10 replies to this topic

[GM1]

Hey guys Ive been lurking here for a bit and am very glad I found this site, tons of useful information.

Background: Im 20 years old and am going to be a senior in college in the fall. Im looking to start a regimen that will help with memory, comminication, social anxiety, and attention span. I also play poker somewhat competivetly and having a sharp mind is obviously important. I was a farily heavy pot smoker over the last year and a half or so and have grown tired of all the debilitating cognitive side effects that came with it. Ive decided to make some life changes and have started eating better as well as lifting weights and playing basketball a few times a week

I have limited experience with nootropics, started a smallish stack last semester of piracetam, choline citrate, ginko, fish oil and a multi last semester and saw decent results but ran out and have yet to restock except for purchasing Aniracetam which I am definitely a fan of. After doing some research I was thinking about starting the following stack

Piracetam- start with 800mg 3x daily, might up the dose after a while

Aniracetam- 750mg 2x daily with food

Alpha GPC- 300mg 3x daily with piracetam

ALCAR Arginate- 1g 2-3x daily (should I just get regular ALCAR?)

K-RALA- 600mg 2-3x daily (should I just get the regular stuff?)

Huperzine A- 100mcg?? (still unsure about this one)

Bacopa- 300mg (50% baccosides) 2x daily (everything I read about bacopa is excellent)

Ginko Biloba- 120mg 2x daily

Fish Oil- 3-4g daily

OrthoCare Multi

B Complex

CoEnyzme Q10- 100mg


Considering adding:
Centrophenoxine
Hydergine
P-serine

For extra boost/mood when needed
Rhodiola
Siberian Ginseng
Adrafanil
SAMe
St. Johns Wort/5HTP
L-tyrosine


Any suggestions on dosages, timing, and whether to take with food or not would be great. Thanks for any help!

Edited by GM1, 04 June 2008 - 08:46 PM.

[Mr.Bananas]

Try adding the supplements one at a time to see what happens and how you respond.

[Zoroaster]

Hey guys Ive been lurking here for a bit and am very glad I found this site, tons of useful information.

Background: Im 20 years old and am going to be a senior in college in the fall. Im looking to start a regimen that will help with memory, comminication, social anxiety, and attention span. I also play poker somewhat competivetly and having a sharp mind is obviously important. I was a farily heavy pot smoker over the last year and a half or so and have grown tired of all the debilitating cognitive side effects that came with it. Ive decided to make some life changes and have started eating better as well as lifting weights and playing basketball a few times a week

I have limited experience with nootropics, started a smallish stack last semester of piracetam, choline citrate, ginko, fish oil and a multi last semester and saw decent results but ran out and have yet to restock except for purchasing Aniracetam which I am definitely a fan of. After doing some research I was thinking about starting the following stack

Piracetam- start with 800mg 3x daily, might up the dose after a while

Aniracetam- 750mg 2x daily with food

Alpha GPC- 300mg 3x daily with piracetam

ALCAR Arginate- 1g 2-3x daily (should I just get regular ALCAR?)

K-RALA- 600mg 2-3x daily (should I just get the regular stuff?)

Huperzine A- 100mcg?? (still unsure about this one)

Bacopa- 300mg (50% baccosides) 2x daily (everything I read about bacopa is excellent)

Ginko Biloba- 120mg 2x daily

Fish Oil- 3-4g daily

OrthoCare Multi

B Complex

CoEnyzme Q10- 100mg


Considering adding:
Centrophenoxine
Hydergine
P-serine

For extra boost/mood when needed
Rhodiola
Siberian Ginseng
Adrafanil
SAMe
St. Johns Wort/5HTP
L-tyrosine


Any suggestions on dosages, timing, and whether to take with food or not would be great. Thanks for any help!

I would say lay off the Huperzine-A as part of a daily stack as it needs to be cycled. It can/will lower your acetocholine receptors if you use it long enough and that's not good at your age. Taken like 3 times a week, however, it shouldn't cause you any problems, but its still one I'm a little wary off. I know there are various opinions on this issue but what I've stated above seems to be the consensus as far as I can find.

