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> questions about piracetam and alpha-gpc
eraser
post Jan 09, 2009, 06:01 AM
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hi,

i just ordered some piracetam powder in bulk and i've also ordered some alpha-gpc. i've tried piracetam once before with excellent results, the problem being that they did not last for more than a few weeks. i believe this may have been because i decided to remove alpha-gpc from the regimen and the choline bitartrate that i replaced it with wasn't cutting it. i also may have noticed the alteration before this. i made some dosing changes, tried taking the alpha-gpc again (i may have only done this for a day or two, so perhaps it didn't fully build up within my system) but alas, i couldn't get the same results that i had within the first few weeks, and was almost out of piracetam, so i stopped taking it altogether. i also became somewhat dehydrated and sickly around the time that i stopped taking it, and several days after i noticed some of the initial effects (like influxes of memories flashing triggered by objects or things in my environment, cross-association and visual supplementation that wasn't as present before) but i'm not sure if this sicklyness had to do with the piracetam/alpha-gpc withdrawal or was unrelated. nonetheless, the initial results were so helpful and impressive to me that i've decided to give it another shot.

my main questions are:

1. being 19 years old, do i really know what i'm getting into by taking alpha-gpc on a daily basis? i did not seem to have any negative side effects from taking it, though would it be safe to take on a daily basis? what if i continued it for years, with how much certainty am i not doing harm to myself? would i be best to use a more basic form of a choline precursor?

2. does any sort of tolerance develop with piracetam? how could i attenuate/prevent this?

3. what would the nature of the long term benefits from this treatment be? if my brain was structurally altered by this regimen, could i expect to retain some degree of effect after i stop taking them, say, after six months? are the structures created dependent on the substances i'm adding to my brain's equation, and will they still function once created but without the addition of piracetam/alpha-gpc? (i'm mostly interested in cross-hemispheric communication, here).


thanks in advance,

m
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GodConsciousness
post Jan 09, 2009, 07:00 AM
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Alpha GPC is generally very well tolerated and can be used for extended periods of time. Alpha GPC is also arguably the most powerful of the choline precursors. The debate whether or not permanent brain changes ensue after treatment seems to still be open. However, you should not be experiencing any withdrawal symptoms from the racetams. A true nootropic (such as the racetams) is not addictive and should not lead to withdrawal symptoms.
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eraser
post Jan 09, 2009, 03:20 PM
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thanks for the reply, GodConsciousness. i have another question. would i benefit from adding dmae to my stack? apparently the mechanism of action is poorly understood, and it may actually 'block' choline from entering the brain, while somehow withholding choline that already exists inside of the brain. my understanding here is probably poor. i'm wondering if this could interfere with the alpha-GPC's function or if the two will have a synergistic effect. i don't really want to take an especially high dose of alpha-gpc, and will probably stick to 300 mg/day, which worked well for me before. i'm also considering taking cdp-choline one day and alpha-gpc the next, to avoid development of tolerance. i don't know if this makes sense or not or would be helpful. again, thanks for any replies.
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GodConsciousness
post Jan 16, 2009, 06:02 AM
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DMAE is definitely synergistic with the racetams and alternating with Alpha GPC may not be a bad idea.
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LifeMirage
post Jan 19, 2009, 11:13 PM
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QUOTE(eraser @ Jan 09, 2009, 08:01 AM) *
hi,

i just ordered some piracetam powder in bulk and i've also ordered some alpha-gpc. i've tried piracetam once before with excellent results, the problem being that they did not last for more than a few weeks. i believe this may have been because i decided to remove alpha-gpc from the regimen and the choline bitartrate that i replaced it with wasn't cutting it. i also may have noticed the alteration before this. i made some dosing changes, tried taking the alpha-gpc again (i may have only done this for a day or two, so perhaps it didn't fully build up within my system) but alas, i couldn't get the same results that i had within the first few weeks, and was almost out of piracetam, so i stopped taking it altogether. i also became somewhat dehydrated and sickly around the time that i stopped taking it, and several days after i noticed some of the initial effects (like influxes of memories flashing triggered by objects or things in my environment, cross-association and visual supplementation that wasn't as present before) but i'm not sure if this sicklyness had to do with the piracetam/alpha-gpc withdrawal or was unrelated. nonetheless, the initial results were so helpful and impressive to me that i've decided to give it another shot.

