questions about piracetam and alpha-gpc Options

[eraser]

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

[eraser]

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

: 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.

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.

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?