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#1 Kylixer

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Posted 30 June 2003 - 12:46 AM

I've done a lot of research on nootropics, and think I am finally ready to delve into buying/experimenting with some stacks...

I'm going to check out the most popular it would seem first, UCB Nootropil (Piracetam), coupled with Choline. I will try out a does of Piracetam around 2400 mg (upping if I don't notice much of an effect, or tapering down to a 'maintenence dose), coupled with at least 1000 mg Choline.

I am then goin to add in Intelectol (Vinpocetine), starting with a dose of 30 to 40 mg, then following with a maintenence dosing of 10 to 15 mg a day.

I will also purchase Hydergine (Ergoloid Mesylates), experimenting probably in a varied dosing schedule (one night, see how I like it, take it from there), of 4.5 mg. This will be coupled with Piracetam and Choline first, then maybe adding in the Vinpocetine.


Oh yeah, at the time, I am also doing what was coined as the "Anarchy Stack," consisting of 3-5 mg of Acetyle-L-Carnitine, 600-900 mg of R-ALA, 5000-10000 mcg of boitin, 12-15 mg of 70% CLA, and about a gallon of Green Tea a day (soon to be extract pills when they come).

Nootropics have ALWAYS intrigued me, and I finally have some money, and what seems like some reliable sources to play around with, so I'm going to be giving it a go.

I would seriously appreciate ANY feedback / suggestions / comments on these dosing schedules and nootropic pics.

Many thanks friends

#2 shpongled

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Posted 30 June 2003 - 03:43 AM

For piracetam, 2400 mg should definitely be plenty, if taken with choline. Your schedule looks good, especially considering that we already know from studies that piracetam + hydergine is synergistic. Looks like you've thought this out well. What form of choline will you be taking?
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#3 nightop

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Posted 30 June 2003 - 03:57 AM

This reminded me... someone posted this link on the CEM board a few days back, its a nootropic forum which might be of useful (can't vouch for it directly though) = http://www.imminst.o....php?act=SF&f=6
READ MIND & MUSCLE ARTICLES FROM PAST ISSUES.

#4 shpongled

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Posted 30 June 2003 - 03:10 PM

QUOTE(nightop @ Jun 30 2003, 12:57 AM)
This reminded me... someone posted this link on the CEM board a few days back, its a nootropic forum which might be of useful (can't vouch for it directly though) = http://www.imminst.o....php?act=SF&f=6

I have not found that place very useful at all, except for finding sources.
-David Tolson
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#5 nightop

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Posted 30 June 2003 - 03:17 PM

QUOTE(shpongled @ Jun 30 2003, 02:10 PM)
QUOTE(nightop @ Jun 30 2003, 12:57 AM)
This reminded me... someone posted this link on the CEM board a few days back, its a nootropic forum which might be of useful (can't vouch for it directly though) = http://www.imminst.o....php?act=SF&f=6

I have not found that place very useful at all, except for finding sources.

As I just posted in another thead, it is primarily useful as you said for the source list/info, but for someone like me who doesn't have much nootropic experience there is some basic info.
READ MIND & MUSCLE ARTICLES FROM PAST ISSUES.

#6 ergoman500

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Posted 02 July 2003 - 07:48 AM

QUOTE(Kylixer @ Jun 30 2003, 12:46 AM)
I've done a lot of research on nootropics, and think I am finally ready to delve into buying/experimenting with some stacks...

I'm going to check out the most popular it would seem first, UCB Nootropil (Piracetam), coupled with Choline.  I will try out a does of Piracetam around 2400 mg (upping if I don't notice much of an effect, or tapering down to a 'maintenence dose), coupled with at least 1000 mg Choline. 

I am then goin to add in Intelectol (Vinpocetine), starting with a dose of 30 to 40 mg, then following with a maintenence dosing of 10 to 15 mg a day.

I will also purchase Hydergine (Ergoloid Mesylates), experimenting probably in a varied dosing schedule (one night, see how I like it, take it from there), of 4.5 mg.  This will be coupled with Piracetam and Choline first, then maybe adding in the Vinpocetine.


Oh yeah, at the time, I am also doing what was coined as the "Anarchy Stack," consisting of 3-5 mg of Acetyle-L-Carnitine, 600-900 mg of R-ALA, 5000-10000 mcg of boitin, 12-15 mg of 70% CLA, and about a gallon of Green Tea a day (soon to be extract pills when they come).

Nootropics have ALWAYS intrigued me, and I finally have some money, and what seems like some reliable sources to play around with, so I'm going to be giving it a go.

I would seriously appreciate ANY feedback / suggestions / comments on these dosing schedules and nootropic pics.

Many thanks friends

In healthy people, short-term memory loss is likely to be related to decreased acetylcholine-activity. Since GPC supplementation can raise acetylcholine levels in the brain, researchers reason that we might be able to reverse some mental deficits and brain function alterations.

Benefits of acetylcholine precursor compounds such as lecithin and choline have not been consistently repeated unfortunately. Choline we know is also an important constituent for phosphatidylcholine.

An example of the body's amazing adaptability is that the body can sometimes makeup for acetylcholine deficits by plundering existing phosphatidylcholine for conversion to acetylcholine. However, the result of this process is decreased cell membrane integrity via depleted phosphatidylcholine stores.