my main questions are:

1. being 19 years old, do i really know what i'm getting into by taking alpha-gpc on a daily basis? i did not seem to have any negative side effects from taking it, though would it be safe to take on a daily basis? what if i continued it for years, with how much certainty am i not doing harm to myself? would i be best to use a more basic form of a choline precursor?

2. does any sort of tolerance develop with piracetam? how could i attenuate/prevent this?

3. what would the nature of the long term benefits from this treatment be? if my brain was structurally altered by this regimen, could i expect to retain some degree of effect after i stop taking them, say, after six months? are the structures created dependent on the substances i'm adding to my brain's equation, and will they still function once created but without the addition of piracetam/alpha-gpc? (i'm mostly interested in cross-hemispheric communication, here).


thanks in advance,

m


0. What are your cognitive goals?
1. I would suggest using it as needed or taking a few day off every week.
2. Tolerance can occur to some degree with most nootropics when taken daily or in higher doses. Taking a few days off each week may be of benefit.
3. Piracetam and Alpha GPC can cause long term changes in brain function. After a period of 6-12 months of use some people notice the effects can last years afterwards.

QUOTE(eraser @ Jan 09, 2009, 05:20 PM) *
thanks for the reply, GodConsciousness. i have another question. would i benefit from adding dmae to my stack? apparently the mechanism of action is poorly understood, and it may actually 'block' choline from entering the brain, while somehow withholding choline that already exists inside of the brain. my understanding here is probably poor. i'm wondering if this could interfere with the alpha-GPC's function or if the two will have a synergistic effect. i don't really want to take an especially high dose of alpha-gpc, and will probably stick to 300 mg/day, which worked well for me before. i'm also considering taking cdp-choline one day and alpha-gpc the next, to avoid development of tolerance. i don't know if this makes sense or not or would be helpful. again, thanks for any replies.


Considering the lack of good human studies on DMAE and it's unknown interactions with Alpha GPC I would avoid it. Cycling between CDP-Choline and Alpha GPC would be a good idea.
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eraser
post Jan 21, 2009, 09:24 PM
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QUOTE(LifeMirage @ Jan 19, 2009, 11:13 PM) *

QUOTE(eraser @ Jan 09, 2009, 08:01 AM) *
hi,

i just ordered some piracetam powder in bulk and i've also ordered some alpha-gpc. i've tried piracetam once before with excellent results, the problem being that they did not last for more than a few weeks. i believe this may have been because i decided to remove alpha-gpc from the regimen and the choline bitartrate that i replaced it with wasn't cutting it. i also may have noticed the alteration before this. i made some dosing changes, tried taking the alpha-gpc again (i may have only done this for a day or two, so perhaps it didn't fully build up within my system) but alas, i couldn't get the same results that i had within the first few weeks, and was almost out of piracetam, so i stopped taking it altogether. i also became somewhat dehydrated and sickly around the time that i stopped taking it, and several days after i noticed some of the initial effects (like influxes of memories flashing triggered by objects or things in my environment, cross-association and visual supplementation that wasn't as present before) but i'm not sure if this sicklyness had to do with the piracetam/alpha-gpc withdrawal or was unrelated. nonetheless, the initial results were so helpful and impressive to me that i've decided to give it another shot.

my main questions are:

1. being 19 years old, do i really know what i'm getting into by taking alpha-gpc on a daily basis? i did not seem to have any negative side effects from taking it, though would it be safe to take on a daily basis? what if i continued it for years, with how much certainty am i not doing harm to myself? would i be best to use a more basic form of a choline precursor?

2. does any sort of tolerance develop with piracetam? how could i attenuate/prevent this?

