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ALCAR and other Nootropics for coming off cycle


New member
Feb 21, 2003
Pure speculation...

Acetyl L-carnitine has been shown to partially diminish stress induced decreases in gonadotropin secretion in cold swimming rats and amennhoreic athletic women. I would venture to guess that some of the other nootropic agents (piracetam, phosphatidylserine etc.) might do the same thing.
smart drugs

1st. let it be known I don't sell nootropics but am still biased due to the fact I feel these drugs help recovery and the actual recruitment of muscle fibers during exercise and I have absolutely not one fucking study to back me up on that. I just know its working for me.

2nd. Everyone is different. A search on google groups and you get literally dozens of different reactions to drugs, some good, some bad, some nothing at all.

I've been playing with Piracetam with very good results in the past. But I recently refined and upgraded my stack and talk about a SMART BOMB.

Piracetam; I notice alot of indivduality on which dose gets it going. I've heard as low as 2,400mg for 2 days, I've heard as I high as 8,000mg for a week! (there have been studies done on ederly using up to 36grams for extended periods of time; not saying go high just its not easy to OD on).

For myself I got it down pat. 1st day 5,600mg. 2nd day 4,800mg. 3rd thru 7th day 2,400mg. From there on out I use 800mg a day, someday I feel I need to double dose.

Idedenone; there's a whole thread about it on this board and a shit load of info on the net. I use 45mg morning, 45mg night.

Vinpocetine; now this right here alone is a sick little bastard. Try it by itself, I dont know maybe Im just sensitive to it, i *feel* coming on. Vision and hearing enhanced, colors brighter. Makes playing comp games even more addicting LOL. I dose 20mg three times a day. Or when Im off Pir I use Vin in 40mg doses. I love Vinpocetine and will use it as long as I and it is around.

Now the little suble shit to play with:
Choline did jack balls. Then I added some b5 to my choline; THERE WE GO. Energy up, mood up, looking good.

Now the stack starts to intertwine with my bobybuilding supplement regimen.

Acetyl-L-Cartinine, very good shit. Helps the neuro stack and is a anti-aging stack and is synergistic with ALA and it nutrional partioning effects. I was using 500mg twice a day, now that big A got it capped for an unbeatable price Im upping it to 5grams.

Taurine; Im always rebumping that post. Tauring = under rated. Take 4 grams at time with some b6, feel the energy.

ALA has some protective properties on the brain too.

GT has a ton of research on it(either the brew or the extract, and its one of the better ways to get a little caffiene in the system).

What do we humans use? I think its 1/10 of 1% of our brain. I may have just upp'd mine up a notch!
Last edited:
Its commonly agreed there's a "muscle-mind" link. A body doesnt just physcially lift weight. The brain recieves the information of the physical stress and recruits muscle fibers (i may not be explaining this perfectly as i dont have any studies in front of me). So, I feel if the nootropic stack *works* and in my case I definetly feel it does, so perhaps, it strengthens the minds ability to recruit fibers during exercise and recognize the damage done to the cells due to microtrauma and help recovery. Keep in my mind this is all bullshit I have made up in my head. Just speculation.
I assume you are taking all this post/off cycle?!?

Nootropics and anabolics have no none interactions. No reason to stop taking smarties while on. In fact Test in itself enhances cognitive abilities, should work well with the stack.
Id also imagine that you may be able to focus better during training, in the same way as ephedrine as a stimulant makes you more alert. Is ginko worth a crap for this? Are all the other drugs prescription? Can you use overseas RXs since Im sure they are not scheduled?
Smarties dont boot you in the ass like Eph does but does heighten senses/alterness.

Piracetam is not Schelduled and I know a domestic source that offers its at 100 bucks for 1000grams, which blows out any overseas company.

Vinpoceptine can be found in most health food stores.

As a matter of fact for the month of February www.VitaminShoppe.com has a 70% off sale on a ginko/hupa A combo which works very well with Pir.
I have read alot of good things about piracetam! I think I am going to give that stuff a try. I dunno if I am ready for the whole thing you got posted but anthing to increase my concentration is a good thing!!
Piracetam is a good way to introduce yourself to the smartie world. However if you go with just Pir at least supplement your meal with extra Choline (gram range) and Vitb5 (500mg).

