the other source and see what happens.

I'll try to be as impartial as I can but bare with me and let me know if you have any suggestions or criticisms, thanks.

Edited by jackj, 19 January 2010 - 03:16 PM.

[babcock]

I started taking my noot regimen of:

4g SmartPowders Piracetam with water after eating
500mg Jarrow Formulas CDP Coline with water after eating
400mg Pyritinol with water after eating
All taken at the same time after breakfast.

I started these yesterday and haven't noticed any effects yet (I know I have to give it two weeks). The only thing I noticed was yesterday my head felt a little "disconnected" almost medicine head like about 1.5 hours after taking the noots. Today I have not noticed any effects (now 4.5 hours after I took the noots).

Let me know if you guys have any suggestions.

[nito]

So I got my supply of original piracetam the other day so I thought I would give an update as a possible "non-responder", when I was prior.

My daily intake (prior) was mainly fish oil and sometimes royal jelly (still testing it) and Alcar and ALA. I exercise almost daily and eat well for a late 20's guy.

Seven days ago I started taking the mucuna powder (500mg) in attempt to boost my dopamine. Three days ago I took a daily dose of 5htp along with a complex multi and vitamin C perhaps level it out a bit.

Yesterday I started taking the new source of piracetam (2400mg once and then 1200mg twice a day with food).

So far I have noticed that the almost depressing effects that I was feeling with the other piracetam source are not there (I have not taken any choline yet). I mean I have been feeling pretty sleepy but I think that might be due to the 5htp which I am taking late in the day. I hope to get a decent sleep tonight as havent in the past few days due to other reasons.

Now I know it doesn't rule out one piracetam source as bad but I'm going to give it a week or a few days and switch to the other source and see what happens.

I'll try to be as impartial as I can but bare with me and let me know if you have any suggestions or criticisms, thanks.

Which two sources of piracetam did you use?

[brain]

I started taking my noot regimen of:

4g SmartPowders Piracetam with water after eating
500mg Jarrow Formulas CDP Coline with water after eating
400mg Pyritinol with water after eating
All taken at the same time after breakfast.

I started these yesterday and haven't noticed any effects yet (I know I have to give it two weeks). The only thing I noticed was yesterday my head felt a little "disconnected" almost medicine head like about 1.5 hours after taking the noots. Today I have not noticed any effects (now 4.5 hours after I took the noots).

Let me know if you guys have any suggestions.

might want to take the piracetam on an empty stomach, then the CDP after food. not sure about the pyritinol.

[brain]

by the way, guys, from what i've found so far, progesterone doesn't appear to be a risk factor for causing any kind of hormone imbalance in males. women take it to keep excess estrogen in check - it appears to have the same effect in males. the progesterone comes in a cream form which can be bought at most vitamin/supplement shops. it's usually marketed towards middle aged women, but it can also be used to help treat prostate issues. anyone who's been taking piracetam for a while want to give this a go?

Edited by brain, 19 January 2010 - 09:10 PM.

[Andrew Shevchuk]

I started taking my noot regimen of:

4g SmartPowders Piracetam with water after eating
500mg Jarrow Formulas CDP Coline with water after eating
400mg Pyritinol with water after eating
All taken at the same time after breakfast.

I started these yesterday and haven't noticed any effects yet (I know I have to give it two weeks). The only thing I noticed was yesterday my head felt a little "disconnected" almost medicine head like about 1.5 hours after taking the noots. Today I have not noticed any effects (now 4.5 hours after I took the noots).

Let me know if you guys have any suggestions.

I started a similar regimen about three days ago, only I've been spreading out my piracetam and CDP choline intake throughout the day. The "disconnected" feeling that you mention occurred in conjunction with the pyritinol, particularly when I took it for the first time. The piracetam doesn't seem to have had any effect yet, but I'm going to continue this for at least a few weeks to see if it kicks in. I've read suggestions that it can take the better part of a month to work.

I feel that upping the dosage of pyritinol could have a more pronounced and positive effect. The bottle recommends a dosage of 800-1200mg a day (in 400mg capsules) whereas I am currently only taking 400mg. I am aware of the hepatotoxicity history in a small selection of pyritinol users and so I am hesitant to use 1200mg a day at this point, although I suppose I could go for it and stop immediately if I notice any health problems. Any suggestions?

