18 replies to this topic

[quazi]

Hay!

How much huperzine A are you taking? I have capsules 50 mcg and I take only one capsule daily. Is this enought?
I take ginko biloba (40 mg 3 times a day), Gin-chia (ginseng 70 mg + chia 190 mg daily), alpha GPC (500 mg daily), multivitamin, fish oil too.

I was taking piracetam, aniracetam about two months and I felt no effects so I stoped.

[teak]

I think many bottled Hyperzine A products state 50mcg 1-3 times a day (with meals?), so 50-150mcg ED? Though one website claims higher:

http://www.wilkereso.../Huperzine.html

The literature reports that the effective daily dosage of Huperzine A to be in the 200 to 400 microgram range. Most dietary supplement manufacturers are formulating capsules and tablets containing 50 to 100 micrograms.

But they only cite a 5 week human test that such doses showed no statistically significant side effects. Where as I've read long-term doses of 100mcg or more might not be good for you. For example, Ray Sahelian M.D author of Mind Boosters warns:

http://www.raysaheli...huperzinea.html

Continuous use of high doses of huperzine A --such as 100 mcg or more-- may be toxic. Due to its strong anticholinesterase activity, huperzine a could cause a cholinergic reaction. Side effects could include sweating, nausea, vomiting, dizziness, and cramps.

So you might be fine with your current 50mcg ED dose?

Edited by teak, 13 January 2005 - 03:34 PM.

[teak]

Also, while on the subject....

Huperzine A inhibits the acetyl-cholinesterase (AChE) enzyme from breaking down the neurotransmitter acetyl-choline (ACh). Thus keeping acetyl-choline levels high, which is meant to improve (short-term?) memory. However, noticed this article which might suggest not to take acetyl-choline boosting supplements near bedtime. Don't know the half-life of Huperzine A though, so not sure what the cut off time should be before sleep.

http://www.post-gaze...4032/267587.stm

In the new study, Dr. Steffen Gais of the University of Lubeck in Germany tested memory in 29 men given bedtime doses of a drug that keeps acetylcholine levels high. The men were young, aged 18-35, and healthy.

The drug seriously impaired their memories. Men given the drug were less able to remember words learned the previous day than men who took none.

In Alzheimer's patients, brain cells that make acetylcholine have been damaged, resulting in lower levels of the chemical. During the day, drugs like Aricept keep acetylcholine levels high and boost memory.

The Gais' study, however, revealed that the brain needs a temporary drop in acetylcholine during sleep so that it can upload data from a temporary storage depot to another region that holds more permanent memories.

"This study teaches us that although patients may need increased acetylcholine during waking, keeping it constantly elevated may block a certain component of memory consolidation that requires a temporary drop in acetylcholine," Power said.

Both she and Gais said physicians should consider advising Alzheimer's patients to take medicine during the day, rather than at bedtime.

Edited by teak, 13 January 2005 - 03:18 PM.

[dopamine]

Unless you have a physical condition corresponding to very low levels of acetylcholine, I would recomend sticking to the lowest effective dosage of Huperzine A, which is generally within the 50 mcg range.

Also, as discussed prior, acetylcholine esterase inhibitors over time may decrease the density of cholinergic receptors in various brain regions. For otherwise healthy individuals, this could potentially have adverse effects on memory in the post-use phase of the drug. There may also be a similar effect on the density of dopamine and norepinephrine receptors, as HupA has been shown to increase levels of these neurotransmitteres as a result of AchE inhibition.

[stellar]

Is it safe to take Ginko and Huperzine at the same time? Both are vasodilators

[dopamine]

Is it safe to take Ginko and Huperzine at the same time? Both are vasodilators

There is a low probability of the two interacting negatively with each other. Ginkgo biloba is very safe is moderate doses (120 - 160 mg), and it may have a protective synergy with HupA (via NMDA antagonism).

Just throw caution to the wind when combining any more substances which act as vasodialators and/or decrease platlet aggregation. Symptoms of excessive thinning of the blood are generally in the area of feeling lightheaded and faint, as a result of decreased blood pressure.

