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> Metylphenidate & Racetams, Toxicity???
the_newsoul
post Feb 23, 2012, 09:04 AM
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Hello everyone!

I received today Aniracetam and my first plan was taking 750 mg in the morning and 750 mg again at lunch.

After doing some research (I don't know if what I found is corrcect), it appears that aniracetam has two phases. In phase 1, which lasts for about 2 hours, aniracetam works as an anxiolytic. And then, the nootropic effects start in phase two lasting for another 6-8 hours. Overall, the effects would last for about 8-10 hours.

If that is correct, your brain perfomance would decrease in phase 1 and boost in phase 2. Therefore, taking aniracetam in two separate times would not be the best if you are looking to improve your cognition.

It would be great if someone could give me an answer!

Thank you =)

P.S.: I have also ordered ALCAR (500mg) and Choline&Inositol (250 mg of each per pill)
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the_newsoul
post Feb 23, 2012, 03:54 PM
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So, after taking my first dosage of aniracetam today (1500 mg):

The first 1-3 hours were quite great, good mood, chilled but reasoning very well at the same time, and expressing myself really clearly.

After that, i think had a bit of brain fog. Actually its been 10 hours now since I took aniracetam and I dont feel focused, but quite tired.

Second day, downed from 1500 to 750 and added 250mg of choline. Results: less brain fog, but i got a mild headache.

Is it possible that i dont need more choline (I already have 90mg from Vitamin b complex) and that by adding 250mg more I got headache?

I would also appreciate if someone could tell me if its better to take aniracetam once a day or in two times.

Thanx =)
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the_newsoul
post Feb 25, 2012, 04:25 AM
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Day 3:

-Vitamin B complex (with 90mg of choline)
-ALCAR 500mg
-Concerta (methylphenidate) 18 mg
-Aniracetam 750 mg
-Cholina & Inositil -250 mg of each

I think it's working better today. Following Flex's words, you should not feel much taking nootropics. And compared to the first too days, today I dont have any headache, I don't feel tired or with any brain fog so far. I dont really feel anything.

Moreover, I was just reading an old book of mine which explains some stock exchange strategies. I directly went to a passage which I never really understood completly. Today I finally understood it in a way I never did before. It was not so complicated, but I just got it more easily and clearly. I guess this is what all this is about.

So, great news!
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the_newsoul
post Feb 25, 2012, 02:00 PM
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I don't know how to deal with ALCAR and Choline: how much and when to use it. It's been just three days and I have already felt that my memory has already increased, but I also feel demotivated&mentaly tired some hours after taking my current stack. Let me know if you have any suggestions.

Anyone know if Racetams and Metylphenidate do not mix well?

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Denning
post Feb 26, 2012, 01:53 PM
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Thanks for posting these updates. Following along.

You may have said this elsewhere, but were you taking the methylphenidate prior to introducing the Aniracetam/ALCAR/choline or was this stack all started at the same time?
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the_newsoul
post Feb 26, 2012, 03:57 PM
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QUOTE(Denning @ Feb 26, 2012, 01:53 PM) *

Thanks for posting these updates. Following along.

You may have said this elsewhere, but were you taking the methylphenidate prior to introducing the Aniracetam/ALCAR/choline or was this stack all started at the same time?


Been taking metylphenidate for some months now. Started with the rest few days ago. Metyl works well for focus and motivation for me, but i am seeking to improve cognition.

Would like to know ig racetams and cholinergics can be mixed with racetams. I am finding contradictive infos
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the_newsoul
post Feb 27, 2012, 05:48 AM
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RACETAMS VS METYLPHENIDATE

VERSION 1

piracetam will turn the afterburners on for your NMDA receptors. amphetamine elicits glutamate release. prolonged calcium influx through NMDA recetors = NEUROTOXICITY.