And when you refer to K-RALA or the "regular stuff" what are you comparing it to? Regular ALA or R-ALA? I don't know that there's a big difference between R-ALA and K-RALA in terms of absorption except that K-RALA is much more stable as a powder (though still not great). At least that's my understanding. So if you're going to cap it yourself or mix it in a drink then K-RALA would be the way to go. If you are just buying pre-mad caps then I don't think there's much advantage of K-RALA over R-ALA. But RALA is def better than ALA.

I don't know much about alcar arginate so maybe someone else can help you on this one. But normal alcar words pretty well as is for most people.

My only other comment is that Ortho-Core is way overpriced. I'm pretty anti Ortho-anything come to think of it. There are plenty of multivitamins chock full of phytonutrients, with Q10, and well mixed tocopherols and all that good stuff that cost a quarter of what that supplement costs. And you can get them from reputable companies with USP certification. I'd say just pick up a multi at Costco. They have an assortment of decent ones for crazy-cheap. And if you get one formulated for "atheletes" they'll have way boosted B vitamins and you won't have to buy a seperate B complex.

As far as your other stuff goes centrophenoxine is good stuff, as is Rhodiola. Ginseng doesn't do anything for me. I don't have experience with the other stuff on the list.

[FunkOdyssey]

The price on Ortho-core came down under $40, I don't think its bad at that price considering everything in there. Na-RALA is what you want, but 600mg two or three times daily is a massive massive amount and would be super expensive. The monthly cost is about $15 per 200mg daily you take, so you see how that math gets out of control quickly. You may also suffer symptoms of hypoglycemia if you take a large enough dose of Na-RALA on an empty stomach.

[zoolander]

I would say lay off the Huperzine-A as part of a daily stack as it needs to be cycled. It can/will lower your acetocholine receptors if you use it long enough and that's not good at your age.

People keep saying this. I have asked for the people saying this to provide a reference for the comment but no one has provided a reference. Zoroaster can you please provide a reference for the above comment?

Just for the record, huperzine A does not act on the acetylcholne receptor it inhibits an enzyme that breaks down acetylcholine

Here's some recent recearch on huperzine

J Neurochem. 2008 May 31. [Epub ahead of print]Click here to read Links
Huperzine A exhibits anti-inflammatory and neuroprotective effects in a rat model of transient focal cerebral ischemia.
Wang ZF, Wang J, Zhang HY, Tang XC.

State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zu Chong Zhi Road, Zhangjiang Hi-Tech Park, Shanghai 201203, P.R. China.

Huperzine A, a reversible and selective acetylcholinesterase (AChE) inhibitor, has been reported to display neuroprotective properties. The present study investigated the protective effects of huperzine A in a rat model of transient focal cerebral ischemia created by middle cerebral artery occlusion (MCAO). Huperzine A (0.1 mg/kg), administrated intraperitoneally at the onset of occlusion and 6 h later, markedly restored regional cerebral blood flow, reduced infarct size, and decreased neurological deficit score at 24 h after reperfusion. Along with inhibiting AChE activity, huperzine A inhibited nuclear translocation of transcription factor nuclear factor-kappa B, decreased overexpression of proinflammatory factors in both ipsilateral cortex and striatum, and suppressed activation of glial cells in the ischemic penumbra. Neurological deficit and glial cells activation were also reduced by daily administration of huperzine A for 14 days. Mecamylamine, a nicotinic acetylcholine receptor (nAChR) antagonist, totally abolished the inhibitory effects of huperzine A on ischemia-induced glial cells activation. Meanwhile, mecamylamine partially reversed the infarct size-reducing effects of huperzine A. In conclusion, our results demonstrate that huperzine A exhibits neuroprotective effects against transient focal cerebral ischemia-induced brain injury and suggest that the protection mechanism may involve a cholinergic anti-inflammatory pathway, in which nAChR plays an essential role.

