Is Aniracetam just suppose to be stronger...
nhlgoducks 11 Nov 2008
Overall, what do YOU think is better and why? Any objective studies to determine efficacy are also appreciated.
jackinbox 12 Nov 2008
Ghostrider 13 Nov 2008
"More potent" generally only mean that the optimal dose is lower. Each nootropic acts differently and have different effects. While piracetam is tolerated by most people, many people dislike aniracetam because it make them feel dizzy or drowsy. The only one to know if it work for you is to try it. 1fast400.com sell it.
Tried various dosages of both, both did nothing for me that I could tell.
medicineman 13 Nov 2008
-NMDA receptors and AMPA receptors are both major players in memory formation. They are both activated by glutamate. And they are both ionotropic (meaning they allow influx and efflux of ions such as Calcium, Sodium, and Magnesium.) In some really complex circuit of synaptic restructuring, memory is formed through mechanisms allowed by the two receptors mentioned. Aniracetam, like piracetam, is a receptor modulator. It doen't cause firing of any neuron, but it primes your neuron to fire well when it does fire. Aniracetam though, unlike piracetam, has activity on the AMPA site, where as piracetam doesn't. Aniracetam also has some slight activity on Dopamine and Serotonin, and possibly GABA (since it desensitizes Glutamergic Receptors, its very possible it does so by acting on GABA), hence it acts as an anxiolytic. Im not sure how it works there, but I think it might be similar, but weaker, in activity to Bupropion on anxiety (though thats complete speculation on my part, and just on anxiety. bupropion is not a nootropic!). I just felt they did the same thing to my anxiety when I took them.
ImmortalisRX 16 Nov 2008
Galantamine 18 Nov 2008
I have tried both, I feel the Aniracetam is a better stand alone drug but if you are taking other nootropics then it seems to interact more strongly with others nootropics. At least with my brain chemistry.
Like I've said before, piracetam has zero affinity to AMPA receptors, whereas aniracetam does. This is a very important characterization. Piracetam is more of a NMDA receptor modulator. The two are definitely stackable.
VespeneGas 18 Nov 2008
http://www.ncbi.nlm....7?dopt=Abstract
the racetams just make me sleepy, even in really low doses with a high quality choline source :(
medicineman 23 Nov 2008
I'm pretty sure aniracetam has no GABAergic effects. This study suggests "[the] involvement of nicotinic acetylcholine, 5-HT2A and dopamine D2 receptors in the anxiolytic mechanism."
http://www.ncbi.nlm....7?dopt=Abstract
the racetams just make me sleepy, even in really low doses with a high quality choline source :(
I did not mean it exerted its anxiolysis via GABA at all. I said, that possibly, through GABA, it desentisizes Glutamate receptors, thus potentiating the effect of Glutamate on the AMPA and NMDA receptors. Here are two studies, first one bringing forward the idea of an intimate relationship between GABA and NMDA receptors.
"N-methyl-D-aspartate (NMDA) receptors are commonly found post-synaptically; they mediate fast excitatory neurotransmission in the central nervous system. In this study, we provide immunocytochemical data supporting the existence of presynaptic NMDA receptors in GABAergic terminals using polyclonal antisera raised against the C-terminus of the NMDAR1 subunit. At the light microscope level, rich plexuses of NMDAR1-positive varicose fibers were found in various nuclei in the basal forebrain (bed nucleus of stria terminalis, septum, parastrial nucleus, vascular organ of the lamina terminalis), thalamus (paraventricular nucleus, midline nuclei), and hypothalamus (parvocellular paraventricular nucleus, arcuate nucleus, preoptic nucleus, suprachiasmatic nucleus). In the brainstem, labeled fibers were much less abundant and were confined to the ventral tegmental area, periaqueductal gray, parabrachial nucleus, and locus coeruleus. At the electron microscope level, NMDAR1-immunoreactive terminals examined in the bed nucleus of stria terminalis, parvocellular paraventricular hypothalamic nucleus, and arcuate nucleus formed symmetric synapses, contained darkly stained large dense-core vesicles, and displayed gamma-aminobutyric acid (GABA) immunoreactivity. Terminals with similar ultrastructural features were found in the paraventricular thalamic nucleus. These findings demonstrate the existence of NMDAR1 subunit immunoreactivity in subsets of GABAergic terminals, which raises questions about the potential roles and mechanisms of activation of presynaptic NMDA heteroreceptors in the rat central nervous system. The pattern of distribution and ultrastructural features of these boutons suggest that they may arise from local GABAergic projections interconnecting a group of brain structures mediating stress responses and/or other endocrine, autonomic, and limbic functions."
