Supplements to increase mental clarity
- 10-03-2012, 03:30 AM
- 10-03-2012, 03:34 AM
10-03-2012, 04:57 AM
My functional memory is usually pretty good, i use noots et al for different effects like increasing energy, clarity, motivation, wit, humor, communication and creativityOriginally Posted by mr.cooper69
10-03-2012, 08:58 AM
Since I started taking the ALCAR (1 g A.M. and 0.5g P.M.) and Bacopa I have noticed a few things. I feel like my 'brain' is more calm and relaxed. Usually I have a million thoughts running through my head 24/7 and while I still do its seems to have slowed down slightly. For me this is obviously a good thing. The biggest thing I have noticed is with sleep. I have slept a good bit better but I CANNOT wake up in the mornings. For the first time ever, I have had to set multiple alarms. I have slept through my first alarm every single morning for about a week now and even slept through my phone alarm one day. I like the sleep but it feels like I am drugged when I wake up. May only take the ALCAR in the A.M. and see if any changes occur.
10-03-2012, 09:59 AM
So, D-Serine is "limited" by prior AMPA activation (among other criteria)? Could it still lead to over activation of the NMDA receptor? I guess this is something that everyone worries about when messing with the NMDA receptor?
Now, what about allosterism? So, piracetam (and others) don't directly activate any receptor, but it modulates glutaminergic receptors through allosteric activation. Now, aniracetam has a high affinity binding to the AMPA receptor. Will modulating the AMPA receptor lead to over-activation of the NMDA receptor?
Alright, I was pretty long winded, but I needed to work through that post to help myself understand.
So, hypothetically speaking, is it safer (avoiding NMDA excitotoxicity) to modulate the AMPA receptor through the use of -racetams, or to activate the NMDA receptor through the use of D-Serine (and follow the cascade of preceding criteria prior to agonism of the NMDA receptor)?
10-03-2012, 04:44 PM
10-03-2012, 04:51 PM
I didn't follow certain parts of your post, but no, aniracetam would not potentiate excitotoxicity (there are far more mechanisms in place than basic AMPA modulation). In fact, aniracetam would probably prove neuroprotective to any such effect from the combo.
10-03-2012, 05:30 PM
I'll just ask this question while I do some more reading:
Can D-Serine or Sarcosine potentiate excitotoxicity?
I would like to investigate the racetams, D-Serine, Sarcosine, and DAA, but I just don't want to be messing with neuronal death, excitotoxicity, etc.
They all show great potential as cognitive enhancers, but I would like to read up on their pharmacodynamics and pharmacokinetics. I want to know what the drug does to my body and what my body does to the drug.
10-03-2012, 08:05 PM
10-03-2012, 08:37 PM
If the BBB will prevent excitoxic insult from oral compounds, when does the fascination with creating compounds with the ability to cross the BBB become a waste of time?
It seems as if creating a compound with even more ability to have BBB permeability has diminishing return (e.g. Magnesium Threonate vs. Any Chelated Magnesium).
Do you have any suggested readings that deal with the NMDA and AMPA receptors?
10-03-2012, 10:18 PM
What do you mean by diminishing return of magnesium l-threonate? I was under the impression supplementation was specifically to increase magnesium levels in the brain and it was effective.
Edit: maybe mg for mg total absorption and/or levels throughout the body?
"Jackie Treehorn treats objects like woman man."
10-03-2012, 10:40 PM
So, Magnesium Threonate may be able to cross the BBB better than Magnesium Glycinate, but how much magnesium from Magnesium Threonate is still being deterred at the BBB? Do we keep trying to create compounds that have greater BBB permeability only for our BBB to still block entry?
10-03-2012, 11:02 PM
Ahhh, I gotcha now. Thanks for clearing that up. Sorry for the derail!
"Jackie Treehorn treats objects like woman man."
10-03-2012, 11:05 PM
10-04-2012, 12:50 AM
It's not all about the BBB, this is just one example! Certainly if you take a highly penetrating compound at even a microdose, you can induce some sort of pathological outcome (methylmercury, anyone?). Your question is very different because we are talking about endogenous substances that are under tight regulation in the body (see all the channels at the NMDAR, for instance. Aniracetam in particular should actually reduce any excitotoxic potential of DAA since it regulates the AMPAR (this is in stark contrast to an AMPAR agonist, which may have totally different effects). Piracetam would also prove useful in exerting neuroprotective effects (this time more specifically to the NMDAR).
10-04-2012, 08:24 AM
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