2626 replies to this topic

[rikelme]

The body can adapt to millions of things as we all know. It's best to break from it at this point and try something entirely new. In essence, you're also stating that you felt no discernible effect from using NADH as well? Have you ever used it by itself? I ask because it was on my list of things to try. Also, was it in a capsule or tablet taken sublingually?

Actually NADH + methylcobalamin combo works quite well for me: clears my head, and gives me quite an [mental] energy boost - I do feel sharper. As a quick [objective?] test if something works for me or not I do mental (in head) multiplications of two two-digit numbers larger than 50. When on NADH + methylcobalamin combo I can finish the calculations much quicker compared to my baseline (15-16 secs compared to 20 secs for baseline).

I'm taking 10mg NADH and 5mg methylcobalamin sublingual.

[xsiv1]

The body can adapt to millions of things as we all know. It's best to break from it at this point and try something entirely new. In essence, you're also stating that you felt no discernible effect from using NADH as well? Have you ever used it by itself? I ask because it was on my list of things to try. Also, was it in a capsule or tablet taken sublingually?

Actually NADH + methylcobalamin combo works quite well for me: clears my head, and gives me quite an [mental] energy boost - I do feel sharper. As a quick [objective?] test if something works for me or not I do mental (in head) multiplications of two two-digit numbers larger than 50. When on NADH + methylcobalamin combo I can finish the calculations much quicker compared to my baseline (15-16 secs compared to 20 secs for baseline).

I'm taking 10mg NADH and 5mg methylcobalamin sublingual.

Thanks for the feedback. I take some Methylcobalamin in the morning that's already in my B-Complex and then I'll take 5mgs sublingually at around 2:30pm along with a capsule of Peak ATP and find that it helps some. I'd like to add NADH since I've never tried it and am actually looking for that bit of a mental & physical boost. I usually switch things up after some time aside from my staple vits/mins, antioxidants and efas. So, then I'm understanding the combination of those two made no difference to the actual effects that the CILTEP regimen once gave you. I'm curious as to whether or not using the dopamine precursors have played a role in it's diminished effects.

[chung_pao]

Tolerance, people. It develops to almost anything.
The higher you dose, the faster it sets in.
That is why I take weekends, or at least 1 day/week, off.

There's nothing wrong with the stack. You're just growing tolerant.
The only substances I've found not to have tolerance issues, are certain Receptor modulators (AMPAkines, hormones, neurosteroids, certain minerals) and Nutrients (creatine, CoQ10, ALCAR).

Focus on your hormonal health, CNS function and nutrition. Complement with things like CILTEP.

[Tumah]

After about three days I've finally finished all 55 pages of this thread. Now on to the questions:

1. Is there any preference to NALT over L- Tyrosine here?
2. I have some generalized anxiety and mild OCD and intend to add L- Theanine to the stack (and of course MgT at night). I was wondering if NAC might be something I could add as well? Daily? Rhodiola was mentioned earlier in the thread as well. Would that be a better/ safer route?
3. On the same note, much of my learning difficulty stems from anxiety. Is there any likelihood of the stimulants exacerbating that problem, which might be counterproductive?
4. I haven't really seen much discussion about oxiracetam here. I am leaning towards adding piracetam since phenylpiracetam doesn't seem to be sustainable due to tolerance and aniracetam induces fog. Does anyone have any experience with oxiracetam?
5. If I am already taking a B- complex are activated forms of B contraindicated? If not, is the additional benefit of the activated forms worth the additional expenditure?

For me, NALT seems to be more effective at a lower dose of 350mgs vs 500 of l-tyrosine. I seem to get more side effects from l-tyrosine i.e., jitters, irritability etc.

In my opinion, NAC is a wonderful supplement for nearly anyone because of its antioxidant role and it's purported neuroprotective effect against the likes of excess glutamate. One thing to look into is taking at least an equal amount of vitamin C since some of it could be metabolized into homocysteine iirc. Someone correct me here if I'm in error.

If you're already prone to anxiety, then yes, adding a dopamine precursor may exacerbate the condition, especially over time. L-theanine may help you enough with that or it may not. If you're currently on any antidepressant that also acts in an anxiolytic manner, I'd double check on your use of Rhodiola. Some can take it while on an AD, while others cannot.