Since choline and lecithin do not significantly inhibit cognitive decline, researchers are studying and focusing more so on GPC.

Several clinical trials have investigated the efficacy and safety of GPC in animal models and in humans. These studies have without exception - demonstrated beneficial results and an excellent safety/ tolerability profile.

Many studies have focused on: changes in learning, memory and brain structure in rats, stroke-induced cognitive deficits in humans, and also induced/restored - memory function decreases in animals.

When GPC has been directly compared to oxiracetam and acetyl-L-carnitine, cognitive improvement scores among GPC are usually similar to those seen in patients taking oxiracetam. GPC versus acetyl-L-carnitine research, demonstrates that GPC also provides similar, if not superior cognitive improvements.

If you meant to say "3-5grams of Acetyl-l-carnitine", IMO that amount is extremely unnecessary and will likely produce the common side-effects associated with this supplement. Did you also mean to say 12-15 GRAMS/DAY of "70% CLA" ? Im curious what results you have noticed if you have been using the CLA and ALCAR in those doses.
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#7 ergoman500

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Posted 02 July 2003 - 09:55 AM

On a variety of scales designed to assess the progression of Alzheimer's disease, GPC-treated patients score more favorably than patients from the control/placebo groups.

GPC has been shown to actually be superior to Reminyl (galantamine hydrochloride) in the treatment of AD patients, and also with fewer side effects.

The most common complaints among GPC users include: mild constipation/nervousness and dizziness which occur in less than 8% of GPC users long-term. I do not believe that brain physiology/cognition is a perfectly clear and simple biochemical process. Numerous complex interrelated processes are associated to mental/cognitive health and decline.

GPC also stimulates release of GABA, raising the amount available for use by the brain.

ALCAR we know plays a key role in memory, attention and also sleep physiology. Adequate acetylcholine balance is VITAL for healthy/refreshing sleep. Acetylcholine also is important for humans to be able to screen out distractions while concentrating on a task, while also allowing one to ignore disrupting sounds when sleeping. Insomnia often becomes severe in advanced Alzheimer's disease.

Rats that received GPC for six months experienced increased expression of nerve growth factor receptors in the cerebellar cortex. Nerve growth factor is crucial to the regulation of acetylcholine receptor function. It influences receptor growth and maturation and is involved in receptor repair, maintenance and regeneration. NGF-receptors are known to deteriorate with advancing age. GPC - in the rat model, at least - appears to further reverse this deterioration.

GPC supplements also cost around 75% LESS than the acetylcholinesterase inhibitors Aricept and Exelon do.

Moreno M et al. Cognitive impairment in mild to moderate Alzheimer's dementia after treatment with the acetylcholine precursor choline alphoscerate: a multi-center, double-blind, randomized, placebo-controlled trial. Clin Therap 2001; Oct: 178 193.

Hofman A et al. The prevalence of dementia in Europe: a collaborative study of 1980-1990 findings. Int J Epidemiol 1991; 20: 736-748.

Zhang M et al. The prevalence of dementia and Alzheimer's disease in Shangai, China: impact of age, gender and education. Ann Neurol 1990; 27: 428-437.

Bartus RT et al. The cholinergic hypothesis of geriatric memory dysfunction. Science 1982; 217: 408-414.

Etienne P et al. Alzheimer's disease: lack of effect of lecithin treatment for 3 months. Neurology 1981; 31: 1552-1554.

Pomara N et al. Failure of single-dose lecithin to alter aspects of central cholinergic activity in Alzheimer's disease. J Clin Psych 1983; 44: 293-295.

Smith RC et al. Comparison of therapeutic response to long-term treatment with lecithin versus piracetam plus lecithin in patients with Alzheimer's disease. Psychopharmacol Bul 1984; 20: 542-545.

Thal LJ et al. Choline chloride fails to improve cognition of Alzheimer's disease. Neurobiol Aging 1981; 2: 205-258.

Barbagallo SG et al. Glycerylphosphorylcholine in the mental recovery of cerebral ischemic attacks. An Italian multi-center clinical trial. Ann N Y Acad Sci
1994; 717: 253-269.

Ricci et al. Oral choline alphoscerate counteracts age-dependent loss of mossy fibers in the rat hippocampus. Mech Ageing Dev 1992; 66 (1): 88-91.

Amenta F et al. Cholinergic neurotransmission in the hippocampus of aged rats: influence of alpha-L-glycerylphosphorylcholine treatment. Ann N Y Acad Sci 1993Sept: 24: 695: 311-313.

Zaudig M. Mild cognitive impairment in the elderly. Curr Opin Psychiatry 2002; 15: 387-393.

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): 547-552.

Ceda GP et al. Alpha-glycerylphosphorylcholine administration increases the GH responses to GHRH in young and elderly subjects. Horm Metab Res 1992 Mar; 24(3): 119-121.

Vega JA et al. Nerve growth factor receptor immunoreactivity in the cerebellar cortex of aged rats: effect of choline alphoscerate treatment. Mech Ageing Dev 1993 Jun;69(1-2): 119-127.

