Galantamine vs Huperzine A? Which is more effective at immediately increasing ach receptor activity? What are the various pros and cons of each? Do they need to be stacked with choline precursors? If so, which choline precursors are the most potent by weight at increasing levels of choline and acetyl-choline?
Are there any other potent ACH releasers, CHAT inducers, or ACHE inhibitors that are effective at minus 250 mg doses? Preferably dietary or natural in origin.
I am also interested in Butyrylcholinesterase inhibitors of natural origin or of dietary supplement status.
I am looking for both personal anecdotal experiences and scientific data.
Thank you!
Both. Huperzine is a an ACHE Inhibitor and galantamine is mainly a positive allosteric modulator. Bacopa increases choline through serotonin receptor + concentration increase (which is amazing, one decreases the other usually)
Was not aware of the serotonin/choline antagonism, knew of the dopamine/ach antagonism though which is essentially what I am trying to counter. So galantamine is more nicotinic I had read while huperzine is a hybrid nmda antagonist with potent ache inhibiting activity.

Think I may test ashwagandha with my stack today, but the huperzine/galantamine are really calling for me, especially with that sweet dosage range.

I think both deserve their own testing after a bit of info, and may even be best combined. Thanks for the info
It's technically serotonin/choline agonism and a slight decrease in dopamine spikes, especially in the addiction centers of the brain like the striatum (bacopa)
in my experience bacopa does not subtly decrease dopamine, I cannot use it in this specific formula and already have 5ht/da agonism going on. Just need to keep ach flowing, my memory is awful with amines so elevated.
"Bacopa has also shown anti-dopaminergic effects in the striatum (location associated with Caffeine and morphine, and highly associated with dopamine induced locomotion) and prevented surges in dopamine when fed at a low dose of 5-15mg/kg bodyweight daily.[49] This anti-dopaminergic effect may be useful in situations of drug dependence[49] Additionally, one study measuring levels of dopamine in the hindbrain noted statistically significant (91% of control).[23]"

Qualitative analysis shows similar. No good.
Actually this is beneficial in my case. I use D2 agonists which upregulate D1. By having slightly less dopamine to agonize D1, it should upregulate and render one more sensitive. It would also curb addictiveness while letting some dopamine effects take place. Even with Kratom I find it is strongly potentiated, because of it's POTENT p450 enzyme inhibition.
In some cases bacopa is excellent it just totally inhibits much of the point of the formulation I am making, which yes, part of is dopamine release in the striatum.
Ashwagandha does not interfere with the effects of the dopamine reward nearly as much, and even provides neuroprotective properties specific to da release, yes bacopa can prevent some toxicity too related to dopamine,there are lot's of reviews on reddit, but in bacopas case it seems like it does much of this by tanking dopamine levels, which ashwagandha only reduces them to a mild, if even noticeable level, while still providing much anti-oxidant, gaba, endorphin, and hopefully ach support.
9% decrease isn't really tanking it that bad. I find that at first it may dull but later on (4+ weeks) most euphoric drugs start getting more euphoria and last longer due to enzyme stuff. It also increases GABA receptors which I think would disinhibit dopamine release, perhaps it simply changes the storage of dopamine like lobelia which forces dopamine in an area which it cannot be released as much by amphetamines and similar addictive drugs
From my personal experiences, Bacopa was not only potent enough at reducing DA levels that it completely stopped my drug induced dyskenisia with a single dose, but it completely eliminated much of the perceivable effect of the dopaminergics I was experimenting with. What is on paper, determined from a rat study or test tubes, is not always how it translates in the physical world.

I do agree bacopa is quite useful, but I would make a formulation based around bacopa rather than add it to an anti-depressant/euphoric mood lifting stimulant stack.
Bacognize is almost as powerful as Cerebrolysin in memory retention imo. Huperzine A is one hell of an enzyme inhibitor, and would be best for study sessions, all nighters, etc but it's mainly focus not retention or recall.
Bacopa is good for an everyday use. Huperzine, I take only when I need it. It seems to have a sustained inhibition of achetylcholinesterase. I prefer bacopa on the reg because it has the choline actyltransferase activity and promotes ngf and bdnf.
Galantamine did well for memory for me, huperzine not so much. Galantamine is really fun as a lucid dreaming product as well, though low-quality products give me a headache for some reason.
Bacopa did nothing for me in 12 weeks. I'm allergic to something in the Huperzine A i took, got welts on my skin.
Galantamine is awesome :3 But brahmi and piracetam are better for memory since they can be taken on a daily basis. Galantamine.. needs to be cycled, and has temporary effects, I use it when I need a creative/imaginative boost, for writing or something else. As for huperzine.. I used a premade stack which had loads of other noots, it had amazing effects.. Yes, super-sharp memory, like.. My whole life was in my fingertips when I was on it.. Galantamine too kinda enhances memory, basically it makes thoughts and memories more vivid.. Thus easier to recall.
I would rate Huperzine as the best AChE-Inhibitor, it increases NGF as well and seems to get along with most everything else rather well. I like Vinpocetine as well, but some people get adverse effects from the vasodilation (helps me since I am prone to headaches from overstimulation). Havent tried Galantamine
I didn't like Huperzine. It made me pee a lot. And even if i didn't need to pee i felt like i did. I read something at the time i was taking it that it can have long term effects on smooth muscle control which can be permanent. So i stopped taking it.

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