2626 replies to this topic

[Lister]

Please do try and avoid derailing the topic. I'm speaking in general of course unless one of your posts was hidden in which case I might be talking to you.

Domo Arigato Gozaimashita!

[medievil]

I requested a split i think? just throw it in the bin otherwise lol

[medievil]

Brain renin-angiotensin system in cognitive function: pre-clinical findings and
implications for prevention and treatment of dementia.

Angiotensin II
Angiotensin II is the main effector of the reninangiotensin system (RAS). The actual role of Ang II
on learning and memory processes has been difficult
to comprehend. This is probably due to the fact that
the cognitive effects of this peptide are highly dependent on different methodological issues, particularly time and via of administration, number and frequency of training sessions as well as the type of
learned response evaluated. For example, it has been
reported that centrally administered Ang II improves
aversive memory (Braszko, 2002), but using similar
learning tasks, others have shown that this peptide
either impairs or has no action at all on memory
retention (Kerr et al., 2005; Bonini et al., 2006).
Similarly, when angiotensin II is injected directly
into the dorsal neostriatum, retention of a step-down
receptors (Kerr et al., 2005). There is also a possible
role of hippocampal angiotensin II receptors in
voluntary exercise-induced enhancement of learning
and memory in rat (Akhavan et al, 2008).
Some authors indicate that data suggesting the
facilitator effect of angiotensin II on learning and
memory must be interpreted with care, since Ang II
is also a precursor for neuroactive angiotensin
fragments like Ang IV. Thus, different results might
be obtained depending on the time intervals between
the injection of Ang II and the tested behavioral
paradigm (Braszko et al., 2006).
The Ang II receptor antagonists, losartan and
PD123177, which are selective for the AT1 and AT2
receptor subtypes respectively, constitute important
pharmacological tools for the assessment of
behavioral consequences through the modulation of
Ang II function (von Bohlen and Albrecht, 2006;
Hritcu et al., 2009). Several studies have shown that
low doses of losartan and PD123177 improved
scopolamine-impaired performance in a light/dark
box habituation task. Similarly countering effect was
observed in the case of captopril and ceranopril
(Chalas and Convay, 1996).
Long-term potentiation (LTP), a specific form of
synaptic plasticity, is thought to represent a correlation of processes attributable to learning and memory
and has been extensively studied in terms of both its
underlying mechanisms and its behavioral significance. Injection of angiotensin II just above the CA1
field in rats has been shown to block the induction
of LTP (von Bohlen and Albrecht, 1998). Further
experiments have demonstrated that this inhibition
can be blocked by the administration of AT1-receptor antagonists (von Bohlen and Albrecht, 2006).
Recent studies demonstrated that Ang II modulates long-term depression (LTD) in the lateral
amygdala of mice. This effect on synaptic plasticity
may be dependent on AT1 receptors, since losartan
blocked the Ang II induced effect on LTD, whereas
AT2 receptors seem not to be involved. Also, the importance of L-type calcium channels on this process
was demonstrated (Tchekalarova et al., 2007).

[medievil]

"
Yakugaku Zasshi. 1991 Nov;111(11):695-701.
[The study of Chinese herbal medicinal prescription with enzyme inhibitory activity. V. The study of hange-shashin-to, kanzo-shashin-to, shokyo-shashin-to with adenosine 3',5'-cyclic monophosphate phosphodiesterase].

[Article in Japanese]
Suzuki M, Nikaido T, Ohmoto T.

Source

Toho University, School of Phamaceutical Sciences, Chiba, Japan.

Abstract

Fifty-nine species of extracts of Chinese herbal medicinal prescription were tested for inhibitory activity of adenosine 3',5'-cyclic monophosphate (cAMP) phosphodiesterase (PDE). Kanzo-shashin-to showed the highest activity in these prescriptions. Kanzo-shashin-to, Hange-shashin-to and Shokyo-shashin-to, whose contracting crude drugs were very similar, were especially studied among these prescriptions. Pinellia tuber acted as an ascent component for Scutellaria root and a mitigatory component for Giycyrrhiza. Jujube acted as a mitigatory component for Glycyrrhiza. Ginger acted as an additional component for Scutellaria root in cAMP PDE test. This additional effect of 6-gingerol, 6-shogaol from Ginger and baicalin from Scutellaria root were investigated

Ill get a needle later on for my ginseng ginger ampoules, am i the only one here finding this odd? lol
A pharmacy i could get losartan.