3. what would the nature of the long term benefits from this treatment be? if my brain was structurally altered by this regimen, could i expect to retain some degree of effect after i stop taking them, say, after six months? are the structures created dependent on the substances i'm adding to my brain's equation, and will they still function once created but without the addition of piracetam/alpha-gpc? (i'm mostly interested in cross-hemispheric communication, here).


thanks in advance,

m


0. What are your cognitive goals?
1. I would suggest using it as needed or taking a few day off every week.
2. Tolerance can occur to some degree with most nootropics when taken daily or in higher doses. Taking a few days off each week may be of benefit.
3. Piracetam and Alpha GPC can cause long term changes in brain function. After a period of 6-12 months of use some people notice the effects can last years afterwards.

QUOTE(eraser @ Jan 09, 2009, 05:20 PM) *
thanks for the reply, GodConsciousness. i have another question. would i benefit from adding dmae to my stack? apparently the mechanism of action is poorly understood, and it may actually 'block' choline from entering the brain, while somehow withholding choline that already exists inside of the brain. my understanding here is probably poor. i'm wondering if this could interfere with the alpha-GPC's function or if the two will have a synergistic effect. i don't really want to take an especially high dose of alpha-gpc, and will probably stick to 300 mg/day, which worked well for me before. i'm also considering taking cdp-choline one day and alpha-gpc the next, to avoid development of tolerance. i don't know if this makes sense or not or would be helpful. again, thanks for any replies.


Considering the lack of good human studies on DMAE and it's unknown interactions with Alpha GPC I would avoid it. Cycling between CDP-Choline and Alpha GPC would be a good idea.



0. my cognitive goals are essentially a treatment for depression and adhd, an increase in my memory/recall, higher mental energy, quicker reading comprehension/retention, enhancing my creativity and imagination, and my associative faculties. when i'm on this stack i also notice that i'm more comfortable around people and that my thought is more fluid/flexible in general. it really levels out my brain chemistry in a perfect way, and it doesn't have any of the hideous downsides that taking adderall does.


lifemirage, because i have something along the lines of adhd, i'm wondering how you might interpret this study on cdp-choline and how it might tie into things for me:

QUOTE
Effects of CDP-choline on striatal dopamine level and behavior in rats.
Shibuya M, Kageyama N, Taniguchi T, Hidaka H, Fujiwara M.

To further assess the effects of CDP (cytidine diphosphate)-choline on Parkinsonian symptoms, striatal dopamine (DA) was measured fluorometrically in rats after injection of CDP-choline. CDP-choline (300 mg/kg, i.p.) increased the DA content in the striatum (p less than 0.05) one hour after injection. The behavioral effect of CDP-choline was then tested in rats in which the unilateral nigro-striatal DA neurons had degenerated following an intranigral injection of 6-hydroxydopamine (6-OHDA). CDP-choline alone did not produce behavioral changes in these rats. However, pretreatment with a single dose of CDP-choline (900 mg/kg, i.p.) suppressed both the apomorphine-induced contralateral and the d-amphetamine-induced ipsilateral circling. The same dose of CDP-choline suppressed the number of treadmill revolutions in mice. On the other hand, a 7-day consecutive treatment with 300 mg/kg of CDP-choline enhanced the apomorphine-induced contralateral circling (by 42%, p less than 0.05). The same treatment with CDP-choline raised the striatal DA content by 29% (p less than 0.05) on the intact side, but not on the 6-OHDA injected side. These results indicate that CDP-choline has either a direct nor an indirect DA agonistic effect. The increase in DA content, decrease in locomotion and enhancement of the effect of apomorphine can be explained on the hypothesis that CDP-choline may act as an antagonist on the DA neurons and receptors. The validity of this apparently paradoxical use of CDP-choline with antagonistic effect on DA neurons in the treatment of Parkinson's disease is discussed.


the supposed simultaneous antagonistic effect on DA neurons and the increase in DA levels has me a little confused. thanks!
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peisistratids
post Jan 22, 2009, 04:08 PM
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QUOTE
Considering the lack of good human studies on DMAE and it's unknown interactions with Alpha GPC I would avoid it. Cycling between CDP-Choline and Alpha GPC would be a good idea.