[brain]

for some reason i'm not able to edit my post, and i'm sorry for all the posting here, but i wanted to retract my previous suggestion that someone should try progesterone, also my statements that it's likely safe in men - it may not directly effect a testosterone/estrogen balance negatively, but it still may cause some sort of negative imbalance between some of these hormones. i think it might be neat to test it out for a week or so to see if anything miraculous happens - but these are very delicate hormone pathways and i don't think half-blind guessing games at supplementation are a very wise idea. likewise, piracetam effects the same pathways, which to me is also leading me to believe it's something i don't want to take on a regular basis until this is sorted out - if it's sorted out.

where to go from here? personally, i think we need to look very carefully into the function and role of every steroid produced by the adrenal glands - i feel it's clear at this point that this is a key area in both piracetam's efficacy and in it's drawbacks. we need to try and figure out as precisely as possible how piracetam alters adrenal function, speculate as to the total alteration of pathways and individual hormone dominance within pathways. the relationship between NMDA/glutamate and adrenal hormones needs to be very clearly understood. since there is very clear research about how piracetam effects NMDA receptors and glutamate - when we truly understand this relationship it might then become apparent how exactly it is that piracetam is effecting adrenal hormones. it's easy to see how preexisting knowledge effects understanding of new information, and how understanding of whatever phenomena/idea is shaped by whatever resources one already has available. if we really become well versed in these systems, and don't merely approach it from the perspective of piracetam efficacy, we would much increase our chances at trying to figure this out. this problem obviously involves a synthesis of a wide array of physiological functions, and once we combine our own subjective experiences from the new perspective of this body of knowledge (which i'm sure some here already have, i myself don't) more connections are going to be made.

i'd like to add that the study which shows that piracetam is ineffective when the adrenals are cut out does not necessarily mean that piracetam's effects are directly mediated by the adrenals or that some increase/decrease in adrenal hormones is causing it's effects or mediating it's effects. it might merely mean that another mechanism which piracetam does act on is dependent on these functions as a co-factor. however, my own subjective experience - and these instances of possible aldosterone deficiency, seem to suggest otherwise.

aldosterone is available as an individual supplement, as well. as it's at the end of the adrenal pathway, it may be safer to test out than some of the others - but it still has a diverse array of functions within the body, and as far as i'm aware, none of them have much to do with the brain in any direct sense - but i have wikipedia level knowledge on that one.

[acantelopepope]

I'm reposting my response to the NMDA/AMPA thread here because it's extremely relevant to our discussion.

medicineman posted:
http://www.sumanasin.../receptors.html

This will clear up alot of questions regarding how the racetams work, how calcium can cause toxic effects if unchecked, and how nmda antagonists work...


acantelopepope posted:

Good video, but it didn't explain 'how calcium can cause toxic effects if unchecked,' did it?

Here's some additional information on NMDA/AMPA receptors taken from the springerlink encyclopedia of neuroscience [which explains calcium's role in NMDA/AMPA receptors]:

Many other drugs have been investigated for possible
efficacy in the treatment of cognitive deficits, including
▶memantine, selegiline, modafanil, vitamin E, Ginkgo
biloba extracts and a variety of other herbal extracts,
and▶α-amino-3-hydroxy-5-methylisoxazole-4-propionic
acid (AMPA) receptor potentiators. Of these, only
memantine and AMPA receptor potentiators have been
shown to have any clinical effect [4]. Memantine
blocks the calcium ion channel associated with the
▶N-methyl-D-aspartate (NMDA) subtype of glutamate
receptor (an uncompetitive NMDA antagonist). Since
the NMDA receptor is involved in increases in synaptic
efficacy associated with LTP, it may at first seem
paradoxical that memantine could benefit cognition.
However, over-stimulation of theNMDAreceptor causes
neurotoxicity and therefore memantine may improve
cognition in diseases such as Alzheimer’s disease by
limiting this form of neural damage [3,4,6,7]. ▶Piracetam
is one of a number of AMPA receptor potentiators
that has been actively researched but is not yet prescribed
for Alzheimer’s disease. Along with aniracetam, it is a
pyrrolidone that increases the response of the AMPA
subtype of glutamate receptor [9]. Other AMPA receptor
potentiators, sometimes referred to as “▶ampakines,”
include benzylpiperidines such as CX-516 and CX-546,
which are in clinical trials [1,9].
Most of the drugs that are used clinically in the
treatment of cognitive disorders do not enhance cognition
in people without a neurological deficit. However, many
drugs that were first investigated for their general
nootropic effects, were then tested in patients with
Alzheimer’s disease and other neurological disorders to
determine whether they would have any beneficial
clinical effect. Some herbal drugs such as Ginkgo biloba
extracts have been claimed to improve memory in
both Alzheimer’s disease patients and in neurologically
intact individuals; however, there is no convincing
evidence for a consistent effect in either case [4,10].
Summary of Nootropic Sites of Action
Where in the brain do nootropic drugs act to produce
their effects? Many areas of the brain are involved in the Areas such as the hippocampus and other areas of the
medial temporal lobe are believed to be important for
encoding new memories; the neocortex is thought to be
important for long-term storage of memories [1,2].
Molecular Mechanisms of Action of Nootropic Drugs
The precise mechanisms of the formation and retrieval
of memories are not understood and therefore the
precise mechanisms of action of nootropic drugs are not
known. However, it is well established that acetylcholine
is important for the formation new memories.
Activation of acetylcholine receptors causes intracellular
changes in neurons that result in the activation of
proteins such as the cyclic adenosine monophospshate
(cAMP) response element binding protein (▶CREB),
which many researchers regard as a form of “molecular
switch” that converts short-term memories into longterm
ones [2]. The neural model of memory, LTP, has
been used to better understand the increases in synaptic
efficacy that are likely to underlie the formation of
memories. In LTP, the activation of post-synaptic
NMDA receptors is thought to be a critical step in
producing the biochemical changes that lead to enhanced
synaptic efficacy. While excessive activation of NMDA
receptors results in excessive calcium influx and
neurotoxicity, a smaller elevation of NMDA receptor
activation may enhance memory. For example, the
ampakines have been developed so that they elevate
NMDA receptor activation indirectly, by potentiating
AMPA receptor activity, which then leads to increased
depolarization, thus lowering the threshold for NMDA
receptor activation [1,9]. The downstream effects of
AMPA receptor modulation include an increase in
growth factors such as brain-derived neurotrophic factor
(BDNF), which is known to be important in synaptic
plasticity [9].While still in clinical trials, these drugsmay
be one class of nootropic drug that is used to treat
Alzheimer’s disease and other related neurological
disorders in the future. Other possibilities include drugs
that modulate dopaminergic and serotonergic function.
Many researchers believe that no one drug with a single
mechanism of action is likely to provide successful
therapy for cognitive disorders.
Will the same nootropic drugs that are used to treat
cognitive disorders be useful for enhancing cognition in
healthy individuals? It is possible but more likely that
there are natural limits to the extent that the normal
neurochemical machinery of memory can be enhanced
before adverse side effects develop.

[acantelopepope]

By the way, my shipment of Piracetam/Aniracetam arrived from Cerebral Health today. They were kind enough to let me sample the piracetam -- $5 for 50g. However, I'm afraid to try it for fear that it will ruin my day if I experience adverse effects. So I do not know when I'll be able to report on its effects.

[Viscid]

By the way, my shipment of Piracetam/Aniracetam arrived from Cerebral Health today. They were kind enough to let me sample the piracetam -- $5 for 50g. However, I'm afraid to try it for fear that it will ruin my day if I experience adverse effects. So I do not know when I'll be able to report on its effects.

lol.

[Thorsten3]

By the way, my shipment of Piracetam/Aniracetam arrived from Cerebral Health today. They were kind enough to let me sample the piracetam -- $5 for 50g. However, I'm afraid to try it for fear that it will ruin my day if I experience adverse effects. So I do not know when I'll be able to report on its effects.

lol.

indeed...how ironic that one has to suffer a shitty day in order to find out!! good find by the way acantelopepope some useful info in that prior post

[tritium]

By the way, my shipment of Piracetam/Aniracetam arrived from Cerebral Health today. They were kind enough to let me sample the piracetam -- $5 for 50g. However, I'm afraid to try it for fear that it will ruin my day if I experience adverse effects. So I do not know when I'll be able to report on its effects.

"We need to be the change we wish to see in the world" -Gandhi

[jackj]

Well I've been taking this new piracetam source for nearly a week now and I'm seeing a definite increase in concentration levels and general clarity of thought (which is why I take it). I have had no angry moody side effects like I used to see on the bulk source, even on 400mg a day I would see side effects on my mood. I'm taking 1200mg twice a day on an empty stomach with the new source and I honestly haven't noticed anything similar. Once or twice I did notice that on the new source the effect seemed very mild if nothing at all even though the dose was three times what I use to take. Taking it on an empty stomach seems to help though.