[zoolander]

Zoroaster, call me pedantic but I think it would be more useful if you just gave recommendations based on 1. science and 2. science. That goes for everyone in these forums who believe that throw out recommendations willy nilly based on what they've heard and how a supplement affected their functioning. I know a lot of people do it and to me it's such a loose and sloppy way of helping someone achieve their goals through dietary supplementation when there is so much research out there that can be referred to.

Unfortunately, a lot of people are going to be misguided following recommendations based on testimonial reports. At minimum people should be explaining how things work instead of just saying, "I'm not sure but I've heard that it's good"

[Zoroaster]

I would say lay off the Huperzine-A as part of a daily stack as it needs to be cycled. It can/will lower your acetocholine receptors if you use it long enough and that's not good at your age.

People keep saying this. I have asked for the people saying this to provide a reference for the comment but no one has provided a reference. Zoroaster can you please provide a reference for the above comment?

Just for the record, huperzine A does not act on the acetylcholne receptor it inhibits an enzyme that breaks down acetylcholine

Here's some recent recearch on huperzine

J Neurochem. 2008 May 31. [Epub ahead of print]Click here to read Links
Huperzine A exhibits anti-inflammatory and neuroprotective effects in a rat model of transient focal cerebral ischemia.
Wang ZF, Wang J, Zhang HY, Tang XC.

State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 555 Zu Chong Zhi Road, Zhangjiang Hi-Tech Park, Shanghai 201203, P.R. China.

Huperzine A, a reversible and selective acetylcholinesterase (AChE) inhibitor, has been reported to display neuroprotective properties. The present study investigated the protective effects of huperzine A in a rat model of transient focal cerebral ischemia created by middle cerebral artery occlusion (MCAO). Huperzine A (0.1 mg/kg), administrated intraperitoneally at the onset of occlusion and 6 h later, markedly restored regional cerebral blood flow, reduced infarct size, and decreased neurological deficit score at 24 h after reperfusion. Along with inhibiting AChE activity, huperzine A inhibited nuclear translocation of transcription factor nuclear factor-kappa B, decreased overexpression of proinflammatory factors in both ipsilateral cortex and striatum, and suppressed activation of glial cells in the ischemic penumbra. Neurological deficit and glial cells activation were also reduced by daily administration of huperzine A for 14 days. Mecamylamine, a nicotinic acetylcholine receptor (nAChR) antagonist, totally abolished the inhibitory effects of huperzine A on ischemia-induced glial cells activation. Meanwhile, mecamylamine partially reversed the infarct size-reducing effects of huperzine A. In conclusion, our results demonstrate that huperzine A exhibits neuroprotective effects against transient focal cerebral ischemia-induced brain injury and suggest that the protection mechanism may involve a cholinergic anti-inflammatory pathway, in which nAChR plays an essential role.

Obviously huperzine-A doesn't interact with the receptor. Its common knowledge that its an acetylcholinesterase inhibitor. Its a matter of downregulation, which I'm sure you're aware is a well established physiological phenomenon. SSRI's and other reuptake inhibitors all induce downregulation of the natural receptors with long-term use. I would submit that the burden of proof would be on you to demonstrate that Huperzine-A is somehow immune to this extremely common phenomenon. There have also been several threads on this very topic wherein numerous studies have been posted verifying these long term effects of Huperzine-A. RI, in their descriptor for Huperzine-A recomends that it be cycled for this very reason. Nevertheless I will provide a few studies for you if that's what you really want. But not now. As I am already late to take an exam. I know that sounds like a lame excuse to get out of posting studies but it actually is true. But don't worry, I"ll come back to it.

And I really don't want to get contentious about this but while its true that there is a paucity of scientific backing to most people's statements on these boards, I would say that posting superflous studies unrelated to the matter at hand do nothing to advance the discussion either [see above]. And there is genuine value in relating personal experiences. I personally enjoy hearing how a particular substance affected someone in vivo. You can get details you can't get through studies. And when I give someone advice with a qualification that it is just, "something I heard" its meant to be no more than a launching point for their own research.

With that said, your point is well taken and I will spend more time posting specifics and references with my statements in the future.