What about cycling between centrophenoxine and cdp-choline?
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GodConsciousness
post Jan 23, 2009, 07:34 AM
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alpha gpc is generally considered to be superior to cdp choline in bioavailability.
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eraser
post Jan 23, 2009, 08:27 AM
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QUOTE(GodConsciousness @ Jan 23, 2009, 07:34 AM) *

alpha gpc is generally considered to be superior to cdp choline in bioavailability.


ok, sorry for dragging this on and on, but i have one more issue. it seems increasing acetylcholine in general stimulates human growth hormone. now this kind of worries me because i'm under 25. and gah! on the one hand, here i have the regimen thats working perfectly for me, on the other, i have absolutely no idea what long term stimulation of growth hormone might do to me. this is kind of worrying. maybe i'll go for the six-month hopefully-lasting treatment and call it quits. if anyone has any input on what these numbers might mean, or what stimulating HGH to the extent that 'enhancing cholinergic tone' via alpha-gpc/cdp-choline (i've decided to cycle the two, and perhaps take a break on weekends), please let me know as i could use some informed advice on this.

QUOTE
Effects of direct and indirect acetylcholine receptor agonists on growth hormone secretion in humans.

Mazza E, Ghigo E, Boffano G, Valetto M, Maccario M, Arvat E, Bellone J, Procopio M, Müller EE, Camanni F.

Department of Clinical Pathophysiology, University of Turin, Italy.

Cholinergic pathways in the central nervous system positively influence growth hormone (GH) secretion. In fact pyridostigmine, a cholinesterase inhibitor, enhances both basal and GH-releasing hormone (GHRH)-induced GH secretion while, conversely, pirenzepine, an antagonist of muscarinic M1 receptors, inhibits the GH response to GHRH and to other physiological and pharmacological stimuli. The effect of the cholinergic system on GH secretion probably takes place via inhibition of the release of endogenous somatostatin. In this study in 36 normal adults (26 males and 10 females, age 22-35 years) we compared the effects of three cholinesterase inhibitors (pyridostigmine, 120 mg p.o., n = 19; neostigmine, 10 micrograms/kg i.v., n = 6; physostigmine, 12.5 micrograms/kg i.v., n = 6) and bethanechol, a direct muscarinic receptor agonist that is mainly active on muscarinic M3 receptors (25 micrograms/kg i.v., n = 5), on both basal and GHRH (1 microgram/kg i.v.)-stimulated GH secretion. Pyridostigmine, neostigmine and physostigmine induced a significant GH increase (peak vs. basal levels, mean +/- S.E.: 10.4 +/- 1.6 vs. 0.6 +/- 0.2 micrograms/l, P = 0.0001; 13.3 +/- 1.2 vs. 0.5 +/- 1.1 micrograms/l, P = 0.004; and 14.9 +/- 3.1 vs. 2.7 +/- 1.1 micrograms/l, P = 0.025;, respectively). These drugs also induced a similar potentiation of the GH response to GHRH (peak: 48.3 +/- 5.6 vs. 16.2 +/- 2.2 micrograms/l, P = 0.0001; 49.2 +/- 2.2 vs. 19.9 +/- 5.1 micrograms/l, P = 0.006; and 76.9 +/- 12.4 vs. 18.1 +/- 5.3 micrograms/l, P = 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)