[ageless]

I love AOR's Ortho Mind which has many of the best mind boosters (ALC, Ginkgo, Huperzine, Vinpocetine, CDP, Bacopa, Pyroglutamic acid and r-lipoic acid) at good doses all in the one pill.
Works for me!

[ageless]

The does of Huperzine-A in Ortho Mind is (from 20 mg Huperzia serrata 0.5%) 100 mcg in 6 capsules which allows one to adjust their daily amount accordingly. 3 caps usually does it for me (50mcg).

[teak]

While this isn't a medical study, since Huperzine A inhibits acetyl-cholinesterase maybe this is partly why long-term and high doses are not recommended for healthly people, though useful for Alzheimers suffers:

http://en.wikipedia....i/Acetylcholine

Normally, the acetylcholine is quickly removed after having performed its action; this is done by the enzyme acetylcholinesterase which converts acetylcholine into choline and acetate. The devastating effects of nerve agents are due to their inhibition of this enzyme, resulting in continuing stimulation of the muscles, glands and central nervous system. Certain insecticides are effective because they inhibit this enzyme in insects. On the other hand, since a shortage of acetylcholine in the brain has been associated with Alzheimer's disease, some drugs that inhibit acetylcholinesterase are used in the treatment of that disease.

http://en.wikipedia....icholinesterase

An anticholinesterase is a chemical that inhibits a cholinesterase enzyme from breaking down acetylcholine, so increasing both the level and duration of action of the neurotransmitter acetylcholine.

Anticholinesterases occur naturally as venoms and poisons, are used as weapons in the form of nerve agents, and are used medicinally to treat diseases such as myasthenia gravis and Alzheimers disease, and as an antidote to anticholinergic poisoning. In myasthenia gravis, they are used to increase neuromuscular transmission.

http://en.wikipedia....lcholinesterase

A cholinesterase inhibitor is known as an anticholinesterase. Because of its essential function, chemicals that interfere with the action of cholinesterase are potent neurotoxins, causing excessive salivation and eye watering in low doses, followed by muscle spasms and ultimately death. Outside of biochemical warfare, anticholinesterases are used are also used in anesthesia or in the treatment of myasthenia gravis, glaucoma and Alzheimer's disease.

http://en.wikipedia....rase_inhibitors

Acetylcholinesterase (AChE) inhibition was thought to be important because there is selective loss of forebrain cholinergic neurons as a result of Alzheimer's. AChE-inhibitors reduce the rate at which acetylcholine (ACh) is broken down and hence increase the concentration of ACh in the brain (combatting the loss of ACh caused by the death of the cholinergin neurons). Acetylcholinesterase-inhibitors seem to treat symptoms but do not prevent disease progression including cell death.

Edited by teak, 02 January 2006 - 09:59 PM.

[dopamine]

since Huperzine A inhibits acetyl-cholinesterase maybe this is partly why long-term and high doses are not recommended for healthly people, though useful for Alzheimers suffers:

Certainly this is the idea. Receptor downregulation is a well known compensatory mechanism by which the brain adapts to enviroments high in specific neurotransmitters. This is of little concern when treating someone with an illness which manifests a greater density of receptors as a compensatory response to low levels of post-synaptic stimulation, since the drug-induced increase in these levels will (theoretically) normalize the proportion between receptor density and levels of the neurotransmitter.

Acetylcholine esterase inhibitors are starting to have a greater application in other areas besides alzheimers disease, however. Since increasing cholinergic neurotransmission in various regions of the brain can result in increases of various catecholamines (dopamine, epinephrine, norepinephrine) in the post-synaptic space, developments are starting to arise in which these types of drugs are used as antidepressants and ADHD medications. Most results are preliminary, and it will probably be a while until these drugs enter into mainstream as treatment options for a wider variety of mental conditions.

[teak]

Has there been any futher research into the safety of acetyl-cholinesterase inhibitors like Huperzine A and Reminyl? As quoted above, such drugs are supposedly 'potent neurotoxins' as used in nerve agents, insecticides and poisons, so large or long-term dosage might not be suitable for healthy individuals. I know it was reported a year back, the FDA was looking into the safety of Reminyl.