if you're interested in some insane tolerance fast, then try it

- nmda & ampa receptor
---these are the 2 receptors which are glutamergic, as in they respond to glutamate, and in doing so, allow ions such as Calcium and Sodium through...... These 2 receptors are thought to play a very important part in Long term potentiation, whereby short term memory is consolidated into long term memory. Piracetam exerts its effect via the NMDA receptor (not by activating it, but probably by making it more responsive to glutamate....) Aniracetam works mainly via the AMPA receptors
http://www.sumanasinc.com/webcontent/anima.../receptors.html
this should give you some insight into these 2 receptor types
- glutamate excitotoxicity
glutamate toxicity is caused when glutamate causes over excitation of nmda and ampa receptors, allowing excess ions to depolarize and activate cellular cascades, which cause over excitation and neuronal damage.
- amphetamine & glutamate release
some studies show that amphetamines cause an increase in extracellular glutamate.... this can have many repercussions if your NMDA and AMPA receptors are 'primed' or locked and loaded
- nmda receptor agonist & antagonist
chemicals that activate or block activity at receptor binding site.... Ketamine is a NMDA antagonist, and so is huperzine......
- piracetam & nmda receptor
piracetam is thought basically to prime the NMDA receptor for more efficient activity or firing, which would in turn increase memory consolidation and long term potentiation... Our fellow angry poster was just worried that you are over priming your NMDA receptor which can have repercussions theoretically, id be interested in reading research which shows evidence of what our fellow poster is worried about
- vinpocetine & DOPAC
vinpocetine use has been shown to mimic reserpine, a bad ass drug.... reserpine is THE DRUG used to INDUCE depression in mice.... one study showed that enough reserpine actually caused rat mommies to abandon, and sometimes kill their newborns.... DOPAC is a metabolite of dopamine breakdown i think, and an increase levels is seen in CSF in both vinpo and reserpine usage....

VERSION 2

Amphetamine acts as a releasing agent of dopamine, whereas methylphenidate is merely a reuptake inhibitor. Amphetamine is more likely to cause dopamine to diffuse out of the synapses and float around in the extracellular fluid. If the amount of free dopamine is excessive, it can damage non-dopaminergic neurons. Simply put, if a neuron is not equipped to handle dopamine then dopamine can damage it. (Actually, dopamine is even a bit toxic to the neurons that are supposed to use it, but those neurons are usually equipped with stronger mechanisms for preventing and repairing that damage. MAO breakdown of dopamine seems to produce some of the toxic compounds, which may be why selegiline and other MAO inhibitors are neuroprotective against both Parkinson's disease and dopaminergic-induced neurotoxicity.)

Amphetamine also releases norepinephrine, which is excitatory. Excitotoxicity is when neurons are turned on too much, and the products of their metabolism begin to damage and kill cells. Glutamate, as the main excitatory neurotransmitter, plays a big role in this. Piracetam seems to have some excitatory effects. So when you combine regular high doses of amphetamine (enough to cause euphoria) with piracetam, there is a POTENTIAL for damage. Considering that neurons and glia are already not happy with excess dopamine floating around the extracellular fluid, the addition of excitotoxicity would be particularly damaging, if it happened.

But I really don't think an amphetamine + piracetam interaction has been proven to occur! The above is speculation, pieced together from various studies examining different types of things. To my knowledge, nobody has studied mammals given doses of amphetamine and piracetam equivalent to those used by humans for cognitive enhancement or ADHD treatment. Please correct me if I'm wrong because I would love to hear about that research. (I'm not particularly interested in research done on animals given megadoses of amphetamine.)

Now, on to methylphenidate. It's not a releasing agent. It's a dopamine and norepinephrine reuptake inhibitor. That means that when one of those neurotransmitters is released into the synapse during normal neurotransmission, some of it will stay in the synapse longer than usual. However, commonly used doses of methylphenidate only block about 40-50% of the transporters in relevant brain areas. Thus, the dopamine and norepinephrine still get pumped back into the synapses. So unlike strong doses of amphetamine, sub-euphoric doses of methylphenidate do not cause enough dopamine to diffuse out into the extracellular fluid and F**K up the non-dopaminergic neurons.

So yeah, MPH does stimulate excitatory transmission to a degree, because it enhances the activity of noradrenergic signals. But it doesn't provoke a release of norepinephrine, and it doesn't push dopamine out into places it shouldn't be. Furthermore, MPH stimulates the inhibitory circuitry of the prefrontal cortex, which is why it's so helpful in controlling hyperactivity and impulsivity.

Thus, MPH just doesn't present much of a risk for excitotoxicity. Piracetam doesn't appear to either. So, unless somebody has a reason we should suspect a risk, why would you? Sure, there's nothing wrong with caution. But caution does not suggest that one expect damage from the MPH + piracetam combination.

Can anybody give some light to this issue???
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