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Supplements to increase mental clarity

mr.cooper69 said:
For an acute burst of cognitive function, try the NMDA trio of D-Serine, sarcosine, and DAA along with a potentially synergistic AMPA-based agent: aniracetam.
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acute meaning "short-lived and diminishing effects when used repeatedly"?
ive used sarco, daa, and ani together for the last few weeks and while they dont do anything bad for me, i havent experienced SUPER-WOW effects, maybe because i didnt have the d-serine...?
 
dsohei said:
acute meaning "short-lived and diminishing effects when used repeatedly"?
ive used sarco, daa, and ani together for the last few weeks and while they dont do anything bad for me, i havent experienced SUPER-WOW effects, maybe because i didnt have the d-serine...?
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Short-lived, yes. Diminishing effects, no.

None of these should give you wow effects. They aren't stimulants/work on the reticular activating system. They should improve functional memory.
 
mr.cooper69 said:
Short-lived, yes. Diminishing effects, no.

None of these should give you wow effects. They aren't stimulants/work on the reticular activating system. They should improve functional memory.
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My functional memory is usually pretty good, i use noots et al for different effects like increasing energy, clarity, motivation, wit, humor, communication and creativity
 
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.
 
mr.cooper69 said:
For an acute burst of cognitive function, try the NMDA trio of D-Serine, sarcosine, and DAA along with a potentially synergistic AMPA-based agent: aniracetam.
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Can D-Serine, itself, activate the NMDA receptor? Wouldn't a cascade of effects like--preceding agonism of the AMPA receptor, membrane depolarization, NMDA magnesium displacement, and accompanying binding with glutamate--need to be met prior to agonism?

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)?
 
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.
 
mr.cooper69 said:
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.
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Alright, thanks, Coop. I tried to word it the best I could.

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.
 
domore said:
Alright, thanks, Coop. I tried to word it the best I could.

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.
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It is highly unlikely that they would do so unless we are talking about a neuron in vitro. There are influx/efflux control systems in place that go beyond things as simple as co-agonism. The whole neuronal apparatus, including the BBB, is geared to prevent excitoxic insult from oral compounds.
 
mr.cooper69 said:
It is highly unlikely that they would do so unless we are talking about a neuron in vitro. There are influx/efflux control systems in place that go beyond things as simple as co-agonism. The whole neuronal apparatus, including the BBB, is geared to prevent excitoxic insult from oral compounds.
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"You must spread some Reputation around before giving it to mr.cooper69 again."

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?
 
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?
 
rob112 said:
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.
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Well, I just picked it as an example for the statement Coop made. Magnesium Threonate has shown to cross the BBB in some studies. This question was just used as means to help me word my BBB question in regards to D-Serine to which Coop answered. Although compounds can be altered or created to have BBB permeability, "the whole neuronal apparatus, including the BBB, is geared to prevent excitoxic insult from oral compounds." The BBB is an intricately coordinated mechanism for protecting the brain. It won't let things get out of control in most cases.

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?
 
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).
 
mr.cooper69 said:
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).
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I really appreciate it, Coop. Thank you for bearing with me and letting me work through my thought process.

This type of information isn't my line of work, but, man, I am really interested in it.
 
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