This study shows that chronic NMDA exposure accelerates GABAergic inhibition
"Maturation of excitatory synaptic connections depends on the amount and pattern of their activity, and activity can affect development of inhibitory synapses as well. In the superficial visual layers of the superior colliculus (sSC), developmental increases in the effectiveness of gamma-aminobutyric acid (GABA(A)) receptor-mediated inhibition may be driven by the maturation of visual inputs. In the rat sSC, GABA(A) receptor currents significantly jump in amplitude between postnatal days 17 and 18 (P17 and P18), approximately when the effects of cortical inputs are first detected in collicular neurons. We manipulated the development of these currents in vivo by implanting a drug-infused slice of the ethylene-vinyl acetate copolymer Elvax over the superior colliculus of P8 rats to chronically release from this plastic low levels of N-methyl-D-aspartate (NMDA). Sham-treated control animals received a similar implant containing only the solvent for NMDA. To examine the effects of this treatment on the development of GABA-mediated neurotransmission, we used whole cell voltage-clamp recording of spontaneous synaptic currents (sPSCs) from sSC neurons in untreated, NMDA-treated, and sham-treated superior colliculus slices ranging in age from 10 to 20 days postnatal. Both amplitude and frequency of sPSCs were studied at holding potentials of +50 mV in the presence and absence of the GABA(A) receptor antagonist, bicuculline methiodide (BMI). The normal developmental increase in GABA(A) receptor currents occurred on schedule (P18) in sham-treated sSC, but NMDA treatment caused premature up-regulation (P12). The average sPSCs in early NMDA-treated neurons were significantly larger than in age-matched sham controls or in age-matched, untreated neurons. No differences in average sPSC amplitudes across treatments or ages were present in BMI-insensitive, predominantly glutamatergic synaptic currents of the same neurons. NMDA treatment also significantly increased levels of glutamate decarboxylase (GAD), measured by quantitative western blotting with staining at P13 and P19. Cell counting using the dissector method for MAP 2 and GAD(67) at P13 and P19 indicated that the differences in GABAergic transmission were not due to increases in the proportion of inhibitory to excitatory neurons after NMDA treatment. However, chronic treatments begun at P8 with Elvax containing both NMDA and BMI significantly decreased total neuron density at P19 ( approximately 15%), suggesting that the NMDA-induced increase in GABA(A) receptor currents may protect against excitotoxicity."
And here, a study showing relationship between aniracetam and GABA:
"The effects of the nootropic drugs piracetam and aniracetam on antinociception induced by baclofen, bicuculline, and picrotoxin and on baclofen-induced muscle relaxation were studied in mice. Antinociception was investigated using both the hot plate (thermal stimulus) and abdominal constriction (chemical stimulus) tests. Both behaviour inhibition and muscle relaxation were observed by using the rota-rod test. Piracetam (30 mg/kg, IP) and aniracetam (10 mg/kg, PO) reduced baclofen, bicuculline, and picrotoxin antinociception without modifying analgesia induced by non-GABAergic drugs such as morphine, physostigmine, clomipramine, and diphenhydramine. In this concentration range, piracetam, and aniracetam were also able to reduce the inhibition of rota-rod performance. At higher doses piracetam (100 mg/kg, IP) and aniracetam (100 mg/kg, PO) were able to completely prevent baclofen antinociception. However, when prevention of GABAergic antinociception was complete, piracetam and aniracetam were able to block non-GABAergic antinociception also. Comparing the effects of piracetam and aniracetam with those exerted by the GABAB antagonist CGP 35348, a reduction of non-GABAergic analgesia was also observed using higher doses of CGP 35348 (2.5 μg per mouse ICV). The present results indicate that piracetam and aniracetam, by preventing both of the investigated effects of baclofen, have some selectivity against GABAB-mediated inhibition. The well-known activity of piracetam and aniracetam on learning and memory might, therefore, depend, at least in part, on the removal of inhibitory GABAB mechanisms that impair attention and cognitive functions."