As far as your B-Complex vitamin, I'd normally state that utilizing an activated or singular form in addition to the multi will depend on a number of variables. These ranges from your lifestyle, medications you may already be taking, whether you exercise and how often, your nutrition or other things like smoking etc. It's far safer to just stick with a complex and slowly introduce other forms like B12 or B6 like some do. Many people who suffer from anxiety have taken doses of B6, as an example, in excess of 250mgs per day only to find out that those types of doses are actually neurotoxic. I use phenylpiracetam and enjoy it's effects, but I never get to the tolerance issue simply because I don't use it more than a couple days a week. I almost use it solely for its stimulatory properties not unlike sulbutiamine. Both sporadically.

Well I'm not on any meds since my anxiety is tolerable. Or at least I've had it for so long that I'm used to functioning with it. I am working on including p5p, NAC, and inositol and SAMe (because I might be an under methylator).

Tolerance, people. It develops to almost anything.
The higher you dose, the faster it sets in.
That is why I take weekends, or at least 1 day/week, off.

There's nothing wrong with the stack. You're just growing tolerant.
The only substances I've found not to have tolerance issues, are certain Receptor modulators (AMPAkines, hormones, neurosteroids, certain minerals) and Nutrients (creatine, CoQ10, ALCAR).

Focus on your hormonal health, CNS function and nutrition. Complement with things like CILTEP.

Speaking of taking a day/week off, I recall way back in the first half of this thread mention of cycling off CILTEP once a week and taking something else to restore balance, but I can't remember what it was.

[magta39]

After about three days I've finally finished all 55 pages of this thread. Now on to the questions:

1. Is there any preference to NALT over L- Tyrosine here?
2. I have some generalized anxiety and mild OCD and intend to add L- Theanine to the stack (and of course MgT at night). I was wondering if NAC might be something I could add as well? Daily? Rhodiola was mentioned earlier in the thread as well. Would that be a better/ safer route?
3. On the same note, much of my learning difficulty stems from anxiety. Is there any likelihood of the stimulants exacerbating that problem, which might be counterproductive?
4. I haven't really seen much discussion about oxiracetam here. I am leaning towards adding piracetam since phenylpiracetam doesn't seem to be sustainable due to tolerance and aniracetam induces fog. Does anyone have any experience with oxiracetam?
5. If I am already taking a B- complex are activated forms of B contraindicated? If not, is the additional benefit of the activated forms worth the additional expenditure?

For me, NALT seems to be more effective at a lower dose of 350mgs vs 500 of l-tyrosine. I seem to get more side effects from l-tyrosine i.e., jitters, irritability etc.

In my opinion, NAC is a wonderful supplement for nearly anyone because of its antioxidant role and it's purported neuroprotective effect against the likes of excess glutamate. One thing to look into is taking at least an equal amount of vitamin C since some of it could be metabolized into homocysteine iirc. Someone correct me here if I'm in error.

If you're already prone to anxiety, then yes, adding a dopamine precursor may exacerbate the condition, especially over time. L-theanine may help you enough with that or it may not. If you're currently on any antidepressant that also acts in an anxiolytic manner, I'd double check on your use of Rhodiola. Some can take it while on an AD, while others cannot.

As far as your B-Complex vitamin, I'd normally state that utilizing an activated or singular form in addition to the multi will depend on a number of variables. These ranges from your lifestyle, medications you may already be taking, whether you exercise and how often, your nutrition or other things like smoking etc. It's far safer to just stick with a complex and slowly introduce other forms like B12 or B6 like some do. Many people who suffer from anxiety have taken doses of B6, as an example, in excess of 250mgs per day only to find out that those types of doses are actually neurotoxic. I use phenylpiracetam and enjoy it's effects, but I never get to the tolerance issue simply because I don't use it more than a couple days a week. I almost use it solely for its stimulatory properties not unlike sulbutiamine. Both sporadically.

Well I'm not on any meds since my anxiety is tolerable. Or at least I've had it for so long that I'm used to functioning with it. I am working on including p5p, NAC, and inositol and SAMe (because I might be an under methylator).

Tolerance, people. It develops to almost anything.
The higher you dose, the faster it sets in.
That is why I take weekends, or at least 1 day/week, off.

There's nothing wrong with the stack. You're just growing tolerant.
The only substances I've found not to have tolerance issues, are certain Receptor modulators (AMPAkines, hormones, neurosteroids, certain minerals) and Nutrients (creatine, CoQ10, ALCAR).

Focus on your hormonal health, CNS function and nutrition. Complement with things like CILTEP.

Speaking of taking a day/week off, I recall way back in the first half of this thread mention of cycling off CILTEP once a week and taking something else to restore balance, but I can't remember what it was.