So I'm pretty sure I am seeing good results. I'm reluctant to try the old source currently but will do in a few days time.

I still have not taken a choline source. I have noticed a slight headache and neck stiffness but I've found some red meat and eggs in my diet keeps them away for now.

Edited by jackj, 24 January 2010 - 07:18 PM.

[acantelopepope]

"We need to be the change we wish to see in the world" -Gandhi

You're right, tritium. I'm sure that Gandhi would say the same thing today about trying a possibly contaminated source of a psychotropic chemical substance. Definitely an appropriate quote for the occassion.

Jack, good to hear you're getting the better of piracetam once again (or for the first time?) -- Here's what I suggest if you want to see whether it's the source.

1) Measure out doses for a few days from each source.
2) Give them to someone close to you. Clearly tell them which group is "1" and which group is "2" -- but don't tell them what that means.
3) Tell them to separate the two and keep track of which is which.
4) Have them give you group 1 for a few days and group 2 for a few days.
5) Record anything you notice in terms of positive or negative feelings/clarity.
6) At the end of the trial (~6 days should do it), decide if you noticed a substantial difference. Have them identify which group was which.
7) That's it. You just performed a double-blind test upon yourself.

[jackj]

"We need to be the change we wish to see in the world" -Gandhi

Jack, good to hear you're getting the better of piracetam once again (or for the first time?) -- Here's what I suggest if you want to see whether it's the source.

1) Measure out doses for a few days from each source.
2) Give them to someone close to you. Clearly tell them which group is "1" and which group is "2" -- but don't tell them what that means.
3) Tell them to separate the two and keep track of which is which.
4) Have them give you group 1 for a few days and group 2 for a few days.
5) Record anything you notice in terms of positive or negative feelings/clarity.
6) At the end of the trial (~6 days should do it), decide if you noticed a substantial difference. Have them identify which group was which.
7) That's it. You just performed a double-blind test upon yourself.

I have been on and off it for about three years. I started on the source I am on now and did that for about six months. I changed to the bulk supply and due to mixed long term results I never really took a regular dose after that. After the first year I thought the supply might have gone off so I brought another but it didn't seem any different. The moods and "clouded" thoughts continued. I have come full circle

I will give what you suggested a try but the only person I trust to tell right now is my girlfriend and she is away for another month plus one source is a pill and the other is a powder that I put into caps :(.

I'll try two weeks on one and two weeks on the other and keep all other factors a standard as I can in the mean time, cheers.

Edited by jackj, 24 January 2010 - 09:47 PM.

[mulvena312]

Jackj, out of curiosity what is the piracetam source you began using to see piracetam results again?

Acantelopepope, any reason why you chose Cerebral Health as the piracetam source?

This topic is inspiring me to give the racetams a round 2. I used to be a racetam responder before the brain fog began setting in. Failed the eye fluctuation test. I have only tried the bulk powder. I'm going to order some this week (non bulk) hopefully from a reliable source after some researching.

I eliminated alcohol, smoking, and coffee this year. Have been supplementing with sea salt, eluthero, creatine, d-ribose, multi, and B-vitamins for over a month now.

Vinpocetine and green tea help with decreasing glutamate and I'm going to add that to the piracetam stack. For choline source I will use DMAE.

[jackj]

Jackj, out of curiosity what is the piracetam source you began using to see piracetam results again?

Geratam.

[acantelopepope]

Isochroma uses CerebralHealth. I don't want to turn into Isochroma or anything, but it seemed to work well enough for him, consistently.

[Andrew Shevchuk]

Starting getting some headaches yesterday after about a week on the Piracetam/CDP Choline regimen. I guess it's good to know that I'm feeling something from it (because I never get headaches otherwise), but I guess I have to reduce my Piracetam-to-Choline ratio.

[acantelopepope]

Starting getting some headaches yesterday after about a week on the Piracetam/CDP Choline regimen. I guess it's good to know that I'm feeling something from it (because I never get headaches otherwise), but I guess I have to reduce my Piracetam-to-Choline ratio.

Theoretically that means your acetylcholine receptor density is increasing, which is a good thing. Have you tried increasing your intake of eggs and meat?