QUOTE
Author: Ceda GP, Ceresini G, Denti L, Marzani G, Piovani E, Banchini A, et al
Date: 3/1992
Journal: Horm Metab Res
Chair of Gerontology and Geriatrics, University of Parma, Italy. Growth hormone (GH) secretion is decreased during aging in humans and in rodents. This decrease may be due to increased hypothalamic somatostatin release, which is inhibited by cholinergic agonists, or to decreased secretion of GHRH. Alpha-glyceryl-phosphorylcholine (alpha-GFC) is a putative acetylcholine precursor used in the treatment of cognitive disorders in the elderly. In order to learn what effect alpha-GFC had on GH secretion, GH-release hormone (GHRH) was given to young and old human volunteers, with or without the addition of alpha-GFC. GH secretion was greater in the younger subjects than in the old individuals, and both groups had a greater GH response to the GHRH+alpha-GFC than to GHRH alone. The potentiating effect of alpha-GFC on GH secretion was more pronounced in the elderly subjects. These findings confirm the observation that aged individuals respond less well to GHRH than younger subjects, and provides further evidence that increased cholinergic tone enhances GH release.




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post Jan 23, 2009, 09:17 AM
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QUOTE
Titre du document / Document title
CDP-choline increases plasma ACTH and potentiates the stimulated release of GH, TSH and LH: the cholinergic involvement
Auteur(s) / Author(s)
CAVUN Sinan (1) ; SAVCI Vahide (1) ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Department of Pharmacology and Clinical Pharmacology, Uludag University Medical Faculty, 16059 Bursa, TURQUIE
Résumé / Abstract
In the present study, we investigated the effect of intracerebroventricular (i.c.v.) administration of cytidine-5'-diphosphate (CDP) choline on plasma adrenocorticotropin (ACTH), serum growth hormone (GH), thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels in conscious rats. The involvement of cholinergic mechanisms in these effects was also determined. In basal conditions, CDP-choline (0.5, 1.0 and 2.0 μmnl, i.c.v.) increased plasma ACTH levels dose- and time-dependently, but it did not affect the TSH, GH, FSH and LH levels. In stimulated conditions, i.c.v. administration of CDP-choline (1 μmol, i.c.v.) produced an increase in clonidine-stimulated GH, thyrotyropin-releasing hormone (TRH)-stimulated TSH, LH-releasing hormone (LHRH)-stimulated LH, but not FSH levels. Injection of equimolar dose of choline (1 μmol, i.c.v.) produced similar effects on hormone levels, but cytidine (μmol, i.c.v.) failed to alter plasma levels of these hormones. Pretreatment with hemicholinium-3, a neuronal high affinity choline uptake inhibitor, (20 μg, i.c.v.) completely blocked the observed hormone responses to CDP-choline. The increase in plasma ACTH levels induced by CDP-choline (1 μmol, i.c.v.) was abolished by pretreatment with mecamylamine, a nicotinic receptor antagonist, (50 μg, i.c.v.) but not atropine, a muscarinic receptor antagonist, (10 μg, i.c.v.). The increase in stimulated levels of serum TSH by CDP-choline (1 μmol, i.c.v.) was blocked by atropine but not by mecamylamine pretreatment. However, CDP-choline induced increases in serum GH and LH levels were greatly attenuated by both atropine and mecamylamine pretreatments. The results show that CDP-choline can increase plasma ACTH and produce additional increases in serum levels of TSH, GH and LH stimulated by TRH, clonidine and LHRH, respectively. The activation of central cholinergic system, mainly through the presynaptic mechanisms, was involved in these effects. Central nicotinic receptors solely mediated the increase in plasma ACTH levels while the activation of central muscarinic receptors was involved in the increase in TSH levels. Both muscarinic and nicotinic receptor activations, separately, mediated the increases in serum GH and LH levels after CDP-choline.
Revue / Journal Title
Fundamental & clinical pharmacology ISSN 0767-3981 CODEN FCPHEZ



QUOTE
: Endocrinol Jpn. 1980 Jun;27(3):265-71.
Related Articles, Links

Effect of cytidine diphosphate choline on growth hormone secretion in patients with brain or pituitary lesions.

Salvadorini F, Saba P, Forli C, Tusini G, Galeone F.