I think is was galantamine to restore acetylcholine receptor sensitivity

[xsiv1]

How many have tried the CILTEP stack with Phenylpiractam instead of a dopamine precursor? Something similar? I think it was mentioned somewhere in the thread but heck if I know if it was the same question or someone's experience. I can't search the thread using Tapatalk. Rrr

[row1]

Hello forum members,

A very interesting topic

Below is a google translation from dutch

I dig through pages and orderd a basic CILTAP stack.

Artichoke 350mg (2.2% cynarin 7.7 mg) - I used two pieces (firm Nature's Garden)
and
50mg Coleus Forskohlii (18% standard 9mg) - I use half. (firm Enzymatic)

I drink coffee at breakfast

Unfortunately I do not have the above results were achieved only after almost two weeks.
I've always swallowed on an empty stomach in the morning. 45 minutes before breakfast.

Beneith I cant order (yet) in Holland

phenylalanine
Forskohlii replaced by C-bolic

I would be happy if someone could send me a link where ik can order "good" supplements.
I think that the quality/purity of what I bought isnt good.

I've been using Vitamin C (1000mg) Vitamin B complex (high doses)
This after Ciltep stack. (2 to 3 hours after)



I would also add Binaural Beats @ 40-48Hz , there have been serval studies that have given good results
Also anyone here treid Neurofeedback?(zengar and traditional) after of before CIPTEP.




Picture 2 is the things that I treid en still trying.  CIMG5565.JPG   163.51KB   67 downloads  CIMG5562.JPG   161.29KB   73 downloads

[magta39]

I tried oxyracetam with artichoke and forskolin. (and theanine)....I crashed after 3 hrs....I don't think it's worth trying again....

Edited by magta39, 10 July 2013 - 02:52 AM.

[abelard lindsay]

Regarding forskolin as an AChE promoter, I double-checked health_nutty's posted reference. Here is the abstract:
http://www.ncbi.nlm....pubmed/16924422
Molecular and Cellular Biochemistry
October 2006, Volume 290, Issue 1-2, pp 23-32

Title:
Forskolin, an inducer of cAMP, up-regulates acetylcholinesterase expression and protects against organophosphate exposure in neuro 2A cells

Abstract:
Bioscavenger prophylactic therapy using purified human acetylcholinesterase (AChE) or butylcholinesterase (BChE) is a promising treatment for future protection against chemical warfare nerve agent exposure. Potential immune response due to the complex structure of cholinesterases, mutations, post-translational modifications, and genetic variation is a limiting factor against purified enzyme therapy. We investigated an alternative bioscavenger approach using Forskolin, an inducer of intracellular cyclic AMP (cAMP), which activates AChE promoter and up-regulates its expression. A mouse neuronal cell line, Neuro 2A, was treated with various doses of Forskolin and analysis of the expressed enzyme indicates that the AChE activity was significantly increased in cells exposed to repeated administration of the drug every other day for 7–10 days. Cholinesterase enzyme assays showed that the enzyme activity was increased approximately 2-fold for the extracellular enzyme and 3-fold for the intracellular enzyme. The optimal dose found for extracellular enzyme production was 12–24 μM Forskolin, while the optimal dose for intracellular was 12 μM. In parallel with the rise in the AChE level, the morphology of Forskolin-treated cells showed neurite growth with increasing doses. Forskolin treatment protects Neuro 2A cells from Diisopropylflurophophate (DFP), a surrogate of the organophosphate chemical warfare agents soman and sarin, induced toxicity in Neuro 2A cells. These results indicate that transcriptional inducers, such as Forskolin, can sufficiently up-regulate cellular AChE production and protect cells against organophosphate toxicity.
----------------------------------------------------

Thus, it looks like health_nutty was spot on. And that makes me concerned that if I take forskolin, it could counteract (or nullify) the very-beneficial-to-me AChE inhibition that Huperzine A is providing.

I think is was galantamine to restore acetylcholine receptor sensitivity

The sleepiness that shows up after a while is probably due to AChE promoter activity of forskolin. Galantamine is an AChE inhibitor which is why it would counteract this. Perhaps when people take time off the stack AChE levels reset to normal and tolerance lowers. Upregulating AChE expression is certainly an interesting moa of tolerance. Usually tolerance occurs as a result of lowered sensitivity of receptors. IMHO, CILTEP doesn't have this problem because it does not directly stimulate receptors like dopamine affecting stimulants. Instead it appears to act as a positive modulator of dopamine metabolism.

How many have tried the CILTEP stack with Phenylpiractam instead of a dopamine precursor? Something similar? I think it was mentioned somewhere in the thread but heck if I know if it was the same question or someone's experience. I can't search the thread using Tapatalk. Rrr

Phenylpiractam is not a dopamine precursor. In my experience, it goes very well with the stack.

