Hi, i read in some threads that taking huperzine everyday could be dangerous, can you explain me why? What would happen after one month of use without breaks?

8 replies to this topic
#1
Posted 19 March 2014 - 10:14 PM
Hi, i read in some threads that taking huperzine everyday could be dangerous, can you explain me why? What would happen after one month of use without breaks?
#2
Posted 21 March 2014 - 10:47 PM
it inhibits acetylcholinestarase, the enzyme that sops up unused acetylcholine from the synaps, so more ach is available. ach improves memory and concentration but it also causes depression and other problems. also, the brain gets used to having too much ach, and then starts releasing less, so when you stop taking the huperzine, the rebound is less ach, poorer memory and less concentration. nobody can tell you that x amount of time at x dosage will cause x effect in your brain particularly, because everyone's different, each product is different, etc. There's not much research on how to cycle it either, but i've found taking it for 1-3 days while cramming for exams works, though i start to feel anxious and it becomes harder to sleep, and then not take it for a few weeks if possible.
#3
Posted 21 March 2014 - 11:10 PM
i'm having some HORRIBLE nightmares while on huperzine, it's the excess of acetylcholine?
#4
Posted 21 March 2014 - 11:17 PM
yea it's possible, increased ach could mean you're more awake, even when you're asleep (for example the REM phase where you dream). But i know benadryl, which reduces ach could also cause nightmares, so you might already be in the phase where your brains adjusting to constantly being flooded with ach and is now making less of it (same effect as being on benadryl). How long have you been taking hupe?
#5
Posted 21 March 2014 - 11:19 PM
4 days
#6
Posted 21 March 2014 - 11:36 PM
yea it's the increased ach. but 4 days isn't very long, so you're ok, heard of people cycling it for a couple weeks at a time. have you read this thread: http://www.longecity...zine-a-dangers/
#7
Posted 23 March 2014 - 11:37 PM
I used to take both huperzine and benadryl together to help induce lucid dreams, but never had an issue with nightmares at the time.
#8
Posted 26 March 2014 - 07:18 PM
I read somewhere that Longterm it could lead to loss of neurons or(?) Synapses.
I can understand if You are skeptic about my Statement, I will try to find the paper.
Found some further Infos here:
http://www.longecity...zine-a-dangers/
I can understand if You are skeptic about my Statement, I will try to find the paper.
Found some further Infos here:
http://www.longecity...zine-a-dangers/
#9
Posted 07 April 2014 - 02:32 PM
Here is something about cholinesterase inhibitors and Neurotoxicity:
http://www.ncbi.nlm..../pubmed/9589388
Responses induced by tacrine in neuronal and non-neuronal cell lines.
Alzheimer's disease (AD) is associated with a reduction in cholinergic activity as a result of specific neuronal loss. Current potential treatments for the disease include both cholinomimetic drugs and anticholinesterase inhibitors. One of the drugs approved by the FDA is tacrine (9-amine-1,2,3,4 tetrahydroacridine; THA), a strong acetylcholinesterase (AChE) inhibitor. We have studied the effects of tacrine on glial and neuronal cells in culture assessing cell survival and viability and morphology. Lactate dehydrogenase (LDH) activity and methylthiazol-diphenyl-tetrazolium (MTT) reduction were used as toxicity indicators. We found that tacrine toxicity on rat B12 glial cells and mouse Neuro 2A cells was strongly dependent on its concentration (up to 500 microM) and time of exposure. The toxic effect was not prevented by serum factors nor by bovine serum albumin. Fluorescein-conjugated phalloidin was used to examine the arrangement of actin filaments at substrate adhesion regions and cell-cell contacts. Primary events following exposure to tacrine included changes in cell morphology, disappearance of actin filament bundles, and disruption of focal adhesion contacts. At concentrations between 10 and 50 microM, tacrine induced neurite outgrowth in Neuro 2A cells, an effect that was not observed in B12 cells, suggesting that certain tacrine effects could be specific for neuronal cells. Although similar trends of response were observed for both cell types, some differences between undifferentiated and differentiated cells were apparent.
http://www.ncbi.nlm..../pubmed/9589388
Responses induced by tacrine in neuronal and non-neuronal cell lines.
Alzheimer's disease (AD) is associated with a reduction in cholinergic activity as a result of specific neuronal loss. Current potential treatments for the disease include both cholinomimetic drugs and anticholinesterase inhibitors. One of the drugs approved by the FDA is tacrine (9-amine-1,2,3,4 tetrahydroacridine; THA), a strong acetylcholinesterase (AChE) inhibitor. We have studied the effects of tacrine on glial and neuronal cells in culture assessing cell survival and viability and morphology. Lactate dehydrogenase (LDH) activity and methylthiazol-diphenyl-tetrazolium (MTT) reduction were used as toxicity indicators. We found that tacrine toxicity on rat B12 glial cells and mouse Neuro 2A cells was strongly dependent on its concentration (up to 500 microM) and time of exposure. The toxic effect was not prevented by serum factors nor by bovine serum albumin. Fluorescein-conjugated phalloidin was used to examine the arrangement of actin filaments at substrate adhesion regions and cell-cell contacts. Primary events following exposure to tacrine included changes in cell morphology, disappearance of actin filament bundles, and disruption of focal adhesion contacts. At concentrations between 10 and 50 microM, tacrine induced neurite outgrowth in Neuro 2A cells, an effect that was not observed in B12 cells, suggesting that certain tacrine effects could be specific for neuronal cells. Although similar trends of response were observed for both cell types, some differences between undifferentiated and differentiated cells were apparent.
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