Plasma GH levels basally and after CDP-Choline (300 mg) i.v. administration were evaluated by radioimmunoassay in patients with brain lesions variously located (frontal lobe, temporal lobe or hypothalamus) as well as in subjects with pituitary lesions. The results were statistically analyzed and compared with those obtained in normal subjects. A lack of response to CDP-Choline was observed in patients with pituitary adenomas or hypothalamic lesions. The GH response was delayed in patients with frontal lobe diseases. On the basis of the results obtained, we discuss the role of the different central nervous structures on the control of the GH activating system.


QUOTE
Effects of cytidine 5'-diphosphocholine administration on basal and growth hormone-releasing hormone-induced growth hormone secretion in elderly subjects.
Ceda GP, Ceresini G, Denti L, Magnani D, Marchini L, Valenti G, Hoffman AR.

Chair of Gerontology and Geriatrics, University of Parma, Italy.

The basal and GH-releasing hormone-stimulated secretion of GH declines in the elderly. We tested the ability of cytidine 5'-diphosphocholine, a drug used in the treatment of stroke and Parkinson's disease, to alter GH secretion in 11 healthy elderly volunteers, aged 69-84. Each subject received an iv infusion of 2 g of cytidine 5'-diphosphocholine or normal saline. GHRH and TRH were also administered during cytidine 5'-diphosphocholine infusions. The infusion of cytidine 5'-diphosphocholine induced a 4-fold (p less than 0.05) increase in serum GH levels over basal values. A small increase in GH was seen after GHRH administration. However, the addition of GHRH to the cytidine 5'-diphosphocholine infusion resulted in a GH response which was significantly greater than that seen after GHRH alone; the integrated concentration of GH was more than 2-fold greater in the cytidine 5'-diphosphocholine treated group (706.85 +/- 185.1 vs 248.9 +/- 61.4 micrograms.l-1.(120 min)-1; p = 0.01). The PRL and TSH responses to TRH were not significantly affected by cytidine 5'-diphosphocholine infusion, indicating that dopaminergic mechanisms are not involved. These studies demonstrate that cytidine 5'-diphosphocholine can enhance basal and GHRH-stimulated GH release in the elderly, but the mechanism of action of the drug remains unclear.


QUOTE
Effect of cytidine diphosphate choline on growth hormone and prolactin secretion in man.
Matsuoka T, Kawanaka M, Nagai K.

The effect of intravenous infusion of cytidine diphosphate choline (CDP-choline) on the serum levels of growth hormone (GH) and prolactin (PRL) was studied in six normal adult male subjects. Serum GH levels increased and reached a maximum at 60--90 min after the initiation of infusion in all subjects examined. The mean peak value of GH in six subjects was 10.0 +/- 2.1 (mean +/- SE) ng/ml, which was signigicantly higher than the basal level (p less than 0.01). In four subjects, serum PRL levels decreased from 10--24 ng/ml to less than 7.2 ng/ml at 60--120 min, while in the other two no significant change was observed. These results indicate that CDP-choline affects GH and PRL secretion from the anterior pituitary.


conclusion: i don't think that i want to be stimulating my growth hormone release. so i think i am going to have to stop taking acetylcholine precursors or at least use them in moderation. this is a pretty big let down. because i haven't found anything else that works this well for me and covers all of the bases, as this does. i'm also wondering if i have an acetylcholine deficiency or if such a thing exists, and then maybe i'm not really doing all too much harm. i do have a poor memory (mostly verbal/auditory) and you might think that since this seemingly balances everything out so well that it might be correcting an 'imbalance'.

on a side note: are there any other means to facilitate communication between brain hemispheres?
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peisistratids
post Jan 23, 2009, 04:26 PM
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post Jan 23, 2009, 04:30 PM
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QUOTE
on a side note: are there any other means to facilitate communication between brain hemispheres?


master a musical instrument
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GodConsciousness
post Jan 26, 2009, 06:48 AM
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Both CDP choline and Alpha GPC increase GH release. Alpha GPC also increases Nerve Growth Factor.
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post Jan 26, 2009, 10:27 AM
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QUOTE(GodConsciousness @ Jan 26, 2009, 06:48 AM) *

Both CDP choline and Alpha GPC increase GH release. Alpha GPC also increases Nerve Growth Factor.