Edit: Seems like there is a Huperzine A phase II clinical trial in progress run by the National Institute on Aging.

Edited by teak, 02 January 2006 - 11:44 PM.

[teak]

Found this reference which casts doubt on the memory enhancing ability in healthy individuals, or at least the main supporting study:

http://www.butler.or...&chunkiid=21761

Huperzine is also promoted for improving memory in healthy individuals, but the supporting evidence for this claim appears to be limited to one small, poorly designed trial.21

21.   Sun QQ, Xu SS, Pan JL, et al. Huperzine-A capsules enhance memory and learning performance in 34 pairs of matched adolescent students [abstract]. Zhongguo Yao Li Xue Bao. 1999;20:601–603.

Also found this anecdotal experience of an unknown regular dosage of DMAE, Vinpocetine, Huperzine and GHB. Supposedly long exposure to high acetycholine levels caused sleep problems, CEV's, light sensitivity, altered vision, etc. Even claimed after using the stated drugs for a prolonged period of time, it permanently kept levels high or made them hypersenstitve to acetycholine even after discontinuing all but GHB.

http://www.erowid.or...xp.php?ID=36603

I stopped taking all drugs except GHB. I found that although these drugs are meant to always be reversable acetylcholine esterase inhibitors I had taken to much and it was not completly reversable reversable. I found that I couldnt take more than 3g of GHB a day without my acetycholine going back up again. I was now hypersenstitve. So I carried on taking ghb, often with my acetycholine much higher that normal because as long as it wasnt to high it was kinda cool. Having high acetcholine gives me a more powerful imagination and is like a psychedelic drug. Now my final problem was that because I had my acetycholine so high for many months after this hospital visit I found one day when i stopped taking ghb that my acetycholine was stuck at a permanently high level and wont go back down! What does this mean? Well the higher your actylcholine is the harder it is to get to sleep. I have to be up for longer before I can sleep. My imaginaton is perinently in high gear all the time.

Edited by teak, 03 January 2006 - 02:45 AM.

[purerealm]

I normally don't ever remember my dreams but yesterday I exercised for the first time in a while and went to bed with a good dose of ghb and had a very vivid dream. Think acetylcholine levels have to do with dream remembering?

[dopamine]

I normally don't ever remember my dreams but yesterday I exercised for the first time in a while and went to bed with a good dose of ghb and had a very vivid dream. Think acetylcholine levels have to do with dream remembering?

Donepezil, an acetylcholine esterase inhibitor, has been shown to increase REM sleep, which we know is essential for proper memory formation. So it is theoretically possible that increased cholinergic neurotransmission in general could increase one's memory of dreams.

[goku]

But this is weird. Because on this thread previously people were saying that too much aceytlcholine during sleep interferes w/ memory consolidation. So we have completely contradictory info and I don't hav a clue what to do. I've been thinking of using Galantamine for a long time now but now I dunno.

[LifeMirage]

As far as Huperzine A dosage I would recommend anywhere from 100mg to 200 mcg daily....a recruiting US study is planning to use 800 mcg daily.

[Brainbox]

By dopamine: "Also, as discussed prior, acetylcholine esterase inhibitors over time may decrease the density of cholinergic receptors in various brain regions. For otherwise healthy individuals, this could potentially have adverse effects on memory in the post-use phase of the drug. There may also be a similar effect on the density of dopamine and norepinephrine receptors, as HupA has been shown to increase levels of these neurotransmitteres as a result of AchE inhibition."

By LEF, on their site: "Since Huperzine A inhibits the enzyme acetylcholinesterase, it should not be used on a chronic basis. The reason for this is that some acetylcholinesterase is needed to suppress excessive amounts of the neurotransmitter acetylcholine from accumulating in the body. While most people over age 30 need more acetylcholine, too much can cause unpleasant side effects."

By LifeMirage: "As far as Huperzine A dosage I would recommend anywhere from 100mg to 200 mcg daily....a recruiting US study is planning to use 800 mcg daily."