Again,i apologize for posting during benzo withdrawal wich made me manic at first. Id like to make clear im not like that even on a once weekly basis.

Edited by medievil, 27 January 2013 - 04:41 AM.

[abelard lindsay]

A female forum user in the other thread confirmed that yes, CILTEP is a female libido enhancer.

!!!!! I was wondering if my cycle was off. I have noticed increased libido. Fascinating

Edited by abelard lindsay, 27 January 2013 - 07:46 AM.

[medievil]

Taking my first ginseng ampoules, hope i dont hit a vein, lol i wonder why they made it exactly like test e ampoules.

[Galaxyshock]

Taking my first ginseng ampoules, hope i dont hit a vein, lol i wonder why they made it exactly like test e ampoules.

Are you sure it is ginseng in there? and not that they were selling you test e "under the counter" thinking you know what's going on lol

[medievil]

I didnt know the cashier, otherwise i get all sort of white powders and ampoules when asking flour and shit haha

Ginsaforce, not a bad name for test e actually.

Edited by medievil, 27 January 2013 - 09:42 AM.

[medievil]

Agyrax, D2 blocker and neuroprotective, helps hungtingson apperantly, its also a antihistamine perhaps good for those that have a hard time sleeping, another potential good addition as D2 blockade increases cyclic AMP. I take it now but need to find the right dose as i dislike the excessive d2 on cilltep, too much talk rather then studying etc. Its a antimuscarinic tough as a bad thing.

[medievil]

Another no for a job, oh well gotta keep looking.

Do you guys notice enhanced social skills?

[alecnevsky]

Medievil,

You should really make your own thread and document your withdrawal symptoms. It would be a lot more useful for you and others in that context. I find it somewhat difficult to be subscribed to this thread at the moment. I do wish you a speedy recovery however.

Edit: Never mind, just saw that you got 3 active threads going.

Edited by alecnevsky, 27 January 2013 - 08:26 PM.

[GetOutOfBox]

I'm wondering what the effects of the CILTEP stack are on ADHD/ADD. On one side, low-levels of cAMP can cause some ADHD/ADD-like issues, however, ADHD/ADD themselves are being more and more associated with Prefrontal-Cortex Dysfunction. cAMP at elevated levels effectively blocks PFC regulation of various parts of the brain by opening up HCN (hyperpolarization-activated cyclic nucleotide-gated channels), which interfere with the PFCs neurons ability to communicate with the rest of the brain. In fact, one novel ADHD treatment, Guanfacine, aka Intuniv, work by actually reducing cAMP.

[abelard lindsay]

I'm wondering what the effects of the CILTEP stack are on ADHD/ADD. On one side, low-levels of cAMP can cause some ADHD/ADD-like issues, however, ADHD/ADD themselves are being more and more associated with Prefrontal-Cortex Dysfunction. cAMP at elevated levels effectively blocks PFC regulation of various parts of the brain by opening up HCN (hyperpolarization-activated cyclic nucleotide-gated channels), which interfere with the PFCs neurons ability to communicate with the rest of the brain. In fact, one novel ADHD treatment, Guanfacine, aka Intuniv, work by actually reducing cAMP.

cAMP signaling is complex and highly compartmentalized.

I went through this already briefly:

http://www.longecity...post__p__557966

and here is me explaining it a little more exhaustively to unbeatable king about 10 pages ago at the end of a rather epic argument:

http://www.longecity...post__p__557966

The upshot of the whole thing was that the right mix of PDE inhibition that luteolin (artichoke) provides works better than quercetin or other PDE inhibitors which are less effective. Also, Rolipram reverses guanfacine's effects to levels slightly better than saline. On its own it does slightly better than saline so it doesn't make things worse than baseline.

Edited by abelard lindsay, 29 January 2013 - 04:45 AM.

[peakplasma]

I'm wondering what the effects of the CILTEP stack are on ADHD/ADD. On one side, low-levels of cAMP can cause some ADHD/ADD-like issues, however, ADHD/ADD themselves are being more and more associated with Prefrontal-Cortex Dysfunction. cAMP at elevated levels effectively blocks PFC regulation of various parts of the brain by opening up HCN (hyperpolarization-activated cyclic nucleotide-gated channels), which interfere with the PFCs neurons ability to communicate with the rest of the brain. In fact, one novel ADHD treatment, Guanfacine, aka Intuniv, work by actually reducing cAMP.

cAMP signaling is complex and highly compartmentalized.