well, i noticed as much. the problem is whether or not this is safe.
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Nadir
post May 08, 2009, 08:54 AM
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I know this is a few months old, but I'm curious as to whether or not its safe too.
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GodConsciousness
post May 13, 2009, 09:43 AM
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The racetams and choline donors are exceptional in safety and non-addictive.
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LifeMirage
post May 16, 2009, 09:00 AM
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QUOTE(eraser @ Jan 22, 2009, 12:24 AM) *
QUOTE(LifeMirage @ Jan 19, 2009, 11:13 PM) *

QUOTE(eraser @ Jan 09, 2009, 08:01 AM) *
hi,

i just ordered some piracetam powder in bulk and i've also ordered some alpha-gpc. i've tried piracetam once before with excellent results, the problem being that they did not last for more than a few weeks. i believe this may have been because i decided to remove alpha-gpc from the regimen and the choline bitartrate that i replaced it with wasn't cutting it. i also may have noticed the alteration before this. i made some dosing changes, tried taking the alpha-gpc again (i may have only done this for a day or two, so perhaps it didn't fully build up within my system) but alas, i couldn't get the same results that i had within the first few weeks, and was almost out of piracetam, so i stopped taking it altogether. i also became somewhat dehydrated and sickly around the time that i stopped taking it, and several days after i noticed some of the initial effects (like influxes of memories flashing triggered by objects or things in my environment, cross-association and visual supplementation that wasn't as present before) but i'm not sure if this sicklyness had to do with the piracetam/alpha-gpc withdrawal or was unrelated. nonetheless, the initial results were so helpful and impressive to me that i've decided to give it another shot.

my main questions are:

1. being 19 years old, do i really know what i'm getting into by taking alpha-gpc on a daily basis? i did not seem to have any negative side effects from taking it, though would it be safe to take on a daily basis? what if i continued it for years, with how much certainty am i not doing harm to myself? would i be best to use a more basic form of a choline precursor?

2. does any sort of tolerance develop with piracetam? how could i attenuate/prevent this?

3. what would the nature of the long term benefits from this treatment be? if my brain was structurally altered by this regimen, could i expect to retain some degree of effect after i stop taking them, say, after six months? are the structures created dependent on the substances i'm adding to my brain's equation, and will they still function once created but without the addition of piracetam/alpha-gpc? (i'm mostly interested in cross-hemispheric communication, here).


thanks in advance,

m


0. What are your cognitive goals?
1. I would suggest using it as needed or taking a few day off every week.
2. Tolerance can occur to some degree with most nootropics when taken daily or in higher doses. Taking a few days off each week may be of benefit.
3. Piracetam and Alpha GPC can cause long term changes in brain function. After a period of 6-12 months of use some people notice the effects can last years afterwards.

QUOTE(eraser @ Jan 09, 2009, 05:20 PM) *
thanks for the reply, GodConsciousness. i have another question. would i benefit from adding dmae to my stack? apparently the mechanism of action is poorly understood, and it may actually 'block' choline from entering the brain, while somehow withholding choline that already exists inside of the brain. my understanding here is probably poor. i'm wondering if this could interfere with the alpha-GPC's function or if the two will have a synergistic effect. i don't really want to take an especially high dose of alpha-gpc, and will probably stick to 300 mg/day, which worked well for me before. i'm also considering taking cdp-choline one day and alpha-gpc the next, to avoid development of tolerance. i don't know if this makes sense or not or would be helpful. again, thanks for any replies.


Considering the lack of good human studies on DMAE and it's unknown interactions with Alpha GPC I would avoid it. Cycling between CDP-Choline and Alpha GPC would be a good idea.