[zoolander]

thank you Zoroaster

[Zoroaster]

thank you Zoroaster

Well that exam was quick. Always a pleasant surprise. Anyway, I found this study which seems like it should settle this issue pretty definitively.

Regulation of muscarinic acetylcholine receptor function in acetylcholinesterase knockout mice.

Li B, Duysen EG, Volpicelli-Daley LA, Levey AI, Lockridge O.

Eppley Institute, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Acetylcholinesterase (AChE) hydrolyzes acetylcholine to terminate cholinergic neurotransmission. Overstimulation of cholinergic receptors by excess acetylcholine is known to be lethal. However, AChE knockout mice live to adulthood, although they have weak muscles, do not eat solid food, and die early from seizures. We wanted to know what compensatory factors allowed these mice to survive. We had previously shown that their butyrylcholinesterase activity was normal and had not increased. In this report, we tested the hypothesis that AChE-/- mice adapted to the absence of AChE by downregulating cholinergic receptors. Receptor downregulation is expected to reduce sensitivity to agonists and to increase sensitivity to antagonists. Physiological response to the muscarinic agonists, oxotremorine (OXO) and pilocarpine, showed that AChE-/- mice were resistant to OXO-induced hypothermia, tremor, salivation, and analgesia, and to pilocarpine-induced seizures. AChE+/- mice had an intermediate response. The muscarinic receptor binding sites measured with [3H]quinuclinyl benzilate, as well as the protein levels of M1, M2, and M4 receptors measured with specific antibodies on Western blots, were reduced to be approximately 50% in AChE-/- brain. However, mRNA levels for muscarinic receptors were unchanged. These results indicate that one adaptation to the absence of AChE is downregulation of muscarinic receptors, thus reducing response to cholinergic stimulation.

While this obviously isn't a test of Huperzine-A specifically (one wouldn't expect to find a study that specific about a neutraceutical) these researchers used knockout mice created to lack AChe (Acetylcholinesterase), which as we've established is inhibited by Huperzine-A. In essence, these mice are somewhat analogous to someone who took a buttload of Huperzine-A for a long period of time.

As you can see from the bolded sections the hypothesis tested was that in the absence of AChe, the mice avoided acetylcholine poisoning by downregulating Acetylcholine receptors. The results were positive and they found that Muscarinic receptors (one of the two types of acetylcholine receptors) were indeed downregulated (reduced in number and/or sensetivity) in the presence of excessive acetycholine caused by the lack of AChe.

This essentially establishes the principle of muscarinic downregulation as a result of AChe inhibition, now its just a matter of degrees. The body maintains a very precise homeostasis and lessons from other uptake inhibitors can tell us that it doesn't take much to induce downregulation. Indeed the very fact that you can "feel something" when Hup-A works means that you are inhibiting AChe enough to cause an unnatural pooling of Acetylcholine at the receptor sites. While I would have to admit that we don't have specific evidence on whether chronic use of Hup-A causes downregulation, I would say it would almost be a violation of the laws of physiology (if there were such things) if it did not.

Of course then there's the question of whether or not the downregulation is reversible and what the specific effects would be of living with a reduced number of acetylcholine receptors, but I think we've had enough science for one post.


I apologize for not being more thorough in my initial response.

[edward]

Try adding the supplements one at a time to see what happens and how you respond.

Definitely, it looks like your stack has a lot of overlaps. I would start off with Piracetam 2400 mg and a Choline source wait a few weeks then add something else (or try something else instead), wait a week or so add something else (or try something else instead) and so on and so forth, or else you dont know what is working and what isn't

Edit: Furthermore it looks like your stack is really hitting the Acetylcholine system hard (which may not be a bad thing, it just depends on your needs). Dopamine, serotonin, glutamate, gaba etc. etc. etc. all have influence on memory and cognition and boy is it a balancing act...

For a young person taking so many acetylcholine nootropics you are going to quickly end up on the other side of the U shaped response curve as in you will begin to get less of an effect and even negative effects.

Edited by edward, 05 June 2008 - 03:13 AM.

[zoolander]

Thanks again Zoroaster that was a very thorough response. The information you supplied will come in handy