Edited by abelard lindsay, 10 July 2013 - 06:53 PM.

[VCPRO]

Abelard or anyone else who may be able to answer this. I am confused as to the correct dosage of Forskolin. You mention that the dose you are using is "5mg of Forskolin from 150mg of uncapped Better Body Sports 95% pure C-Bolic capsules." Each capsule contains 25mg. Where does the 150mg come from? I measured the powder in one of the pills and it was .6 grams or 600 milligrams. If a take 1/5 of that it would be .12 grams or 120 milligrams. Any guidance on the correct weight would be greatly appreciated.

[xsiv1]

Thanks AL. I knew phenylpiracetam wasn't a dopamine precursor and wanted to use it to replace NALT for a while but was unsure how they'd interact. So, thanks for the reply.

[KoolK3n]

I apologize if this question has already been asked. Why are we aiming for a selective PDE inhibitor? Particularly PDE4 (obviously). Why not use a potent nonselective PDEI like Trental over a weak PDE4 inhibitor like Artichoke, etc?

[norepinephrine]

After an extended break, I'm having great results with the 'classic' CILTEP stack (i.e., artichoke for PDE inhibition). As well, I'm again finding that fasting for a few hours after dosing seems to be one of the most important factors governing how I respond.

Chung_pao - if I recall, you go to school in a quantitative/technical field, yeah? Have you noticed much of a difference for how CILTEP affects your reasoning abilities versus modafinil? It's been too long since I've taken the former before a math test, but the latter seems to hurt my reasoning skills insofar as I become to 'linear' and mechanical in my thought processes and have considerable difficulty coming up with a novel or insightful solution. For example - solving an integral in calculus that depends on an arcane method to compute is a complete shitshow if I've had >100mg moda, but doing computations that I've done many times in the past is a breeze. Cautiously looking forward to seeing what happens the next time I take a test on CILTEP...

[lostfalco]

Phenylpiractam is not a dopamine precursor. In my experience, it goes very well with the stack.

Hey Abelard, Opaque and I have been experimenting recently (with extremely promising results) with PQQ + CoQ10 + 808nm laser and we were wondering about a CILTEP-ish stack with this. What would you recommend here? I'm just gonna copy and paste Opaque's recent post on my thread because it was so good. Hopefully, that will give you some context. Thanks again for all your work on this and your Linux-like approach. Respect.

" lostfalco, on 09 July 2013 - 11:18 PM, said:

This brings me to my last point. I don't see any reason why this wouldn't stack amazingly well many of the traditional nootropics. Does anyone see any possible problems combining this with CILTEP? Anybody want to try it and report back?

OpaqueMind
I tried combining it with CILTEP and got a minor headache. Nothing too severe, but definitely out of the ordinary as I never get them. I have however used it on days inbetween laserings to good effect. I have a vague, potential hypothesis - cAMP overload

According to the PQQ wiki page -

• PQQ triggers the CREB signaling protein (cAMP-response element-binding protein), which plays a pivotal role in embryonic development and growth. It also beneficially interacts withhistones, proteins involved in the packaging and nuclear organization of cell DNA.^[14] CREB also stimulates the growth of new mitochondria.

It also seems that Low-level laser therapy (LLLT) acts as cAMP-elevating agent in acute respiratory distress syndrome. [source] Since the mechanism of action on the mitochondrial metabolic level is universal, and cAMP is an aspect of the metabolic process, then cAMP is elevated in the brain also. [see diagram on page 10 of this pdf for confirmation].

Two parts of the CILTEP stack also raise cAMP (forskolin) and inhibit it's degradation(PDE4 inhibitor of choice).

I think this four-fold action causes just way too much cAMP for the brain to deal with, causing headaches and other unpleasantries."

[chung_pao]

After an extended break, I'm having great results with the 'classic' CILTEP stack (i.e., artichoke for PDE inhibition). As well, I'm again finding that fasting for a few hours after dosing seems to be one of the most important factors governing how I respond.

Chung_pao - if I recall, you go to school in a quantitative/technical field, yeah? Have you noticed much of a difference for how CILTEP affects your reasoning abilities versus modafinil? It's been too long since I've taken the former before a math test, but the latter seems to hurt my reasoning skills insofar as I become to 'linear' and mechanical in my thought processes and have considerable difficulty coming up with a novel or insightful solution. For example - solving an integral in calculus that depends on an arcane method to compute is a complete shitshow if I've had >100mg moda, but doing computations that I've done many times in the past is a breeze. Cautiously looking forward to seeing what happens the next time I take a test on CILTEP...