0. my cognitive goals are essentially a treatment for depression and adhd, an increase in my memory/recall, higher mental energy, quicker reading comprehension/retention, enhancing my creativity and imagination, and my associative faculties. when i'm on this stack i also notice that i'm more comfortable around people and that my thought is more fluid/flexible in general. it really levels out my brain chemistry in a perfect way, and it doesn't have any of the hideous downsides that taking adderall does.


lifemirage, because i have something along the lines of adhd, i'm wondering how you might interpret this study on cdp-choline and how it might tie into things for me:

QUOTE
Effects of CDP-choline on striatal dopamine level and behavior in rats.
Shibuya M, Kageyama N, Taniguchi T, Hidaka H, Fujiwara M.

To further assess the effects of CDP (cytidine diphosphate)-choline on Parkinsonian symptoms, striatal dopamine (DA) was measured fluorometrically in rats after injection of CDP-choline. CDP-choline (300 mg/kg, i.p.) increased the DA content in the striatum (p less than 0.05) one hour after injection. The behavioral effect of CDP-choline was then tested in rats in which the unilateral nigro-striatal DA neurons had degenerated following an intranigral injection of 6-hydroxydopamine (6-OHDA). CDP-choline alone did not produce behavioral changes in these rats. However, pretreatment with a single dose of CDP-choline (900 mg/kg, i.p.) suppressed both the apomorphine-induced contralateral and the d-amphetamine-induced ipsilateral circling. The same dose of CDP-choline suppressed the number of treadmill revolutions in mice. On the other hand, a 7-day consecutive treatment with 300 mg/kg of CDP-choline enhanced the apomorphine-induced contralateral circling (by 42%, p less than 0.05). The same treatment with CDP-choline raised the striatal DA content by 29% (p less than 0.05) on the intact side, but not on the 6-OHDA injected side. These results indicate that CDP-choline has either a direct nor an indirect DA agonistic effect. The increase in DA content, decrease in locomotion and enhancement of the effect of apomorphine can be explained on the hypothesis that CDP-choline may act as an antagonist on the DA neurons and receptors. The validity of this apparently paradoxical use of CDP-choline with antagonistic effect on DA neurons in the treatment of Parkinson's disease is discussed.


the supposed simultaneous antagonistic effect on DA neurons and the increase in DA levels has me a little confused. thanks!


Extrapolating the meaning of this study for humans is difficult for several reasons. However the complexity of 1 compound having multiple and even seemingly counteracting effects is not uncommon. In time human research into oral doses should shed some light on this subject producing more useful data.


QUOTE(peisistratids @ Jan 22, 2009, 07:08 PM) *
QUOTE
Considering the lack of good human studies on DMAE and it's unknown interactions with Alpha GPC I would avoid it. Cycling between CDP-Choline and Alpha GPC would be a good idea.

What about cycling between centrophenoxine and cdp-choline?


For the purpose of determining how it effects you I think it would be interesting and would like to see your experiences doing this.

QUOTE(eraser @ Jan 26, 2009, 01:27 PM) *
QUOTE(GodConsciousness @ Jan 26, 2009, 06:48 AM) *

Both CDP choline and Alpha GPC increase GH release. Alpha GPC also increases Nerve Growth Factor.


well, i noticed as much. the problem is whether or not this is safe.
QUOTE(Nadir @ May 08, 2009, 11:54 AM) *
I know this is a few months old, but I'm curious as to whether or not its safe too.


Both compounds are present in the human diet and our brains to that end research done examining their functions would confirm at some level in our bodies they are not only safe but required for proper functioning. Excessive doses and/or long term doses have not been proven safe, however from the limited research so far I don't see any serious concern from semi regular usage.
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Isochroma
post Aug 16, 2009, 06:45 PM
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Take the Piracetam alone for a few weeks and feel what it's like. Alpha-GPC is an enormously profitable ripoff.
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post Aug 17, 2009, 07:34 AM
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QUOTE(Isochroma @ Aug 16, 2009, 10:45 PM) *

Take the Piracetam alone for a few weeks and feel what it's like. Alpha-GPC is an enormously profitable ripoff.


Iso- Alpha GPC is a bit pricey but quite a few people have found it helpful in augmenting the racetams. There is also solid research in its ability to cross the BBB and increase NGF secretion
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