Or get Hupa A with acts as Cholingenic system inhibitor.
I already take about 400mgs of the choline do oyu think that would be enough???
I would up it up to 1-2 grams a day if you go with Pir. I'll post other things to use instead of choline or injunction with. Stick with the 400mg if you want but its pretty cheap to go higher.
Yea its not the expense I am worried about, its the fact that I forget to take so many pills! I know you with your super inttelenct can remember to take the 96 pills you swollow a day but lessor individuals like myslef have trouble remembering to take 15. Also I always forget were I put my car keys but thats another story...... hopefully this shiyt works
Funny how close your are with that 96 estimation...
As far as "ordinary" Choline is concerned... it doesn't easily pass the blood-brain barrier so people tend not to get much out of it. There is a special type of Choline called CDP-Choline which can easily pass the blood-brain barrier and is much more effective than "ordinary" Choline.

As far as Piracetam is concerned, I suppose that's better than nothing but Oxiracetam, Pramiracetam, and Aniracetam are all a lot more powerful. I personally prefer Aniracetam.
Ah we got a smartie. Yes the oxy is the best you can get but unless you got better hook-ups than I, it can get pricey. As for the choline issue you are correct that form is better but not the best, Im just trying to warm these guys up;

Glycerylphosphorylcholine is a drug prescribed in Europe to treat
neurological disease. It is sold in the United States as a dietary
supplement to protect against age-related brain deterioration and memory

In the November 2001 issue of Mechanisms of Ageing and Development, an
extensive review was published about the muliple effects of
glycerylphosphorylcholine (GPC).[1] The analysis covered thirteen published
clinical trials examining a total of 4,054 patients with various forms of
brain disorders including adult-onset cognitive dysfunction, Alzheimer's
disease, stroke and transient ischemic attack. The overall consistent
finding was that "administration of GPC significantly improved patient
clinical condition."

The researchers stated that the effects of glyceryl-phosphorylcholine (GPC)
were superior to the results observed in the placebo groups, especially with
regard to cognitive disorders relating to memory loss and attention deficit.
They noted that the therapeutic benefits of GPC were superior to those of
acetylcholine precursors used in the past, such as choline and lecithin.
What most impressed the researchers was data indicating that GPC helps
faciliate the functional recovery of patients who have suffered a stroke.

Brain aging is characterized by cerebral circulatory deficit and
neurotransmitter deficiency, along with structural deterioration to neurons
and their connective transmission lines (axons and dentrites). A significant
body of research indicates that glyceryl-phosphorylcholine (GPC) may be of
benefit in helping to prevent every one of these pathological events. It may
thus be possible to both protect against underlying causes of brain aging
while partially restoring cognitive function.
This article describes the scientific studies that substantiate the benefits
of glycerylphosphorylcholine.

Choline-fuelled signalling molecules are at the seat of learning, memory and
behavior. As a result, there has been a lot of buzz around manipulating
cholinergic neuronal transmission in order to slow or undo the neurologic
effects of aging.
The tricky part is not how much choline can be pumped into the brain, but
how efficiently this critical raw material can be transported to various
regions of the brain. Otherwise, it's like gassing up a car that has a
clunked out engine.

A large problem in aging and diseased brains is the slowing of cholinergic
transport, while cholinergic neurons drop in number. In Alzheimer's disease,
cholinergic cells shrivel up and die at a fast-forward pace. Scientists
believe that even in healthy aging people, malfunctioning and decreased
numbers of choline-powered neurons are somewhat to blame for short-term
memory loss and cognitive decline.

The reason why choline has to get where it's going in the brain is that it
has a big to-do list. In addition to being the precursor for the
neurotransmitter acetylcholine, choline also synthesizes
phosphatidylcholine. Brain cell membrane integrity is dependent on
phosphatidylcholine. When choline levels are low, phosphatidylcholine can
function to produce more acetylcholine. The problem with low choline is that
it compromises the integrity of brain cell membranes, since boosting the
production of acetylcholine diverts phosphatidylcholine away from its
critical job of maintaininig cell membranes. This all explains why the brain
has such a voracious appetite for choline.
Help on the way

Enter L-alpha glycerylphosphoryl-choline (GPC), a byproduct of
phosphatidylcholine, and a precursor that's useful in stoking the
cholinergic neurotransmitter system. More specifically, it aids in the
synthesis of several brain phospholipids, which increases the availability
of acetylcholine in various brain tissues. The GPC form of choline has been
shown in studies to reverse the cognitive and behavioral glitches seen in
aging, Alzheimer's disease (AD), stroke and memory loss.