Govoni S et al. PKC translocation in vivo and in vitro by alpha-glycerylphosphorylcholine, a cognition-enhancing drug. Ann N Y Acad Sci 1993 Sep; 24; 695: 307-310.
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#8 shpongled

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Posted 03 July 2003 - 12:41 AM

QUOTE(ergoman500 @ Jul 2 2003, 04:48 AM)
If you meant to say "3-5grams of Acetyl-l-carnitine", IMO that amount is extremely unnecessary and will likely produce the common side-effects associated with this supplement.

What side effects do you refer to?

Can you back up this statement?
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#9 shpongled

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Posted 03 July 2003 - 12:48 AM

QUOTE(ergoman500 @ Jul 2 2003, 06:55 AM)
GPC supplements also cost around 75% LESS than the acetylcholinesterase inhibitors Aricept and Exelon do.

That's because those are prescription drugs.

The naturally occuring AchE inhibitor huperzine A is about 5 times as cheap as AGPC.


Like I said, I think the stack looks good - it will be significantly more effective than Alpha GPC would be. Adding some AGPC in wouldn't hurt but I wouldn't start out too many things at once.
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#10 ergoman500

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Posted 03 July 2003 - 01:50 AM

QUOTE(shpongled @ Jul 3 2003, 12:41 AM)
QUOTE(ergoman500 @ Jul 2 2003, 04:48 AM)
If you meant to say "3-5grams of Acetyl-l-carnitine", IMO that amount is extremely unnecessary and will likely produce the common side-effects associated with this supplement.

What side effects do you refer to?

Can you back up this statement?

Huperzine A has been nonprescription and easily available OTC in the USA for several years. I mentioned the 2 drugs precisely because they are prescription drugs. Huperzine A and GPC have many contrasting effects and very little in common witheachother when it comes to their biochemical effects in humans.


When I post research/data/info, it is because it already has been substantiated and "backed up" by scientific data/experimentation.

So the answer is yes...

The side-effects of 3 grams + per day of ALC are "backed up" and well known as I stated... Huperzine A has been nonprescription and easily available OTC in the USA for several years.

I mentioned the 2 drugs precisely because they are prescription drugs. Huperzine A and GPC have many contrasting effects and very little in common with eachother when it comes to their biochemical effects in humans.
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#11 ergoman500

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Posted 03 July 2003 - 02:42 AM

Donepezil produces poor to modest improvements in cognitive function.
Common adverse effects include: nausea, vomiting, diarrhea, and anorexia. (Birks et al. 2000b).

Tacrine (Cognex) is another acetylcholinesterase inhibitor with many liver-toxic effects. 75% of patients receive NO benefits from this medication on average. (Birks et al. 2000b).


Rivastigmine is an acetylcholinesterase inhibitor that has been found to be as effective as donepezil with similar side effects. (Birks et al. 2000a; Wettstein 2000).

Thomas (2000) -- suggested that stimulation of nitric oxide production could be central to the action of Selegilene. Deprenyl stimulates vasodilation and increases nitric oxide production in brain tissue and cerebral blood vessels. Because nitric oxide modulates activities including cerebral blood flow and memory, and reduced nitric oxide production has been observed in brains affected by Alzheimer's disease, stimulation of nitric oxide production by deprenyl could contribute to the enhancement of cognitive function in Alzheimer's disease. Studies in rats show that the combination of selegilene with tacrine was remarkedly more effective than either agent alone (Dringenberg et al. 2000).

Nicotine causes acetylcholine transmitter release and, therefore, is theoretically of benefit in Alzheimer's disease with its decrease in acetylcholine levels. Some studies have shown a reduced incidence of Alzheimer's disease among light smokers (fewer than 10 cigarettes per day), but an increased incidence of the disease among heavy smokers (more than 20 cigarettes per day). A pilot study with six patients using nicotine patches showed some improvement in a learning task, but no effect on global cognition or short-term memory. The scientific studies, however, are not conclusive (Lopez-Arrieta et al. 2001).


Hydergine (ergoloid mesylates) is used in Europe for Alzheimer's disease and other forms of dementia. It acts as a mild vasodilator. A meta-analysis of studies using Hydergine showed modest improvement for Alzheimer's symptoms, but only in dosages of 4-9 mg a day, rather than the typical dose of 3 mg a day. Hydergine increased the number of neuronal synapses and the plasticity of synaptic junctions in a rat study. However, when the dose is translated to human equivalents, about 2000 mg a day would be required and has never been used in humans (Bertoni-Freddari et al. 1987).

Hydergine decreases hypoxia in the early stages of Alzheimer's disease but not in the late stages. In a PET scan analysis in multi-infarct dementia (not Alzheimer's patients) and at a dose of 2.4 mg a day, Hydergine showed an improvement on the PET scans (Nagasawa et al. 1990).

A meta-analysis of the published research on hydergine found significant treatment effects in 13 of the trials that met the selection criteria. The overall review was very positive despite the small number of trials (Olin et al. 2000).
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#12 ergoman500

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Posted 03 July 2003 - 02:48 AM

QUOTE(ergoman500 @ Jul 3 2003, 02:42 AM)
Donepezil produces poor to modest improvements in cognitive function.
Common adverse effects include: nausea, vomiting, diarrhea, and anorexia. (Birks et al. 2000b).

