Aniracetam

Aniracetam, a compound belonging to the racetam group, was developed in the 1970s by a Belgium lab and was brought to market as a nootropic supplement in 1979. Since then, it has undergone continuous research in an effort to pin point its precise effects and mechanisms of action, with several theories being suggested. The general consensus, however, is that the nootropic supplement targets neurotransmitters in the brain, enhancing both mood and cognition immensely.
Nonetheless, before starting on a supplementation course with Aniracetam, it can be helpful to know how the smart drug acts on the body along with the results others have achieved from using it.

How it works

aniracetam how it worksAniracetam is able to effortlessly cross the blood-brain barrier making it easier to target the brains neurotransmitters, which are chemicals that pass on signals from one neuron to another.

One such neurotransmitter is acetylcholine, which is involved in areas of the brain associated with a number of cognitive processes including memory, learning ability and attention span. Aniracetam binds to acetylcholine receptors, decreasing the rate of their desensitization as well as promoting greater acetylcholine release at neuron synapses. As a result, acetylcholine activity in the brain is prolonged.

Aniracetam also targets the neurotransmitter Glutamate, specifically modulating its AMPA receptors. The supplement binds to these receptors when they are inactive, increasing the rate of transfer by which Glutamate (and the signal it carries) is received in the synaptic receptors of the next neuron. AMPA receptors are also concerned with long term potentiation and synaptic plasticity, the process by which the brain learns and stores new memories. Aniracetam is thought to optimize this process by facilitating the building of new synapses and neuronal connections.

Aniracetam is renowned as the most effective mood enhancing nootropic, as it stimulates the AMPA receptors that control glutamate. Glutamate is necessary for the production of GABA (gamma aninobutryic acid). Low levels of GABA in the brain are associated with anxiety disorders and can induce seizures and panic attacks. However, GABA supplements are unable to effectively reduce anxiety as they cannot cross the blood-brain barrier. Whereas, Aniracetam is able to leave the blood stream and enter the brain tissue allowing it to effectively inhibit brain signals that cause anxiety.

Benefits

Memory and Learning

Aniracetam has exhibited positive effects on both short-term and long-term memory. By increasing acetylcholine and glutamate activity in areas responsible for long-term memory formation, like the hippocampus, Aniracetam assists with learning new information and recalling past memories more proficiently.

However, memory improvement may vary. For instance, some users report being able to remember detailed facts and figures more easily, whilst others are able to recall dreams and conversations more vividly.

Improved learning capacity is also due to the role of Glutamate receptors in maintaining synaptic plasticity. Greater plasticity of the brain improves the ability to learn new things and adapt to changing environments with ease.

Studies have further shown that Aniracetam optimizes communication between the left and right hemispheres of the brain while some users note an increase in their attention span and concentration. This enhanced fluidity between the ‘creative’ and ‘logical’ sides of the brain, along with Aniracetam's role as a focusing agent has resulted in many users being able to read, write and communicate effectively, with less strain.

Mood

Aniracetam is also known as an anxiolytic nootropic, for its modification of dopamine and GABA levels, resulting in mood enhancing and anti-depressant qualities. In many parts of Europe, the compound is administered as treatment for depression and anxiety disorders, despite both conditions having different symptoms. This is due to Aniracetam’s effect being determined by one’s current mood. For example, users who felt fatigued and depressed prior to the supplementation program, felt stimulated by Aniracetam, whereas, people who were otherwise nervous and stressed felt a calming and relaxing effect. Potential users should take into consideration that a loss of inhibition is likely.

Owing to its effect on Serotonin levels, people who suffer from insomnia could use Aniracetam to regulate their sleep patterns.

Protection

In addition, Studies claim that Aniracetam has a protective function against external damage to the brain. In some instances it has been shown to reverse harmful effects of excessive alcohol consumption.

Cognitive decline due to aging is also slowed down as Aniracetam optimizes learning and memory processes that would otherwise be damaged.

aniracetam side effectsSide Effects

Aniracetam is known for its mild side effects and non-toxic compound. Nevertheless, potential users should consult a medical professional as to whether their medical history or current prescriptions support an Aniracetam supplement program. Pregnant or nursing mothers are advised not to use the supplement.

Headaches are the most commonly reported side effect of Aniracetam usage and are more frequent amongst those who are taking a dosage higher than the recommended amount. The addition of a choline supplement, such as Alpha GPC or Citicholine, has been shown to reduce these headaches.

Exhaustion and mild nausea may occur but these side effects should lessen eventually. A decrease in dosage should be considered if these effects do not fade and become more uncomfortable.