Studies suggest that glyceryl-phoshorylcholine is effective in slowing the
expression of structural changes that occur in the brain as a result of age.
These changes result in the loss of neuronal function, as well as a decline
in the number of neurons and their receptors. One study found that long-term
treatment of rats with GPC in their drinking water was effective in
countering the loss of neuro-connecting fibers and brain cells that are
consistent with aging. In GPC-treated rats, both the area occupied by
neuro-connecting fibers and their density were significantly higher than in
age-matched controls. Moreover, the number of granule neurons of the
hippocampus (nerve cells that transmit information to the cerebellum) was
higher in GPC-treated animals than in control 24-month-old rats. The authors
stated that is appears that "glycerylphosphorylcholine treatment counteracts
some anatomical changes of the rat hippocampus occurring in old age."[2]

Other research shows similar findings. Scientists looked at the density of
nerve cells in the hippocampus and in the cerebellar cortex in adult
(12-month-old) and old (24-month-old) rats. Results showed that a six-month
treatment with GPC countered the age-dependent reduction of nerve cells.[3]

A number of studies have also demonstrated the ability of GPC to help
restore muscarinic M1 receptors in old rats. These are a type of
acetylcholine receptor whose number of sites tend to decrease with age.
Italian researchers assessed the effects of aging and of GPC treatment on
the hippocampus of experimental rats. Treatment with GPC restored, in part,
choline acetyltransferase immunoreactivity and acetylcholinesterase
reactivity in the hippocampus of aged rats. The treatment also countered, in
part, the age-related loss of M1 receptors in old rats.[4]

In a later study, this scientific team examined specifically how six-month
treatment with GPC would affect the density and pattern of M1 cholinergic
receptors in rat brains. And again, they found that GPC treatment countered,
in part, the loss of muscarinic M1 receptor sites in old rats. The authors
suggest that the reduction in muscarinic M1 sites noticeable in aging rats
may reflect a loss of nerve cells and/or terminals in these hippocampal
fields, and that GPC increased the expression of muscarinic M1 cholinergic
receptors.[5] Likewise, other researchers concluded that chronic treatment
of aged rats with GPC restored the number of M1 receptors to levels found in
the striatum and hippocampus from young animals, and partially reversed
membrane stiffness in both regions.[6]

The idea that cholinergic treatments might help dementia of the Alzheimer's
kind goes back to what's known as the "cholinergic hypothesis" set forth
about 20 years ago.[7] That's when a U.S. researcher found and reported that
the number of cholinergic neurons in the basal forebrain was substantially
lower in Alzheimer's disease patients than in healthy individuals, and that
the loss of cholinergic innervation from this area of the brain might be the
basis of disease-related cognitive changes. Since then, research has
characterized the Alzheimer's brain as having substantive degenerative loss
of cholinergic receptors and a deficiency of acetycholine, which could
explain the breakdown in cholinergic transmission that leads to dementia,
learning and memory impairment.

While certainly not an exclusive theory on the underpinnings of Alzheimer's
disease and how to treat it, the theory has given rise to a number of
cholinergic-based therapies aimed at bettering cholinergic transmission.
Primarily, therapies have included the use of acetylcholine precursors, M1
muscarinic agonists, and acetylcholinesterase or cholinesterase inhibitors
in order to restore cholinergic function in the Alzheimer's disease brain.
Inhibiting the natural breakdown of acetylcholine through esterase
inhibitors and stimulating acetylcholine release with cholinergic
precursors, such as choline and phosphatidylcholine (lecithin), have been
the focus of many clinical trials.

A limited amount of research and small clinical trials have demonstrated
that GPC boosts acetylcholine availability, its release, and even slightly
improves cognitive dysfunction.[8] Moreover, a larger, multicenter,
randomized, controlled study echoed the results of smaller studies.
Researchers compared the efficacy of GPC and acetyl-l-carnitine among 126
patients with probable senile dementia of Alzheimer's type of mild to
moderate degree. Results showed significant improvements in most
neuropsychological parameters in the GPC recipients that was greater than
improvements in the acetyl-l-carnitine group.[9]

Researchers have found that GPC can be useful in the treatment of cognitive
deficits that often arise from cerebrovascular (stroke) events. When blood
flow is disrupted by a stroke, the result is a cascade of events involving
glutamate flooding NMDA receptors (excitotoxicity), which then leads to
neuron death in the affected region of the brain.