Tacrine (Cognex) is another acetylcholinesterase inhibitor with many liver-toxic effects. 75% of patients receive NO benefits from this medication on average. (Birks et al. 2000b).


Rivastigmine is an acetylcholinesterase inhibitor that has been found to be as effective as donepezil with similar side effects. (Birks et al. 2000a; Wettstein 2000).

Thomas (2000) -- suggested that stimulation of nitric oxide production could be central to the action of Selegilene. Deprenyl stimulates vasodilation and increases nitric oxide production in brain tissue and cerebral blood vessels. Because nitric oxide modulates activities including cerebral blood flow and memory, and reduced nitric oxide production has been observed in brains affected by Alzheimer's disease, stimulation of nitric oxide production by deprenyl could contribute to the enhancement of cognitive function in Alzheimer's disease. Studies in rats show that the combination of selegilene with tacrine was remarkedly more effective than either agent alone (Dringenberg et al. 2000).

Nicotine causes acetylcholine transmitter release and, therefore, is theoretically of benefit in Alzheimer's disease with its decrease in acetylcholine levels. Some studies have shown a reduced incidence of Alzheimer's disease among light smokers (fewer than 10 cigarettes per day), but an increased incidence of the disease among heavy smokers (more than 20 cigarettes per day). A pilot study with six patients using nicotine patches showed some improvement in a learning task, but no effect on global cognition or short-term memory. The scientific studies, however, are not conclusive (Lopez-Arrieta et al. 2001).


Hydergine (ergoloid mesylates) is used in Europe for Alzheimer's disease and other forms of dementia. It acts as a mild vasodilator. A meta-analysis of studies using Hydergine showed modest improvement for Alzheimer's symptoms, but only in dosages of 4-9 mg a day, rather than the typical dose of 3 mg a day. Hydergine increased the number of neuronal synapses and the plasticity of synaptic junctions in a rat study. However, when the dose is translated to human equivalents, about 2000 mg a day would be required and has never been used in humans (Bertoni-Freddari et al. 1987).

Hydergine decreases hypoxia in the early stages of Alzheimer's disease but not in the late stages. In a PET scan analysis in multi-infarct dementia (not Alzheimer's patients) and at a dose of 2.4 mg a day, Hydergine showed an improvement on the PET scans (Nagasawa et al. 1990).

A meta-analysis of the published research on hydergine found significant treatment effects in 13 of the trials that met the selection criteria. The overall review was very positive despite the small number of trials (Olin et al. 2000).

Acetyl-L-carnitine can correct acetylcholine deficits and has been tried in rodents (Butterworth 2000). Double-blind studies have been done and have shown some benefit (Pettegrew et al. 2000). Acetyl-L-carnitine was shown to protect neurons from the detrimental effects of beta-amyloid in the cortex of rats (Virmani et al. 2001).

In humans, a one-year controlled trial in early Alzheimer's disease measured ADAS-Cog and the Clinical Dementia Rating Scale in 229 patients. Acetyl-L-carnitine use slowed the clinical deterioration. (Thal et al. 2000).
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#13 shpongled

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Posted 03 July 2003 - 03:10 AM

Schizophrenia is a common mental illness with an incidence of 15 new cases per 100,000 population per year (Kelly et al. 2003). Schizophrenia is characterized by thought disorder, the diminished ability to think clearly and logically. "Often it is manifested by disconnected and nonsensical language that renders the person with schizophrenia incapable of participating in conversation, contributing to his alienation from his family, friends, and society."

Piracetam, a cyclic GABA derivative may be useful in the treatment of schizophrenia (Noorbala 99). Kabes et al. (1979) observed that piracetam significantly increases ATP levels in the brain.

Vitamin D supplements are especially useful for those on a vegetarian diet (Messina 03).


Soares-Weiser KV, Joy C. Miscellaneous treatments for neuroleptic-induced tardive dyskinesia (Cochrane Review). Cochrane Database Syst Rev. 2003;(2):CD000208

Tang WK, Ungvari GS, Leung HC. Effect of piracetam on ECT-induced cognitive disturbances: a randomized, placebo-controlled, double-blind study. J ECT. 2002 Sep;18(3):130-7

Fehr C, Dahmen N, Klawe C, Eicke M, Szegedi A. Piracetam in the treatment of tardive dyskinesia and akathisia: a case report. J Clin Psychopharmacol. 2001 Apr;21(2):248-9

Moreno M et al. Cognitive impairment in mild to moderate Alzheimer's dementia after treatment with the acetylcholine precursor choline alphoscerate: a multi-center, double-blind, randomized, placebo-controlled trial. Clin Therap 2001; Oct: 178 193.

Hofman A et al. The prevalence of dementia in Europe: a collaborative study of 1980-1990 findings. Int J Epidemiol 1991; 20: 736-748.

Zhang M et al. The prevalence of dementia and Alzheimer's disease in Shangai, China: impact of age, gender and education. Ann Neurol 1990; 27: 428-437.

Bartus RT et al. The cholinergic hypothesis of geriatric memory dysfunction. Science 1982; 217: 408-414.

Etienne P et al. Alzheimer's disease: lack of effect of lecithin treatment for 3 months. Neurology 1981; 31: 1552-1554.