A higher dosage than recommended may also lead to anxiety. The following dosage guidelines should help you avoid any serious side effects.

Dosage Guidelines

The generally accepted dosage of Aniracetam ranges between 750 mg to 1500 mg a day. However, a new user should start their course at 750 mg or lower and then gradually increase their dosage if there are no negative side effects. A new user should also note that the supplement may take up to two weeks to build in their system.

Aniracetam has a short half-life of approximately 2 hours and so it is important to supply your body with the compound more than once a day. Therefore the recommended dosage should be divided into at least two or three equal administrations each day, preferably at morning, noon and night.

Aniracetam review and experience

Hello all... I wanna share this frustrating experience that i just had (and kind of still having) on aniracetam. Has anyone experienced the same thing and got any idea as to why the following happened?

I took around 350mg of aniracetam and after about 20 minutes noticed increased physical energy (not so much as on high dose of caffeine but still very noticeable) as well as restlessness. I started jumping from doing one thing to another and couldn't sustain any activity systematically for longer than 10-15 min. Tried reading a book and eyes were jumping from one line to another. I was in such a bag brainfoggy state that I couldn't even pin down what I was thinking about 2-3 hours ago. My thoughts were a complete mess and emotionally I felt really blunt. I wasn't myself. This probably lasted for about 2 hours after which my body felt really weak and all I could do is lie on bed in this hazy state of mind until I fell asleep.

Aniracetam questions and answers

I have read that many racetams are neuroprotective. Yet, if they are AMPA modulators (e.g. oxiracetam and aniracetam) and thus increase glutamate, could they not potentially lead to glutamate excitotoxicity since excess glutamate is the first step in causing it?

Answer 1

Glutamate is necessary for learning. Lots of things will increase glutamate levels. An excessive increase can cause excitoxic problems. I haven't heard of it being a problem with either aniracetam or oxiracetam but I've seen possible evidence with sunifiram.

Answer 2

I do believe they decrease the threshold for excitotoxicity. If you want to combat this, you'll want to supplement Magnesium and either Agmatine or Memantine. After many months of using ampakines and noopept, however, I've made the decision to stay away from them entirely. They gave me increasingly bad hangovers and mental fog and the benefits of taking them just weren't worth it. They were great at first, but towards the end not so much. I feel great now that I'm off of them, and feel that taking noopept had some permanent positive effects on my memory.

Answer 3

Some people report overstimulation with some racetams, yes that can contribute to excitotoxicity. It's the same as any stimulant, some racetams also have that effect. Others do not however, so it just depends on the drug and the person. But if one is already anxious, then adding a stimulating racetam is not a good idea. They are not magic pills for intelligence. They are dirty bombs that may help achieve an intelligence goal. If they improve performance but cause over-excitation, then you might only use them during tests or sporting events.

Answer 4

the glutamate-gaba relationship and the causes of neuronal apoptosis are more complex than you think, so don't worry. And yes, you should stack racetams with magnesium (and some choline source and HUP-A to buffer fast depolarisation, maybe even some ginseng to lower neuronal fatigue via non-specific ACTH way and lowering blood sugar in your brain):
1. First, racetams - especially Noopept as being piracetam analogue with really small molecules as my fav - inhibits slow, inactivated potassium without influencing calcium or fast potassium channels. This results in the most "healthy" way to induce excitation of neurons and promoting intensive learning and deep-thinking process. Opening potassium channels is also associated with protection against stroke.
2. Next mehanism of protection is prevention against unwanted aggregation of proteins on different brain's features. Alfa and beta sheets are second level of brain protein structure and often oversimplified regarded as good and bad. Some of them (again speaking of noopept as "piracetam matching partner", asserting the highest neuroprotective level) are producing beta sheets which are considered a synonym for amyloid diseases. Wait, what? Yes, through the fibrilization of alpha-synuclein noopept produce longer beta sheets, what is believed to be neuroprotective in vivo - a novel doctrine actually suggests that shorter, misfolded oligomergic structures are way more cytotoxic. The form, structure, the lenght is much more decisive as just alpha and beta distinction.
3. Glutamate is the chief excitatory neurotransmitter, while GABA is the main inhibitory. It is not angel vs. devil relationship. NMDA and AMPA receptors can be overactived by the glutamergic storm, leading to aggregation of extracellular plaques or coating of cerebral blood vessels. This is often associated with the reduction of the neurotransmitter GABA that inhibits neuronal firing. So, it is optimal to suppress excessive glutamate which makes the cortical circuits more responsive and selectively susceptible to sensory stimulation. But even this can have adverse effects since rapid desensitization of AMPA receptors leads to so-called excitatory feedback (that is a known cognitive obtruder). You can buffer this using Huperzia serrata extract.
4. Potassium-magnesium relation is even more enteresting (meaning: on good days behaving nice, on bad...worst:D). Magnesium usually reduces amplification of NMDA receptor by blocking calcium out - this is seen as completely normal process of depolarization in which magnesium or calcium is being excpelled out of the receptor. This allows calcium ions into the NMDA channel, what leads to enhanced transmission and long term potentiation. But excitatory cells are one thing which cannot always be understood in an orderly fashion. Weak stimulus alone will not induce LTP, but cooperatively via weaker stimulation of many, they can generate depolarization to induce LTP . Our goal is the activation of NMDA receptors at its weakest possible input by selectively reducing the flux of calcium ions, associated with any uncorrelated activity - this enhances both short-term synaptic facilitation and synaptically induced LTP . The relation between calcium and magnesium ions must be seen as a homeostatic and non-linear mechanism - too much of calcium ions results in apoptosis, too little in long-term synaptic depression and clouding of consciousness. If out brain and nutrition regimen is optimal both of them can act as promoters of LTP - calcium ions promote LTP at high excitation and magnesium ions at low excitation. None of this process is neurotoxic.
5. There are some genotype- and phenotype- related mechanism on which we don't have much of control. GABA and glutamate may produce normal repolarization in must people, but in some may also strengthen glutamergic synaptic transmission while making GABA synapses totally inhibitory. Some of there irregularities, especially when depolarization doesn't happen, may even lead to apoptosis of neurons, since GABA and glutamate add up, leading acutely to jitter, but in long term to excitotoxicity.