An Italian multicenter trial looked at GPC in 2,044 patients suffering from
recent stroke or transient ischemic attacks. GPC was administered, in phase
1, after the attack at the daily dose of 1 gram intramuscularly for 28 days
and, in phase 2, orally at the dose of 400 mg during the next five months.
Using a series of different standard measuring scales, a positive
association was found in all parameters. According to one scale that
measured deterioration (Global Deterioration Scale), "no cognitive decline"
or "forgetfulness" was reported for 71% of the patients.[10]
A review of 13 published clinical trials comprising 4,054 patients in all,
set out to weigh the benefits of GPC treatment for various forms of dementia
disorders, including senile dementia of the Alzheimer's type or vascular
dementia, and in acute cerebrovascular diseases, such as transitory ischemic
attack (TIA) and stroke. Results from 10 controlled trials comparing GPC to
a reference drug or placebo showed that GPC's clinical results were better
or equal to those observed in control groups under active treatment and
superior to the results observed in placebo groups. Meanwhile, three
uncontrolled trials examining the use of GPC in acute cerebrovascular stroke
and transient ischemic attack ("mini stroke") demonstrated promise that it
could help with the functional recovery of patients with cerebral stroke,
but would require further investigation.[1]

Memory loss
Another area of research has focused on the loss of memory function that
occurs due to any number of causes, including disease, trauma or infection.
Since amnesia (partial memory loss) has been related to decreased or blocked
acetylcholine, researchers have set out to examine reversing this damage
using GPC.
In one study, GPC was injected for 20 days into aged male rats (24 months
old) with learning and memory capacity deficits. It was also administered to
rats with amnesia, which was experimentally induced by scopolamine, a drug
that works by blocking acetycholine receptors. Results indicated that
learning and memory capacity improved in both groups.[11]

Other researchers found that oral GPC reverses pharmacologically induced
amnesia and partially counteracts the decrease of brain acetylcholine levels
elicited by scopolamine administration. Additionally, in experiments that
involved analyzing hippocampus slices from rats, scientists found that GPC
was able to increase the amount of acetylcholine released.[12] Another study
showed that administering oral GPC to rats prevented the learning impairment
and reversed amnesia induced by scopolamine. This study showed that GPC
increased acetylcholine release and resulted in acetylcholine formation. The
authors concluded that the behavioral effects of GPC's ability may relate to
its ability to increase hippocampal acetylcholine synthesis and release.[13]

Explaining the effects
Scientists have homed in on a number of means by which GPC may elicit its
various brain fortifying effects. It is believed that GPC's mode of action
may involve the release of free choline, which then aids in the synthesis of
acetylcholine and phosphatidylcholine. A study involving 12 volunteers
compared GPC to CDP-choline and showed that plasma choline was higher after
GPC.[14] Some researchers have suggested that GPC "may result in an
increased rate of phospholipid synthesis, including the phosphoinositides
available for signal transduction at central nervous system level."[15]

In other research, investigators demonstrated how GPC increased
gamma-aminobutyric acid (GABA) release.[16] This amino acid acts as an
inhibitory neurotransmitter in the central nervous system. Decreased amounts
of GABA have been shown to contribute to the dementia, mood disorders and
psychoses related to Huntington's and Alzheimer's disease.[17]

GPC has also been called a growth hormone sensitizer, which basically means
that it has the ability to potentiate the effects of growth hormone
releasing hormone (GHRH) and increase human growth hormone (hGH) secretion,
as one study showed.[18] Researchers wanted to assess what effect GPC would
have on growth hormone secretion, so they administered growth
hormone-releasing hormone (GHRH) to young and old human volunteers, either
in combination with GPC or exclusively. Results revealed a greater growth
hormone response to the GHRH plus GPC than to GHRH alone, and the effect was
more pronounced in elderly subjects.

Moreover, other researchers have been able to show that GPC treatment may
increase the expression of nerve growth factor receptors in the rat
cerebellar cortex. Nerve growth factor is important for regulating the
growth and maturation process of cholinergic neurons in the central nervous
system, as well as their repair, survival and regeneration. Unfortunately,
the receptors for these vital proteins fall prey to the ravages of age,
making them less effective over time at performing their neurprotective
work. However, findings from one study suggest that GPC can undo these
age-related effects, after the daily administration of GPC to rats for six