Pomara N et al. Failure of single-dose lecithin to alter aspects of central cholinergic activity in Alzheimer's disease. J Clin Psych 1983; 44: 293-295.

Smith RC et al. Comparison of therapeutic response to long-term treatment with lecithin versus piracetam plus lecithin in patients with Alzheimer's disease. Psychopharmacol Bul 1984; 20: 542-545.

Thal LJ et al. Choline chloride fails to improve cognition of Alzheimer's disease. Neurobiol Aging 1981; 2: 205-258.

Barbagallo SG et al. Glycerylphosphorylcholine in the mental recovery of cerebral ischemic attacks. An Italian multi-center clinical trial. Ann N Y Acad Sci
1994; 717: 253-269.

Ricci et al. Oral choline alphoscerate counteracts age-dependent loss of mossy fibers in the rat hippocampus. Mech Ageing Dev 1992; 66 (1): 88-91.

Amenta F et al. Cholinergic neurotransmission in the hippocampus of aged rats: influence of alpha-L-glycerylphosphorylcholine treatment. Ann N Y Acad Sci 1993Sept: 24: 695: 311-313.

Zaudig M. Mild cognitive impairment in the elderly. Curr Opin Psychiatry 2002; 15: 387-393.

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): 547-552.

Ceda GP et al. Alpha-glycerylphosphorylcholine administration increases the GH responses to GHRH in young and elderly subjects. Horm Metab Res 1992 Mar; 24(3): 119-121.

Vega JA et al. Nerve growth factor receptor immunoreactivity in the cerebellar cortex of aged rats: effect of choline alphoscerate treatment. Mech Ageing Dev 1993 Jun;69(1-2): 119-127.

Govoni S et al. PKC translocation in vivo and in vitro by alpha-glycerylphosphorylcholine, a cognition-enhancing drug. Ann N Y Acad Sci 1993 Sep; 24; 695: 307-310.

Weir MR et al. Depression of vitamin B6 levels due to
theophylline. Ann Allergy 1990;65:5962.

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S, Camara M, Buchmeier A, et al. Double-blind trial
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treatment by the administration of magnesium sulfate. J Lab
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disturbances. The role of adrenal cortical
hormone-sodium-vitamin C. Am J Dig Dis 1947;14:302306.

Asthma with sulfite intolerance in children: A
blocking study with cyanocobalamin. J Allerg Clin Immunol
1992;90:103109.

Johnson JL et al. Molybdenum cofactor deficiency in a
patient previously characterized as deficient in sulfite
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Flatt A, Pearce N, Thomson CD, et al. Reduced selenium in
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1990;45:9599.

Hasselmark L, Malmgren R, Zetterstrom O, Unge G. Selenium
supplementation in intrinsic asthma.
Allerg 1993;48:3036.

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dietary supplementation with fish oil on asthmatic
responses to antigen. Allerg Clin Immunol 1988;81:183

Broughton KS, Johnson CS, Pace BK, et
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Am J Clin Nutr 1997;65:101117.

Dry J, Vincent D. Effect of a fish oil diet on asthma: results of a 1-
year double-blind study. Int Arch Allerg Appl Immunol
1991;95:15657.

Hajjar IM, Grim CE, Kotchen TA. J Clin Hypertens (Greenwich). Dietary calcium lowers the age-related rise in blood pressure in the United States: the NHANES III survey. 2003 Mar-Apr;5(2):122-6

Shi H, Norman AW, Okamura WH, Sen A, Zemel MB. 1alpha,25-dihydroxyvitamin D3 inhibits uncoupling protein 2 expression in human adipocytes. FASEB J. 2002 Nov;16(13):1808-10. Epub 2002 Sep 05

Zemel MB, Shi H, Greer B, Dirienzo D, Zemel PC. Regulation of adiposity by dietary calcium. FASEB J. 2000 Jun;14(9):1132-8

Chan JM, Stampfer MJ, Ma J, Gann PH, Gaziano JM, Giovannucci EL. Dairy products, calcium, and prostate cancer risk in the Physicians' Health Study.Am J Clin Nutr. 2001 Oct;74(4):549-54.

Berndt SI, Carter HB, Landis PK, Tucker KL, Hsieh LJ, Metter EJ, Platz EA; Baltimore Longitudinal Study of Aging. Calcium intake and prostate cancer risk in a long-term aging study: the Baltimore Longitudinal Study of Aging. Urology. 2002 Dec;60(6):1118-23

Papakonstantinou E, Flatt WP, Huth PJ, Harris RB. High dietary calcium reduces body fat content, digestibility of fat, and serum vitamin D in rats. Obes Res. 2003 Mar;11(3):387-94

Shea B, Wells G, Cranney A, Zytaruk N, Robinson V, Griffith L, Ortiz Z, Peterson J, Adachi J, Tugwell P, Guyatt G; Osteoporosis Methodology Group and The Osteoporosis Research Advisory Group. Meta-analyses of therapies for postmenopausal osteoporosis. VII. Meta-analysis of calcium supplementation for the prevention of postmenopausal osteoporosis. Endocr Rev. 2002 Aug;23(4):552-9

McConnell N, Campbell S, Gillanders I, Rolton H, Danesh B. Risk factors for developing renal stones in inflammatory bowel disease. BJU Int. 2002 Jun;89(9):835-41