This is all a bit confusing for me as a self-educative just-starting bio-chemist'ish non-professional .... [huh]

I cannot find backup for dopamine's statement. But this is quite worrying and would inhibit any possible use of Huperzine for me.
At what doses of Huperzine would this effect be probable in healthy persons and is any practical evidence present to support this?

The statement of LEF, and some other organisations / individuals, seem to be consistent in warning healthy individuals in not taking Huperzine in the standard dose of 50mcg daily during long periods. This to avoid cholinergic side effects. They do not refer to the mechanism that is described by dopamine btw. Some organisations do promote long term usage of Huperzine by healthy individuals however.
Any clue's on why this inconsistency exists? I assume the reason is that (pubmed) information just relates to use of Huperzine in memory-impaired patients and that long-term trails with healthy individuals are not known.

Is the new US study that is mentioned by LifeMirage aimed at memory-impaired patients or healthy individuals?

Thanks ,
Brainbox.

[LifeMirage]

QUOTE
By LEF, on their site: "Since Huperzine A inhibits the enzyme acetylcholinesterase, it should not be used on a chronic basis. The reason for this is that some acetylcholinesterase is needed to suppress excessive amounts of the neurotransmitter acetylcholine from accumulating in the body. While most people over age 30 need more acetylcholine, too much can cause unpleasant side effects."

LEF has a very conservative viewpoint on several supplements (5-HTP, Galantamine, Huperzine A)….too much of anything may cause a problem…it’s a matter of finding the right dose for you.

QUOTE
By LifeMirage: "As far as Huperzine A dosage I would recommend anywhere from 100mg to 200 mcg daily....a recruiting US study is planning to use 800 mcg daily."


This is all a bit confusing for me as a self-educative just-starting bio-chemist'ish non-professional .... 

I cannot find backup for dopamine's statement. But this is quite worrying and would inhibit any possible use of Huperzine for me.
At what doses of Huperzine would this effect be probable in healthy persons and is any practical evidence present to support this?

So far I can find any direct evidence of this and recommend Huperzine A as a safe and highly neuroprotective compound, cycling it is a good idea however.

The statement of LEF, and some other organisations / individuals, seem to be consistent in warning healthy individuals in not taking Huperzine in the standard dose of 50mcg daily during long periods. This to avoid cholinergic side effects. They do not refer to the mechanism that is described by dopamine btw. Some organisations do promote long term usage of Huperzine by healthy individuals however.

Dosing depends on several factors from age to purpose of use….I’ve taken up to 400 mcg for a week (without any other choline compounds) without any problems.

Any clue's on why this inconsistency exists? I assume the reason is that (pubmed) information just relates to use of Huperzine in memory-impaired patients and that long-term trails with healthy individuals are not known.

It’s a matter of a lack of both understanding and experience….3 months is the longest study I’m aware of…

Is the new US study that is mentioned by LifeMirage aimed at memory-impaired patients or healthy individuals?

Alzheimer's disease

[Brainbox]

So far I can find any direct evidence of this and recommend Huperzine A as a safe and highly neuroprotective compound, cycling it is a good idea however.

After indigestion, Hup-A stay's present or in effect for about 6 hours according some studies. So, if I would decide to take one 50 mcg at 6 o’clock and one at 12, it leaves my body with about 12 hours a day of Hup-A inactivity. But probably “present” and “in effect” are not the same thing, as far as I understand, the 6 hours period was determined by measuring it’s effect.

Apart from this short period “cycling”, probably also a long-term cycling is advisable just to be sure. What period could be recommended? Is there a substance I could cycle it with? I do not react very well on AC precursors (slight irritation and anxiety) that I tried for a few days, but Hup-A seems to have very positive effects during a period of 2 days. Could be placebo though…. I also take ALCAR, R-ALA and Rhodiola Rosea. Maybe cycling it with the RR is a good idea since that seems to wear of also….

Edit:
I figure that a cumulative effect of AC build-up or other effects could be predominant as compared to the short hourly breaks......
Maybe this is all basic stuff for you, but I'm trying to find a way to use it as safe as possible......

Edited by brainbox, 29 January 2006 - 09:13 AM.