Other researchers have demonstrated that GPC increases protein kinase C
activity after just one hour following oral administration. And in vitro,
GPC promoted protein kinase C translocation in cortical slices from rats at
GPC also increases the release of the neurotransmitter dopamine, a chemical
messenger in the brain that regulates emotions, sensation of pain and
pleasure and physical movement. This may be useful in the treatment of
Parkinson's disease, which has been found to involve an imbalance between
dopaminergic and cholinergic transmission. In Parkinson's disease,
dopamine-transmitting neurons die. That's why patients are given L-DOPA, a
drug that produces dopamine in the brain as a replacement for endogenous
dopamine. If GPC can perform a similar task, it may become another way to
ameliorate Parkinson's.[21]

Safety profile
At a glance, GPC seems to have much to offer the aging brain by increasing
the bioavailability of choline, restoring the number of acetylcholine
receptors and decreasing progressive cell membrane stiffness that occurs
with cognitive aging. But as anyone knows, the most effective drug therapy
in the world won't work if patients do not, or cannot, take it.

GPC has been shown in numerous human studies to have high tolerability and
safety. In one study, side effects, such as heartburn, nausea-vomiting,
insomnia-excitation and headache were reported by just 2% (44) of patients,
and only four patients dropped out of the study due to unwanted effects. The
authors conclude that, "The trial confirms the therapeutic role of GPC on
the cognitive recovery of patients with acute stroke or TIA, and the low
percentage of adverse events confirms its excellent tolerability."[22]

An open clinical trial was carried out to compare the efficacy and the
tolerability of 1 gram/day GPC with 1 gram/day CDP-choline, both given
intramuscularly for 90 days in 120 patients with mild to moderate vascular
dementia. Besides reporting good symptomatic relief and tolerability with
both treatments, results suggested GPC tested more highly on both accounts,
according to clinical measurements and patients reports, compared with
CDP-choline.[23] Other studies have echoed the same kind of positive

Given the growing evidence that suggests glycerylphosphorylcholine's (GPC)
usefulness in preventing and treating many conditions that tax our mental
faculties, coupled with a vote for its safety and tolerability, it would not
be surprising to see this neuroceutical gaining more ground in
neuropsychiatry circles and popularity among people who want to preserve
their brain power for as long as possible.