Barzel US, Massey LK. Excess dietary protein can adversely affect bone. J Nutr. 1998 Jun;128(6):1051-3

Heaney RP. Excess dietary protein may not adversely affect bone. J Nutr. 1998 Jun;128(6):1054-7

Sakhaee K, Bhuket T, Adams-Huet B, Rao DS. Meta-analysis of calcium bioavailability: a comparison of calcium citrate with calcium carbonate. Am J Ther. 1999 Nov;6(6):313-21

Ishitani K, Itakura E, Goto S, Esashi T. Calcium absorption from the ingestion of coral-derived calcium by humans. J Nutr Sci Vitaminol (Tokyo). 1999 Oct;45(5):509-17
-David Tolson
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#14 ergoman500

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Posted 04 July 2003 - 01:18 AM

QUOTE(shpongled @ Jul 3 2003, 12:41 AM)
QUOTE(ergoman500 @ Jul 2 2003, 04:48 AM)
If you meant to say "3-5grams of Acetyl-l-carnitine", IMO that amount is extremely unnecessary and will likely produce the common side-effects associated with this supplement.

What side effects do you refer to?

Can you back up this statement?

Consumption of too much Acetyl-l-Carnitine-- not L-carnitine - (over 3 grams/day) is known to commonly cause symptoms such as: stiff neck, muscle tension headaches, nausea, irritability/anxiety, diarrhea, stomach cramps, vomiting, and insomnia in healthy adults.

GPC aka glyceryl phosphorylcholine is more expensive than CDP-choline, but the published literature indicates that GPC is the superior form of choline to supplement with.
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#15 shpongled

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Posted 04 July 2003 - 03:48 PM

Ergoman, I'm starting to think that comparing A-GPC and citicoline is apples and oranges. Given a specific condition (like Alzheimer's) A-GPC is more beneficial but I would guess that citicoline would be more effective at enhancing phospholipid synthesis while A-GPC is superior in the acetylcholine department.
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#16 shpongled

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Posted 06 July 2003 - 02:25 AM

QUOTE(ergoman500 @ Jul 3 2003, 10:18 PM)
Consumption of too much Acetyl-l-Carnitine-- not L-carnitine - (over 3 grams/day) is known to commonly cause symptoms such as: stiff neck, muscle tension headaches, nausea, irritability/anxiety, diarrhea, stomach cramps, vomiting, and insomnia in healthy adults.

Would really like a source on this. I haven't seen any reports of side effects other than overstimulation which disappears with repeated treatment.
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#17 ergoman500

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Posted 06 July 2003 - 02:56 AM

QUOTE(shpongled @ Jul 4 2003, 03:48 PM)
Ergoman, I'm starting to think that comparing A-GPC and citicoline is apples and oranges. Given a specific condition (like Alzheimer's) A-GPC is more beneficial but I would guess that citicoline would be more effective at enhancing phospholipid synthesis while A-GPC is superior in the acetylcholine department.

Ideally, the most benefits of these 2 would be combined use of lesser amounts of both. This would benefit the brain optimally and with less expensive money-wize. Acetylcholine's benefits/actions rely upon adequate and optimal phospholipid metabolism...
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#18 ergoman500

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Posted 02 August 2003 - 02:32 AM

Testosterone's effects on verbal memory and overall attention etc...

J Clin Endocrinol Metab. 2002 Jul;87(7):3090-6.

Cognitive effects of short-term manipulation of serum sex steroids in healthy young men.

Cherrier MM, Anawalt BD, Herbst KL, Amory JK, Craft S, Matsumoto AM, Bremner WJ.

Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, 1959 NE Pacific, Seattle, WA 98195, USA. cherrier@u.washington.edu

We examined the effects of sex steroids on cognitive functioning by exogenously manipulating circulating T levels in a group of healthy young men. Thirty-two men were randomized to receive 8 wk of treatment including: 1) im T enanthate 100 mg/wk plus daily oral placebo (T); 2) im placebo/wk plus 125 microg daily oral levonorgestrel (LNG); 3) im T enanthate 100 mg/wk plus 125 microg daily oral LNG (T + LNG); 4) im placebo/wk plus daily oral placebo. Cognitive functions were assessed at baseline and twice during treatment. Serum T and E2 levels were significantly increased in the T and T + LNG groups compared with baseline (P < 0.01) and T levels were significantly decreased in the LNG group (P < 0.05). Verbal memory significantly decreased in the LNG group (P < 0.01) and was maintained by coadministration of T in the T + LNG group. Divided attention was unaffected in the LNG group but improved significantly in the T + LNG group. In summary, decreased serum T levels induced by LNG or direct effects of the progestin, LNG, adversely affects verbal memory in normal young men. These results suggest that short-term changes in sex steroid levels have effects on cognitive function in healthy young men.
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#19 methodice

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Posted 02 August 2003 - 01:48 PM

hmmm well ive been having sleeping troubles lately.. maybe im having a bit too much ALCAR...

is is because it is depleting something too much? I usually have it before lunch in one hit, maybe some the in morning too.