The studies above don't say that aniracetam acts on GABA per say. It shows a somewhat intimate relationship between NMDA, AMPA and GABA receptors. But I just wanted to clarify, I speculated, based on some studies (the above being a couple) I read about the complex relationship between GABA, AMPA, and NMDA receptors, that aniracetam might exert some of its effect by some GABAergic mechanism on its upregulation or modulation of the AMPA receptor. Thats just speculation.
Guest_Isochroma_* 08 Aug 2009
Edited by Isochroma, 08 August 2009 - 04:17 AM.
mentatpsi 10 Aug 2009
For instance, I think Aniracetam is comparable to the effects you might get off of rhodiola rosea. Awhile ago the herb used to give me fogginess, as did Aniracetam. Now when i take rhodiola i get a stimulant type effect and this is also true with Aniracetam. I think it is best to classify Aniracetam as an "adaptogen" for this reason. This is predominately the result of the modulation of the Dopamine-2 (inhibition) and serotonin receptor sites.
Johann 05 Oct 2009
SYNTAX 07 Oct 2009
Is the point of Aniracetam to just last longer than Piracetam? What does it mean to be more potent? Also, does relentless improvement sell Aniracetam, I cant find a reputable dealer that sells this stuff.
Overall, what do YOU think is better and why? Any objective studies to determine efficacy are also appreciated.
I voted in favor of Aniracetam (have not tried Piracetam), but that was a mistake because I didn't take the time to read your poll. I have tried both and my true answer is that I love the two together far more than either of them alone. taking 500mg Piracetam and 200 mg Aniracetam, my naturally strong memory becomes as steel trap. And in my case, the combination (i eat 6 or 7 walnuts one minute before the Aniracetam so that it can bind to an unsaturated fat) with a few soy lethicin pills and a B-complex works every single time. Well, I must be rested too.
425runner 05 Jan 2010
As for a reliable supplier - Smart Powders sells all sorts of nootropics and they're all high quality with COA's....oh and they ship international
Edited by 425runner, 05 January 2010 - 11:05 PM.
csrpj 05 Jan 2010
spider 06 Jan 2010
is it just me, or is this poll really stupidly constructed? only the last two options should be present.
I interpret it the following way. The first two options are for the people that have made a definate decision based solely on the current theories and studies.
The last two options are for members who have actually tried both. They give their oppinion based on their experience.
Tukotih Doji 14 Apr 2010
So the difference is the fact that it is fat soluble, has a shorter half-life, regulates AMPA-receptors and has a higher potency?
Is there anything else?
I've read that people tend to prefer Aniracetam in the long run but prefer Piracetam for single occasions. Perhaps the fact that it is fat-soluble and can have stronger in people that use it regularly.
JonnyDoowop 04 May 2010
Interesting...
So the difference is the fact that it is fat soluble, has a shorter half-life, regulates AMPA-receptors and has a higher potency?
Is there anything else?
I've read that people tend to prefer Aniracetam in the long run but prefer Piracetam for single occasions. Perhaps the fact that it is fat-soluble and can have stronger in people that use it regularly.
Piracetam is a daily thing for me, I wish I could use aniracetam consistently because it has such a noticeable feeling for me.
Guacamolium 04 May 2010
Oxi is my favorite BTW, but damn, if we can get some companies generating new core racetams, I swear they'll be something epic. I understand the ampakine relationship, but the FDA has allowed this so far, let's get the racetams their due!
mentatpsi 04 May 2010
Aniracetam is just so loopy for me. I cannot recall many great experiences from it as an early racetam. I'd rather have a diasteriomer of nicoracetam and see what that's like. Piracetam is just so..... gabanootropic to portmanteau it into a word. Ani just has failed to do it for me - I'm telling you guys it needs alterations molecularly and then it would be fine. It's just so crude to be descriptive.
Oxi is my favorite BTW, but damn, if we can get some companies generating new core racetams, I swear they'll be something epic. I understand the ampakine relationship, but the FDA has allowed this so far, let's get the racetams their due!
Could you go into the molecular alteration notion? Sounds interesting. Also is pharmacology really to the point where slight alterations in chemical structure could be modeled in terms of direct effects or is there still a lot of guesswork?
Also, can you differentiate Piracetam and Oxiracetam for yourself? The two are supposed to be highly similar with mainly strength being the differing quality.
Personally, Aniracetam can work in many ways for me. Sometimes it seems to hinder thought, other times promote it. In general though, I prefer sticking with lower intensity nootropics, but that's a preference thing. The Dopamine augmentation/modulation would be interesting if it didn't come with the Serotonin effect as well. It's somewhat comparable to Rhodiola but much stronger.