So, the apoptosis of neurons is still to complex to be fully understood....eat well, sleep long, exercise and blend reasonable dosage of nootropics with unreasonable high dosege of adaptogens:)

I just got my cdp choline and aniracetam. How often do I take these? Or what has worked best for you? Thanks in advance!

Answer 1

1500 mg Aniracetam in the morning, with food and 400 mg cdp choline with it. Then if you want more - 750 mg Aniracetam in the afternoon, again with some food (fish is the best) and 400 mg cdp choline. Skip the weekend if you can, to not build a tollerance. Don't drink alkohol with it, to keep your GABA receptors safe.

Answer 2

normally go for 750-800mg of ani up to 3 times per day. With a break at weekends or lazy days :)

Answer 3

Only take choline source every other day at most, unless experiencing any headaches then top up accordingly. Choline sources too regularly brings about feelings of depression in me, so I use sparingly.

Is/has anyone taking/taken fasoracetam? What dosage? Any results? I don't feel any real results from it...I'm interested in trying Aniracetam, as I seem to recall reading that it helps with anxiety and promotes creativity. Tianeptine didn't seem to do a single thing for me, and neither did Noopept. Not sure I respond to ANYTHING besides Modafinil.

Answer 1

 I don't remember what dosage I was taking when I had some probably 20-40mg but I've taken up to 100mg. Can get overstimulating at that dosage. Where are you getting your noots? Quality varies from vendors. Aniracetam is great for a calm sense of well being. Tianeptine has been my biggest responder.

Answer 2

I usually only take Faso on days I'm taking Phenibut. I always take A-GPC with racetams, tho sum say it is not needed unless you r experiencing a headache from the racetam. Phenyl-Piracetam and Oxiracetam are quite noticeable do to their stimulant properties.

Answer 3

I've wanted to try Oxiracetam, too. So far, I've tried Noopept, Piracetam, Phenibut, Tianeptine, Modafinil, PEA...a few others. A company called Chaos and Pain used to make a power drink called Aggro that had the perfect blend of Noots in it and I felt amazing on it. I think the FDA gave them grief, as they've completely changed the formula around. It used to contain Noopept, etc...

Should you feel the effects of Aniracetam on the first day? Took 1400mg total yesterday and not sure if I felt anything...

Answer 1

it's cumulative, meaning it takes a while to feel effects. this applies to other racetams as well, but in my experience I've felt everything I've tried the first time, except aniracetam which I took for 3 weeks without ANYTHING... with fat every time of course (fat soluble compound)

Answer 2

 I didn't notice it the first time either but it can really reduce anxiety while sharpening up the brain. Adding it to a blenderized smoothie with some emulsified fats (fat source + lecithin) might help.

Answer 3

 I bought a big tub of it from powder city, I mix it with choline and yogurt every morning for breakfast, took about 3 days to start noticing subtle differences. Went on vacation for 4 days after being on it gor 2 months and didn't have it and could definitely tell I was more foggy.