Also, may I add that it is difficult to extrapolate from rodent-studies since rats do not really have a comparable Prefrontal Cortex ¹.

A more relevant Monkey study revealed no significant effect on normal prefrontal cortical function in Young Adult Monkeys. However, at high doses it significantly impaired working memory performance in Aged Monkeys - the authors attribute this to age-related changes in the cAMP-PKA signaling pathway ²

Here is a figure from the aforementioned study.



So the CILTEP-working memory issue is a moot point. Unless, you're an octogenarian with severe deficits in your PFC cAMP/PKA pathway.

[GetOutOfBox]

I'm wondering what the effects of the CILTEP stack are on ADHD/ADD. On one side, low-levels of cAMP can cause some ADHD/ADD-like issues, however, ADHD/ADD themselves are being more and more associated with Prefrontal-Cortex Dysfunction. cAMP at elevated levels effectively blocks PFC regulation of various parts of the brain by opening up HCN (hyperpolarization-activated cyclic nucleotide-gated channels), which interfere with the PFCs neurons ability to communicate with the rest of the brain. In fact, one novel ADHD treatment, Guanfacine, aka Intuniv, work by actually reducing cAMP.

cAMP signaling is complex and highly compartmentalized.

Also, may I add that it is difficult to extrapolate from rodent-studies since rats do not really have a comparable Prefrontal Cortex ¹.

A more relevant Monkey study revealed no significant effect on normal prefrontal cortical function in Young Adult Monkeys. However, at high doses it significantly impaired working memory performance in Aged Monkeys - the authors attribute this to age-related changes in the cAMP-PKA signaling pathway ²

Here is a figure from the aforementioned study.



So the CILTEP-working memory issue is a moot point. Unless, you're an octogenarian with severe deficits in your PFC cAMP/PKA pathway.

Yeah, I'm not worried that normal people would have issues, since I'd assume it would take a lot of a PDE4 inhibitor/cAMP releaser to increase levels of cAMP to those enough to be pathological. However, I worry that if impaired PFC function is the cause of ADHD symptoms as many newer studies are suggesting, that raising cAMP could worsen the problem.

[abelard lindsay]

Yeah, I'm not worried that normal people would have issues, since I'd assume it would take a lot of a PDE4 inhibitor/cAMP releaser to increase levels of cAMP to those enough to be pathological. However, I worry that if impaired PFC function is the cause of ADHD symptoms as many newer studies are suggesting, that raising cAMP could worsen the problem.

Let me make this really simple. The results of the Rolipram/Guanafacine study is summarized as follows:

1. Guanafacine reduces cAMP in the PFC which improves working memory. (There are many other parts of the brain where cAMP plays different roles and is regulated by different PDE4 enzyme variants e.g PDE4A2, PDE4D5, etc)
2. Rolipram reverses this effect.
3. Rolipram does not make things any worse than baseline on its own. In fact there is slight improvement in performance, but it's not statistically significant.

So the upshot is is that if you love guanafacine's effects more than you like CILTEP's then you're going to have to make a choice between the two because it's likely that the PDE4 inhibition in CILTEP will cancel the effect of CILTEP on working memory but not make it any worse than baseline on its own. So, in conclusion, you should be no worse than baseline with regards to working memory if you take CILTEP based on the study I referenced earlier (http://www.ncbi.nlm....pubmed/17101879).

[GetOutOfBox]

Yeah, I'm not worried that normal people would have issues, since I'd assume it would take a lot of a PDE4 inhibitor/cAMP releaser to increase levels of cAMP to those enough to be pathological. However, I worry that if impaired PFC function is the cause of ADHD symptoms as many newer studies are suggesting, that raising cAMP could worsen the problem.

Let me make this really simple. The results of the Rolipram/Guanafacine study is summarized as follows:

1. Guanafacine reduces cAMP in the PFC which improves working memory. (There are many other parts of the brain where cAMP plays different roles and is regulated by different PDE4 enzyme variants e.g PDE4A2, PDE4D5, etc)
2. Rolipram reverses this effect.
3. Rolipram does not make things any worse than baseline on its own. In fact there is slight improvement in performance, but it's not statistically significant.