Guacamolium 05 May 2010
Aniracetam is just so loopy for me. I cannot recall many great experiences from it as an early racetam. I'd rather have a diasteriomer of nicoracetam and see what that's like. Piracetam is just so..... gabanootropic to portmanteau it into a word. Ani just has failed to do it for me - I'm telling you guys it needs alterations molecularly and then it would be fine. It's just so crude to be descriptive.
Oxi is my favorite BTW, but damn, if we can get some companies generating new core racetams, I swear they'll be something epic. I understand the ampakine relationship, but the FDA has allowed this so far, let's get the racetams their due!
Could you go into the molecular alteration notion? Sounds interesting. Also is pharmacology really to the point where slight alterations in chemical structure could be modeled in terms of direct effects or is there still a lot of guesswork?
Also, can you differentiate Piracetam and Oxiracetam for yourself? The two are supposed to be highly similar with mainly strength being the differing quality.
Personally, Aniracetam can work in many ways for me. Sometimes it seems to hinder thought, other times promote it. In general though, I prefer sticking with lower intensity nootropics, but that's a preference thing. The Dopamine augmentation/modulation would be interesting if it didn't come with the Serotonin effect as well. It's somewhat comparable to Rhodiola but much stronger.
Well, a diasteriomer of nicoracetam SHOULD produce better results than ANI. based on structure. Guesswork is a part of molecular chemistry to a point. Actually - Fun fact - Prozac was the first drug conceived to BE an antidepressant before it was even made.
Oxi equals very intelligent driving force. PIR equals relaxed driving force. That hydroxyl seems to serve well for OXI.
fed_machine 12 Aug 2010
I take Piracetam at 2 grams with a choline source, once a day, an hour before studying.
I take Aniracetam at 600 mg, once a day, an hour or so before studying.
I would take Aniracetam for 4-5 days then get off for the next 4-5 days and then repeat. I would cycle the Piracetam similary.
Am I not taking it long enough or need to take more of it? I'm primarily trying these as concentration-enhancers as I am studying for an important exam. How long before I start to see results?
Thanks a lot in advance!
nito 31 Aug 2010
Spectre 01 Sep 2010
Is it safe to take aniracetam in the mornings and GABA at night before bed? (I also ordered 500 grams of GABA powder, mainly to increase my HGH levels to help stimulate muscle growth and promote deeper sleep). I've heard that SmartPowders is legit and this is my first order from them. Comparable to other vendors, both SmartPowders and Cerebral Health have better priced products. (Other companies selling 60x 750mg aniracetam capsules priced them at $40 on average).
Edited by Spectre, 01 September 2010 - 08:40 AM.
nito 01 Sep 2010
Seems the capsules you buying is cheaper than the powder. I'm just ordering 30 g of ani, alpha, and sulbiatimine right now. I only want 30 because pira never worked for me and i fear ani might end up the same.
health_nutty 02 Sep 2010
Well, I just ordered 60x 750mg aniracetam capsules from SmartPowders today (45 grams for $15), I've never tried aniracetam before but I'm really excited to see how it will affect me. I've only tried piracetam but I'm looking for something stronger and more effective..
Is it safe to take aniracetam in the mornings and GABA at night before bed? (I also ordered 500 grams of GABA powder, mainly to increase my HGH levels to help stimulate muscle growth and promote deeper sleep). I've heard that SmartPowders is legit and this is my first order from them. Comparable to other vendors, both SmartPowders and Cerebral Health have better priced products. (Other companies selling 60x 750mg aniracetam capsules priced them at $40 on average).
It had some weird effects when I took aniracetam close to bed. I would wake up in the middle of the night and be afraid to go back to sleep (no nightmares or any obvious reason). Very very unusual, but happened on three seperate occasions when I took it close to bed. Piracetam at bed did not have this effect. Just something to watch out for.
Introspecta 02 Sep 2010
Spectre 02 Sep 2010
It had some weird effects when I took aniracetam close to bed. I would wake up in the middle of the night and be afraid to go back to sleep (no nightmares or any obvious reason). Very very unusual, but happened on three seperate occasions when I took it close to bed. Piracetam at bed did not have this effect. Just something to watch out for.
I plan on taking only GABA at night, while taking Aniracetam first thing in the morning.
Would taking it with sunflower oil be suitable?