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#20 Tatsuo

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Posted 02 August 2003 - 06:23 PM

I take about 1g ALCAR/day and haven't had any trouble sleeping (although I only allow myself 6-7 hrs sleep per night, so I pass OUT as soon as I hit the pillow each night.)
How do you guys dose out 1fast's ALCAR?? It tastes like really, really salty or sweet or something. I've been using the measuring spoon that came with a previous kilosports 1test order. I am assuming that alcar & 1test are approximately the same density, so the alcar should be about 100mg/scoop.

PS I second whomever said not to take selegiline too late at night. Crazy wicked lucid dreams, and I remembered every last one of them!! wait a minute...

#21 Number 5

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Posted 12 August 2003 - 01:44 AM

kylixer,

about 2400 of piracetam tablets per day did very little for me. once i upped the dossage to about 5-6 g / day (this time kilosports piracetam powder) and added homozon (magnesium oxide powder) i noticed real benefits.

i was also using vinpocetine (which i like a lot, even on it's own) and wellbutrin (which is a prescription drug, it's an antidepressant, but my doc prescribed it for ADD symptoms).

anyway, since you are taking lots of other stuff you might not need a higher dose of piracetam, but i'd try the homozon if you have an extra $30 (take it with lemon juice).

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#22 Panzer

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Posted 14 August 2003 - 11:49 PM

Ergoman,
If you were to pick 2 or 3 things for a nootropic stack, what would they be? I'm just curious what you'd personally use.

Thanks

#23 ergoman500

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Posted 15 August 2003 - 02:09 PM

QUOTE(Panzer @ Aug 14 2003, 11:49 PM)
Ergoman,
If you were to pick 2 or 3 things for a nootropic stack, what would they be? I'm just curious what you'd personally use.

Thanks

Hmmm...Thats a tough question to answer as there are so many. I would have to definitely pick Deprenyl, ALCAR, and Piracetam if I had only 3 to decide upon...
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#24 Panzer

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Posted 15 August 2003 - 09:41 PM

QUOTE(ergoman500 @ Aug 15 2003, 11:09 AM)
QUOTE(Panzer @ Aug 14 2003, 11:49 PM)
Ergoman,
If you were to pick 2 or 3 things for a nootropic stack, what would they be? I'm just curious what you'd personally use.

Thanks

Hmmm...Thats a tough question to answer as there are so many. I would have to definitely pick Deprenyl, ALCAR, and Piracetam if I had only 3 to decide upon...

Thanks! So, do you think Ginkgo is useless or overrated? Or is it just that there are much more powerful compounds?

I'm slightly reluctant to add Deprenyl since I'm on an SSRI, although Novick indicated there shouldn't be an issue. I've wondered about Piracetam and Hydergine too. Would those interact with Effexor XR at all?

I'm looking at upping my dose on Effexor yet again. I feel like its effects are leveling off a little and I'm feeling weird the last few days. It's almost as if it's wearing off late in the day and I get that dizzy feeling as though I didn't take it. So, I'm going to pop another 75mg cap at night the next few days to see if that does it. If so, I'll have my doc just increase the dose.

#25 shpongled

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Posted 16 August 2003 - 01:10 AM

QUOTE(Panzer @ Aug 15 2003, 06:41 PM)
QUOTE(ergoman500 @ Aug 15 2003, 11:09 AM)
QUOTE(Panzer @ Aug 14 2003, 11:49 PM)
Ergoman,
If you were to pick 2 or 3 things for a nootropic stack, what would they be? I'm just curious what you'd personally use.

Thanks

Hmmm...Thats a tough question to answer as there are so many. I would have to definitely pick Deprenyl, ALCAR, and Piracetam if I had only 3 to decide upon...

Thanks! So, do you think Ginkgo is useless or overrated? Or is it just that there are much more powerful compounds?

I'm slightly reluctant to add Deprenyl since I'm on an SSRI, although Novick indicated there shouldn't be an issue. I've wondered about Piracetam and Hydergine too. Would those interact with Effexor XR at all?

I'm looking at upping my dose on Effexor yet again. I feel like its effects are leveling off a little and I'm feeling weird the last few days. It's almost as if it's wearing off late in the day and I get that dizzy feeling as though I didn't take it. So, I'm going to pop another 75mg cap at night the next few days to see if that does it. If so, I'll have my doc just increase the dose.

Neither piracetam nor hydergine will interact with effexor in a significant way. The literature indicates that the fluoxetine+deprenyl combination is of primary concern, this may be because fluoxetine is an MAO inhibitor itself. I wouldn't worry about it at 5-10 mg daily.
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#26 ergoman500

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Posted 18 August 2003 - 04:45 PM

QUOTE(Panzer @ Aug 15 2003, 09:41 PM)
QUOTE(ergoman500 @ Aug 15 2003, 11:09 AM)
QUOTE(Panzer @ Aug 14 2003, 11:49 PM)
Ergoman,
If you were to pick 2 or 3 things for a nootropic stack, what would they be? I'm just curious what you'd personally use.

Thanks

Hmmm...Thats a tough question to answer as there are so many. I would have to definitely pick Deprenyl, ALCAR, and Piracetam if I had only 3 to decide upon...

Thanks! So, do you think Ginkgo is useless or overrated? Or is it just that there are much more powerful compounds?

I'm slightly reluctant to add Deprenyl since I'm on an SSRI, although Novick indicated there shouldn't be an issue. I've wondered about Piracetam and Hydergine too. Would those interact with Effexor XR at all?