So the upshot is is that if you love guanafacine's effects more than you like CILTEP's then you're going to have to make a choice between the two because it's likely that the PDE4 inhibition in CILTEP will cancel the effect of CILTEP on working memory but not make it any worse than baseline on its own. So, in conclusion, you should be no worse than baseline with regards to working memory if you take CILTEP based on the study I referenced earlier (http://www.ncbi.nlm....pubmed/17101879).

Well, what I'm concerned about is that something like Forskolin, which increases the release of cAMP, will raise cAMP levels in the PFC as well. Normally this is fine, even beneficial, but the issue in ADHD individuals is that excessive cAMP is causing HCNs to open up, temporarily (not physically disconnecting, but preventing electrical propagation) disconnecting affected neurons in the PFC from other neurons. So raising cAMP with something like Forskolin, could worsen behavioral issues by exacerbating the PFC problem. I realize that different PDE4 enzymes regulate cAMP in different parts of the brain, which is why I'm less concerned about the PDE4 inhibition part of CILTEP and more worried about the increased cAMP release brought about by Forskolin, which if I understand correctly, has more of a global effect. Keep in mind that Rolipram is just like the Artichoke part of CILTEP, it's a PDE4 inhibitor. So yes, as you said, assuming the variant of the enzyme it affects does not handle cAMP in the PFC, it shouldn't cause a problem. Additionally note that the studies using Rolipram on monkeys did not test it on monkeys with pathological cAMP levels (such as those possibly brought about by ADHD, or artificially induced with something like high-levels of Forskolin). So in those with normal levels of cAMP, I'm sure it's effect on PDE4 inhibition would be much safer.

But after considering what you've said regarding different variants of the PDE4 enzyme, even if my concerns are founded, the upside is that Guanafacine could theoretically be combined with the CILTEP stack. This would allow for the effects of raised cAMP in unaffected parts of the brain to be enjoyed, while blocking the effects in the PFC.

[usernameiuse]

Abelard, I must thank you for your research. I tried CILTEP a while back.

2x300 mg Twinlab Artichoke Extract
3.85 mg Forskolin Solaray
500 mg Twinlab L Phenylalanine

Didn't feel much for a couple of weeks, but slowly and steadily some glorious effects manifested.

I stopped a month or two ago because money was tight. I'm looking to start it up again, and was looking to combine it with a racetam this time. Noopept seems to work well with CILTEP (A friend of mine combines them and loves it) but I haven't the money for a scale or to buy it pre-capped. Aniracetam is obviously out. Is there any info about prami or oxi combining well with this stack? Those would work for me because I can just do scoops and get the dose right, but if they interact badly like ani then I won't bother.

[health_nutty]

Abelard, I must thank you for your research. I tried CILTEP a while back.

2x300 mg Twinlab Artichoke Extract
3.85 mg Forskolin Solaray
500 mg Twinlab L Phenylalanine

Didn't feel much for a couple of weeks, but slowly and steadily some glorious effects manifested.

I stopped a month or two ago because money was tight. I'm looking to start it up again, and was looking to combine it with a racetam this time. Noopept seems to work well with CILTEP (A friend of mine combines them and loves it) but I haven't the money for a scale or to buy it pre-capped. Aniracetam is obviously out. Is there any info about prami or oxi combining well with this stack? Those would work for me because I can just do scoops and get the dose right, but if they interact badly like ani then I won't bother.

I use Pram with the CILTEP stack and it works great. Note that I also tried with with Ani and CILTEP exaggerated the brain fog I would sometime get from Ani.

Edited by health_nutty, 30 January 2013 - 10:16 PM.

[noos]

Is there any replacement for forskolin?

[abelard lindsay]

Is there any replacement for forskolin?

Sesamin had an interesting study (http://www.ncbi.nlm....pubmed/22293035) that said it raised cAMP levels. However, ZrBarnes tried it a few pages back and said it didn't work very well. The herb coleus forskohlii, which contains forskolin, is available at any vitamin shop and cheap so I don't know why you'd want to replace it in the stack.

[usernameiuse]

Abelard, I must thank you for your research. I tried CILTEP a while back.

2x300 mg Twinlab Artichoke Extract
3.85 mg Forskolin Solaray
500 mg Twinlab L Phenylalanine

Didn't feel much for a couple of weeks, but slowly and steadily some glorious effects manifested.

I stopped a month or two ago because money was tight. I'm looking to start it up again, and was looking to combine it with a racetam this time. Noopept seems to work well with CILTEP (A friend of mine combines them and loves it) but I haven't the money for a scale or to buy it pre-capped. Aniracetam is obviously out. Is there any info about prami or oxi combining well with this stack? Those would work for me because I can just do scoops and get the dose right, but if they interact badly like ani then I won't bother.