[mulvena312]

Isochroma uses CerebralHealth. I don't want to turn into Isochroma or anything, but it seemed to work well enough for him, consistently.

I emailed Cerebral Health and Smart Powders for their Piracetam COAs. Isochroma also mentioned that he was using Smart Powders prior to Cerebral Health. Switched because he had issues with Canadian customs at the below link:

http://74.125.113.13...u...=clnk&gl=us


Based on how recent and how these COAs look I will make a decision. Thought about Relentless Improvement but that price is out of my range right now.

[nito]

Isochroma uses CerebralHealth. I don't want to turn into Isochroma or anything, but it seemed to work well enough for him, consistently.

I emailed Cerebral Health and Smart Powders for their Piracetam COAs. Isochroma also mentioned that he was using Smart Powders prior to Cerebral Health. Switched because he had issues with Canadian customs at the below link:

http://74.125.113.13...u...=clnk&gl=us


Based on how recent and how these COAs look I will make a decision. Thought about Relentless Improvement but that price is out of my range right now.

I have the smartpowder, and i have not felt anything to make any judgements on. I might give the cereberal health a try since Isochroma had success with it. If that don't work i mind as well just give up. I must mention i've only tried the powder - but it wouldn't make sense if the pill worked better, so if powder don't work i guess i'm out!

[John W.]

First of all apologies because this is a kind of off-topic. I was googling a few weeks ago and came upon some articles on VGlut (Vessicular Glutamate Transport) being implicated in vision processes. Which made me think about czukles' post several pages ago, which essentially said: Piracetam modifies cholinergic transmission and therefore seems to require choline supplements, Piracetam also modifies glutamatergic transmission - ergo lack of glutamine supplementation could explain negative effects (brain fog etc.) in the same way lack of choline supplementation could. L-Glutamine is extremely cheap, so I gave it a shot. I took a pretty heavy amount at first, and then took 1 gm L-Glutamine on an empty stomach. A while later I took my Piracetam and some choline. Amazingly, I felt pretty good. Not 'brilliant', but no negative side effects. The most amazing thing though was this: the day before I had taken Piracetam and had all the problems, I was a bit spacey, my pupils fluctuated dramatically, and I was pretty light sensitive. Yet the day of the 1 gm L-Glutamine -- Bam; no spaciness, more or less normal light sensitivity, and most incredibly - my pupils stopped fluctuating. The only thing was though, I didn't feel 'smarter'. Encouraged though since my pupils finally stopped fluctuating so freakishly (and have stayed consistent since), I have continued to take the L-Glutamine. I've been taking the regimen in Central America for the last two weeks though and I believe the nootropic effects have crept up on me. I would take L-Glutamine then Piracetam early in the day, and then note that later in the day my confidence in speaking Spanish (which I haven't studied since High School) dropped dramatically and I was speaking it much slower/laboriously. I'll grant this could be a placebo but there is no doubt that since the day I started taking L-Glutamine the pupil fluctuations and 'objective' negative effects have gone away.

[Andrew Shevchuk]

Starting getting some headaches yesterday after about a week on the Piracetam/CDP Choline regimen. I guess it's good to know that I'm feeling something from it (because I never get headaches otherwise), but I guess I have to reduce my Piracetam-to-Choline ratio.

Theoretically that means your acetylcholine receptor density is increasing, which is a good thing. Have you tried increasing your intake of eggs and meat?

Headaches have since disappeared. I eat very little egg (except if it's in something like baked goods) and I usually avoid red meat. I really don't like either of them and prefer to eat poultry or seafood as protein sources. I realize that red meat and eggs are the largest choline sources in the diet, so perhaps I should supplement with more choline? Because I really don't want to force myself to eat things I've developed a distaste for.

[tritium]

I have the smartpowder, and i have not felt anything to make any judgements on. I might give the cereberal health a try since Isochroma had success with it. If that don't work i mind as well just give up. I must mention i've only tried the powder - but it wouldn't make sense if the pill worked better, so if powder don't work i guess i'm out!

I found that you can buy the same Piracetam for three different prices at Cerebral Health:

http://www.cerebralh.../nootropics.php $59 + $30 shipping in USA

http://www.cerebralh...roceuticals.php $49 + $7 shipping in USA

http://www.cerebralh...supplements.php $35 + $30 shipping in USA

I don't see how they can charge $30 for shipping when it would cost at most $10 within the US. The middle link has the lowest price for those interested.