I'm looking at upping my dose on Effexor yet again. I feel like its effects are leveling off a little and I'm feeling weird the last few days. It's almost as if it's wearing off late in the day and I get that dizzy feeling as though I didn't take it. So, I'm going to pop another 75mg cap at night the next few days to see if that does it. If so, I'll have my doc just increase the dose.

As far as ginkgo biloba, I definitely believe it has its place as a mild nootropic supplement when used along with others synergistically. I do think its "over-rated" as far as benefits for those w/o disease and who are under age 40 however...


Psychopharmacol Bull. 1997;33(4):677-83.

The cognitive, subjective, and physical effects of a ginkgo biloba/panax ginseng combination in healthy volunteers with neurasthenic complaints.

Wesnes KA, Faleni RA, Hefting NR, Hoogsteen G, Houben JJ, Jenkins E, Jonkman JH, Leonard J, Petrini O, van Lier JJ.

Cognitive Drug Research Ltd., Beech Hill, Reading, UK.

We evaluated the effects of a Ginkgo biloba/ginseng combination on cognitive function in this 90-day, double-blind, placebo-controlled, parallel-group study. Sixty-four healthy volunteers (aged 40 to 65 years), selected on the basis of fulfilling the ICD-10 F48.0 criteria for neurasthenia, were assigned randomly to four equal dosing groups, receiving 80, 160, or 320 mg of the combination b.i.d. or placebo. Assessments were performed on the day before dosing, and again at Days 1, 30, and 90 at 1 hour after the morning dose and 1 hour after the afternoon dose. The assessments included the Cognitive Drug Research (CDR) computerized assessment system, the Vienna Determination Unit, cycle ergometry, and various questionnaires. The treatments were well tolerated by all volunteers. On Day 90 at 1 hour post morning dosing, dose-related improvements were seen on the CDR tests, the 320 mg dose being significantly superior to placebo. These effects, however, were reversed 1 hour after the afternoon dose, possibly suggesting that a longer inter-dosing interval would be preferable. The 80-mg dose produced a significant benefit on the ergometry assessment of heart rate at maximum load. There were also several supporting changes from other assessments, including an advantage of 320 mg over placebo on the global score from the Symptom Checklist-90-revised (SCL-90-R) at Day 90.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 9493479 [PubMed - indexed for MEDLINE]
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#27 ergoman500

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Posted 22 August 2003 - 04:21 PM

Good info on how pregnenolone supplements may help improve spatial and overall memory via acetylcholine release...


Brain Res 2000 Jan 3;852(1):173-9

Pregnenolone sulfate increases hippocampal acetylcholine release and spatial recognition.

Darnaudery M, Koehl M, Piazza PV, Le Moal M, Mayo W. Psychobiologie des Comportements Adaptatifs, INSERM U.259, Universite de Bordeaux 2, France.

The pregnenolone sulfate is a neurosteroid with promnesic properties. Recently, a correlation between endogenous levels of pregnenolone sulfate in the hippocampus and performance in a spatial memory task has been reported in aged rats. Cholinergic transmission is known to modulate memory processes and to be altered with age. In the present experiment we investigated the effect of increasing doses of pregnenolone sulfate on hippocampal acetylcholine release. Our results show that intracerebroventricular administrations of this neurosteroid induced a dose-dependent increase in acetylcholine release. Administration of 12 and 48 nmol of pregnenolone sulfate induced a short lasting (20 min) enhancement of acetylcholine output with a maximum around 120% over baseline and the administration of 96 and 192 nmol doses induced a long-lasting (80 min) increase that peaked around 300% over baseline. In a second experiment we have observed that the 12 nmol dose enhanced spatial memory performance, whereas the 192 nmol dose was inefficient. These results are consistent with previous work suggesting that, a modest increase in acetylcholine release facilitates memory processes, while elevation beyond an optimal level is ineffective. Nevertheless, neurosteroids may be of value for reinforcing depressed cholinergic transmission in certain age-related memory disorders.
"What is true is not new and what is new is not necessarily true" -Art Lindsley

#28 Tatsuo

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Posted 31 August 2003 - 09:44 AM

(To everyone) Do you ingest such "nootropic stacks" every day, or as needed? I just purchased piracetam and was curious whether to add to my daily regimen or spare it for when I need to accomplish especially neurally taxing work.

#29 D Sade

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Posted 31 August 2003 - 05:40 PM

QUOTE(Tatsuo @ Aug 31 2003, 07:44 AM)
(To everyone) Do you ingest such "nootropic stacks" every day, or as needed?  I just purchased piracetam and was curious whether to add to my daily regimen or spare it for when I need to accomplish especially neurally taxing work.

They are all different. Piracetam is a definite every day nootropic, and the effects seem to get better with duration. I can definitely notice a difference, though, when I forget a dose.

Some of the others, like Ginkgo and vinpocetine, while I take them daily, they seem to be dose/reaction type (meaning, you can save them for when you definitely need them, if you dont want to do the everyday thing).
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#30 BrooklynJuice

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Posted 31 August 2003 - 08:36 PM

PRAMIRACETAM will soon be available 15 x stronger than piracetam mg per mg
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