I use Pram with the CILTEP stack and it works great. Note that I also tried with with Ani and CILTEP exaggerated the brain fog I would sometime get from Ani.

Yea I've seen several places talking about aniracetam and CILTEP not being good bedfellow due to brainfog. I hear pram has the longest half-life of the racetams but I've also heard it can cause depression in some individuals. Would you mind giving some details about your experience with pram+CILTEP?

[lourdaud]

Where can you get the cheapest forskolin currently?
And does anyone know where to get luteolin and rolipram?

Btw, forskolin should help with caffeine withdrawal right?

[GetOutOfBox]

Where can you get the cheapest forskolin currently?
And does anyone know where to get luteolin and rolipram?

Btw, forskolin should help with caffeine withdrawal right?

It's available at most largish vitamin/health stores. You'll probably have good luck at an alternative-medicine/healthy living type store, before researching into noorotropics I never thought I'd step into one, considering how most of what they sell is BS. However, they do tend to have a much larger selection of the non mainstream type things, so when it comes to things like Rhodiola Rosea or Forskolin, you'd have the best luck there. It should be pretty cheap, my bottle of 60 capsules cost me about $10.

As for caffeine withdrawal, sure it might help part of the effects that are related to caffeine's effect on cAMP, though most of the symptoms are related to other systems of the brain (i.e adenosine, dopamine, etc).

[dreth7]

Would caffeine be recommended on this stack due to it being a non selective phosphodiesterase inhibitor?

[jadamgo]

Yes, some sort of stimulant is often recommended with this stack, and caffeine is a popular choice due to its safety, availability, and as you said PDE inhibition.

On another topic, WhatAreNootropics.com has a great article about this stack. I don't know if you guys have heard of it, or even if one of you might actually run the place or submit articles there, but for anyone interested in a summary, check it out here: http://www.whatareno...ciltep-regimen/

One more thing: I'm trying this today. I've got NOW Artichoke Extract (450mg), and the NOW "Diet Support" formula that contains ~6mg forskolin per capsule. And 125mg L-carnitine, 110mg hydroxycitric acid, 100mg decaf green tea extract, and 25mg of Uva Ursi extract. (Let's hope it's a terrible diet pill, because the last thing my flat ass needs is to lose weight.) Updates will follow.

For reference, I'll be using this with my usual MPH schedule of 2.5mg every 2 hours. (Okay if we're being honest it's actually "every whenever-the-fuck-I-remember hours" and I also do 5mg at "oh shit, I haven't taken any in forever!" o'clock.) And also however much bright light therapy I have the patience for, so up to 2 hours.

[health_nutty]

Abelard, I must thank you for your research. I tried CILTEP a while back.

2x300 mg Twinlab Artichoke Extract
3.85 mg Forskolin Solaray
500 mg Twinlab L Phenylalanine

Didn't feel much for a couple of weeks, but slowly and steadily some glorious effects manifested.

I stopped a month or two ago because money was tight. I'm looking to start it up again, and was looking to combine it with a racetam this time. Noopept seems to work well with CILTEP (A friend of mine combines them and loves it) but I haven't the money for a scale or to buy it pre-capped. Aniracetam is obviously out. Is there any info about prami or oxi combining well with this stack? Those would work for me because I can just do scoops and get the dose right, but if they interact badly like ani then I won't bother.

I use Pram with the CILTEP stack and it works great. Note that I also tried with with Ani and CILTEP exaggerated the brain fog I would sometime get from Ani.

Yea I've seen several places talking about aniracetam and CILTEP not being good bedfellow due to brainfog. I hear pram has the longest half-life of the racetams but I've also heard it can cause depression in some individuals. Would you mind giving some details about your experience with pram+CILTEP?

Pram is the most effective racetam of the major 4 (Pir, Ani, Oxi, Pram). The effects I notice most are motivation and confidence. Executive reasoning is also improved: my ability to determine the correct solution and break it down in managible chunks.

The CILTEP stack has been mildly beneficial for me with increasing motivation. I'm able to add it to Pram without any side effects.

[jadamgo]

Update: After taking 1 of each capsule (450mg Artichoke extract, ~6mg forskolin, plus the other stuff in the "diet support" capsule), I noticed a mild increase of extraversion, energy, and libido above and beyond what the light therapy would ordinarily do. I also find that MPH was slightly potentiated.