1. Parnetti L, et al. Choline alphoscerate in cognitive decline and in acute
cerebrovascular disease: an analysis of published clinical data. Mech Ageing
Dev 2001 Nov;122(16):2041-55.
2. Ricci A et al. Oral choline alfoscerate counteracts age-dependent loss of
mossy fibres in the rat hippocampus. Mech Ageing Dev 1992;66(1):81-91.
3. Amenta F, et al. Long term choline alfoscerate treatment counters
age-dependent microanatomical changes in rat brain. Prog
Neuropsychopharmacol Biol Psychiatry 1994 Sep;18(5):915-24.
4. Amenta F, et al. Cholinergic neurotransmission in the hippocampus of aged
rats: influence of l-alpha-glycerylphosphorylcholine treatment. Ann N Y Acad
Sci 1993 Sep 24;695:311-3.
5. Amenta F, et al. Muscarinic cholinergic receptors in the hippocampus of
aged rats: influence of choline alphoscerate treatment. Mech Ageing Dev 1994
Oct 1;76(1):49-64.
6. Muccioli G, et al. Effect of l-alpha glycerylphosphorylcholine on
muscarinic receptors and membrane microviscosity of aged rat brain. Prog
Neuropsychopharmacol Biol Psychiatry 1996 Feb;20(2):323-39.
7. Whitehouse PJ, et al. Alzheimer's disease and senile dementia: loss of
neurons in the basal forebrain. Science 1982 Mar 5;215(4537):1237-9.
8. Amenta F, et al.Treatment of cognitive dysfunction associated with
Alzheimer's disease with cholinergic precursors. Ineffective treatments or
inappropriate approaches? Mech Ageing Dev 2001 Nov;122(16):2025-40.
9. Parnetti L et al. Multicentre study of l-alpha-glycerylphosphorylcholine
vs ST200 among patients with probable senile dementia of Alzheimer's type.
Drugs Aging 1993 Mar-Apr;3(2):159-64.
10. Barbagallo Sangiorgi G, et al. Alpha-glycerophosphocholine in the mental
recovery of cerebral ischemic attacks. An Italian multicenter clinical
trial. Ann N Y Acad Sci 1994 Jun 30;717:253-69.
11. Drago F, et al. Behavioral effects of l-alpha-glycerylphosphorylcholine:
influence on cognitive mechanisms in the rat. Pharmacol Biochem Behav 1992
12. Lopez CM, et al. Effect of a new cognition enhancer,
alpha-glycerylphosphorylcholine, on scopolamine-induced amnesia and brain
acetylcholine. Pharmacol Biochem Behav 1991 Aug;39(4):835-40.
13. Sigala S, et al. L-alpha-glycerylphosphorylcholine antagonizes
scopolamine-induced amnesia and enhances hippocampal cholinergic
transmission in the rat. Eur J Pharmacol 1992 Feb 18;211(3):351-8.
14. Gatti G, et al. A comparative study of free plasma choline levels
following intramuscular administration of L-alpha-glycerylphosphorylcholine
and citicoline in normal volunteers. Int J Clin Pharmacol Ther Toxicol 1992
15. Aleppo G, et al. Chronic l-alpha-glycerylphosphoryl-choline increases
inositol phosphate formation in brain slices and neuronal cultures.
Pharmacol Toxicol 1994 Feb;74(2):95-100.
16. Ferraro L, et al. Evidence for an in vivo and in vitro modulation of
endogenous cortical GABA release by alpha-glycerylphosphorylcholine.
Neurochem Res 1996 May;21(5):547-52.
17. Cummings JL, et al. Neurobiological basis of behavior. In: Coffey CE,
Cummings JL, eds. Textbook of Geriatric Neuropsychiatry. American
Psychiatric Press;1994:72-96.
18. Ceda GP, et al. Alpha-glycerylphosphorylcholine administration increases
the GH responses to GHRH of young and elderly subjects. Horm Metab Res 1992
19. Vega JA et al. Nerve growth factor receptor immunoreactivity in the
cerebellar cortex of aged rats: effect of choline alfoscerate treatment.
Mech Ageing Dev 1993 Jun;69(1-2):119-27.
20. Govoni S, et al. PKC translocation in rat brain cortex is promoted in
vivo and in vitro by alpha-glycerylphosphorylcholine, a cognition-enhancing
drug. Ann N Y Acad Sci 1993 Sep 24;695:307-10.
21. Trabucchi M, et al. Changes in the interaction between CNS cholinergic
and dopaminergic neurons induced by l-alpha-glycerylphosphorylcholine, a
cholinomimetic drug. Farmaco [Sci] 1986 Apr;41(4):325-34.
22. Barbagallo Sangiorgi G, et al. Alpha-glycerophosphocholine in the mental
recovery of cerebral ischemic attacks. An Italian multicenter clinical
trial. Ann N Y Acad Sci 1994 Jun 30;717:253-69.
23. Di Perri R, et al. A multicentre trial to evaluate the efficacy and
tolerability of alpha-glycerylphosphorylcholine versus cytosine
diphosphocholine in patients with vascular dementia. J Int Med Res 1991

Article From www.lef.org
As far as the Aniracetam is concerned, I am currently taking two 750mg tabs a day. At that rate it's only costing me about $100/month.

The reason I choose Aniracetam over Oxiracetam is because I read somewhere that Piracetam & Oxiracetam are both water soluble molecules but Pramiracetam & Aniracetam are fat soluble molecules. Generally, the fat soluble nootropics have a longer half-life in the brain so you don't have to take them as often.

Piracetam, Oxiracetam, Pramiracetam, and Aniracetam can all be procured at http://www.antiaging-systems.com

CDP-Choline can be acquired at **broken link removed**

BrooklynJuice: where do you get GPC?

Maybe with a little pharmacological help we can all debunk the MuscleHead stereotype.
You are right in regards to the fat solubles having a longer half life. But thats the reason I like Piracetam. Its one of the earlier "cetams." It is well researched and very safe. And after 2 or days on attack dose all I need is one AM dose of 2400mg. The last thing I need is a brain overflowing with thoughts before bed, as Im a boarderline insominiac (BTW high dosing Taurine as been knocking me out).

As for sherwyns, they are a rip-off. Yes its not and easy domestic source but their prices are a joke.

As for GPC sources I'll be back with several sourcing....
Good thread guys

I think very clearly about math, statistics, economics - but can't remember shit about everyday things. I guess I'm just a burnout, but its starting to hold me back. Plus, I can't find my way around (I'm only 35).

I feel a decent little brain boost from 5-HTP and DL phenylaline (probably spelled that wrong hahahaha) but I'd really love to try cheap high-quality piracetam. - CH
Leave it to Brooklyn to just jump in and stir the water. Seems very interesting, but I can't remember what we were talking about so I'll stop my response there LOL

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