The effects seemed to be wearing off after about 4 hours, so I took another 1 of each capsule. The effects are coming up as I type this, and I notice the MPH that was already in my system has been potentiated a lot more than it was with the first dose, leading to a bit of attentional tunnel-vision -- I'm hyperfocused, which is not well-suited to this job. I also feel increased mental energy, though also mild anxiety. It's nothing I can't handle, but I'd prefer not to have to handle it at all. Since MPH doesn't generally make me feel anxious at any dose, I believe that's a side effect of the stack itself, not of potentiating the MPH.

For now, my plan is to dose MPH as needed for the rest of this work shift, which may require a decrease of dosing frequency from every 2ish hours to every 3ish hours.

Tomorrow, I need to either take one forskolin and two artichoke, or one artichoke and two forskolin; two capsules of each component is too much but one of each is not enough to really do anything.

Any suggestions?

[tatu]

Wow, interesting study I stumbled across. It's from 2004! Can't believe nobody brought it up before.

http://en.wikipedia....rm_potentiation

LTP is widely considered one of the major cellular mechanisms that underlies learning and memory.

http://jn.physiology.../91/5/1955.long

Abstract

Chemically induced long-term potentiation (cLTP) could potentially work by directly stimulating the biochemical machinery that underlies synaptic plasticity, bypassing the need for synaptic activation. Previous reports suggested that agents that raise cAMP concentration might have this capability. We examined the cLTP induced in acute slices by application of Sp-cAMPS or a combination of the adenylyl cyclase activator, forskolin, and the phosphodiesterase inhibitor, rolipram. Under our conditions, cLTP was induced but only if inhibition was reduced. We found that this form of cLTP was blocked by a N-methyl-D-aspartate receptor (NMDAR) antagonist and required the low-frequency test stimulation typically used to monitor the strength of synapses. Interestingly, similar LTP could be induced by lowering the Mg²⁺ concentration of the ACSF during forskolin/rolipram or Sp-cAMPS application or even by just lowering Mg²⁺ concentration alone. This LTP was also NMDAR dependent and required only a few (∼5) low-frequency stimuli for its induction. The finding that even low-frequency synaptic stimulation was sufficient for LTP induction indicates that a highly sensitized plasticity state was generated. The fact that some stimulation was required means that potentiation is probably restricted to the stimulated axons, limiting the usefulness of this form of cLTP. However, when similar experiments were conducted using slice cultures, potentiation occurred without test stimuli, probably because the CA3–CA1 connections are extensive and because presynaptic spontaneous activity is sufficient to fulfill the activity requirement. As in acute slices, the potentiation was blocked by an NMDAR antagonist. Our general conclusion is that the induction of LTP caused by elevating cAMP requires presynaptic activity and NMDA channel opening. The method of inducing cLTP in slice cultures will be useful when it is desirable to produce NMDAR-dependent LTP in a large fraction of synapses.

Hi,

I'm curious about this portion of the study cited above:

"Our general conclusion is that the induction of LTP caused by elevating cAMP requires presynaptic activity and NMDA channel opening"

Does this mean that the stack won't work unless we take NMDA channel activating drugs?

I've started taking this stack (CLTEP) for two days now.

In the morning:

1 tab Forskolin (18%)
1 tab Quercetin
1 tab Ginko
750 mg Piracetam
500 mg Choline Bitartrate

and afternoon:

1 tab Forskolin (18%)
1 tab Artichoke Extract
1 tab Ginko
750 Piracetam
500 mg Choline Bitartrate

Objective experience:

I had 2 back to back 40 minute study sessions. I fell asleep from 3-7 pm. Intermittently waking up in between and having a bite to eat. I finished studying at around 8:10 pm.

Also noted a recurrent abnormal sensation, right anterior chest wall. Not painful, but definitely not normal.

The effects are very subtle, if anything... for me at least.

[jadamgo]

No, you don't need to take NMDA agonists. NMDAR activation is a normal feature of the brain -- that's why NMDAR antagonists induce anesthesia in sufficiently high doses.

If you want to improve the CILTEP stack's memory formation benefits, your best options are to increase dose, or add/increase other nootropics like racetams or galantamine. (750mg piracetam 2ce a day isn't really very much, I'd double, triple, or quadruple that amount.)

How much forskolin is in those tablets? And how much quercetin and artichoke?