Fasting really helps to preserve cAMP (proven). I also have a layman hypothesis about "more blood" being available for mental activity when it's not directed towards the digestive system. (not proven)
Ketones also have very interesting nootropic properties; experimentation with coconut oil and ALCAR has validated this lately.

I don't work in a quantative field, but I study a lot, and I enjoy calculations.
I think I understand what you're saying about the thought processes. The creative process has really fascinated me lately.
I've realized how complex this actually is; it's not about single neurotransmitters, like amping up dopamine, but more about excitation in parts of the brain not previously activated simultaneously, resulting in new insights... I'm not going to even try to understand what constitutes it. I can only study Cause-and-effect and offer my observations.

I don't think Modafinil directly antagonizes these thought processes and make you mechanical in your thinking. It has that effect on me sometimes, but only after continued use. My brain sort of gets "worn down" and tired. Maybe it has with myelin-breakdown to do, or downregulation... Because good fats (coconut oil, eggs), DHEA and a nap always restores me, as if it rebuilds the catabolized parts.
(DHEA I only use on Modafinil, since Moda completely wrecks my endogenous hormone-production...)

Anyhow, the following has produced the best effects for me: (consider it one stack)
By best effects, I also refer to the creative aspect; spontaneous recollection of relevant facts, even ones you didn't even know you had memorized...
*Forskolin: Keep the dose LOW. Anything above your minimal effective dose will completely shut down the creative/imaginative parts of the brain.
*500 mg Artichoke extract, 1x Zembrin. (zembrin offers very interesting mechanisms which artichoke doesn't, involving GABA, serotonin, other PDE-subtypes and... opioid receptors?!)
*No tyrosine/phenylalanine. (taking this quells my creativity and inner dialogue)
Dietary: I do Intermittent fasting (+ ALCAR) until I start feeling depleted. When I do, it's refuelling with veggies, coconut oil and eggs.

*Piracetam: Produces short bursts of very interesting (exciting!) mental activity. Don't know if it's the AMPA-potentiation, but recollection of relevant facts definitely improves, almost to a ridiculous degree: Both in my inner and outer dialogue... It becomes extremely fluent, and I'm completely bombarded with memorized facts that are retrieved through the present memory cues. It's short lived however, and only happens during fasting...
I never use Piracetam after eating anything containing choline... The increased choline uptake often causes ACh-overload symptoms for me.
*Modafinil: This is a wildcard. Most of the times, it gives me incredible cognitive skills on most levels (even mathematical and creative), but the impressive effects wear off after a few hours, and I start just feeling depleted. Bad risk:benefit-ratio.

IMO, stick to CILTEP (preferably including zembrin), Fasting, and attack doses of ALCAR (500-1000 mg) + Piracetam (max 4.8g), and some caffeine (preferably tea). This will definitely spark your creativity and facilitate recollection of any stored information you have and utilize a lot of your creative potential.
Piracetam never has any side-effects for me (aside from almost giving me Tourette's in social situations), so I'd definitely recommend using it with CILTEP. Keep the choline low, however... or use ALCAR instead.

I think it's the positive modulation of both glutamate (Piracetam) receptors and dopamine metabolism (CILTEP) that synergizes and makes both INPUT and Recollection so effortless. But that's just a guess.

If anyone has any ideas to contribute on the subject of increasing Creativity; stimulating never-thought-of insights and ideas, as opposed to just memorization, please do.

I apologize if this question has already been asked. Why are we aiming for a selective PDE inhibitor? Particularly PDE4 (obviously). Why not use a potent nonselective PDEI like Trental over a weak PDE4 inhibitor like Artichoke, etc?

We have combined available studies with a lot(!) of trial-and-error. The application of Zembrin or Artichoke extract has reliably produced the best nootropic effects. (taking into account potency, duration, minimizing side-effects and results from actual quantitative testing)
If you decide to try Trental however, please report your observations!

Edited by chung_pao, 11 July 2013 - 02:53 AM.

[xsiv1]

^^^ Interesting thread you have going there. I'm going to read it all tomorrow and see what's up. I may cycle to that when it's time if it's working for you guys. I like the commentary about the MCT oils and breathing techniques. Sounds like it doesn't jibe well with CILTEP though, so perhaps it'd be more of an option during one's "break" from CILTEP which many of us have done. I've normally taken weekends off and after 90 days, I now take it only on weekends with positive effects. I'm going to try it (the original stack) and then dose 50mgs Phenylpiracetam about 1 hour after CILTEP ingestion. I'd like to see how my focus is or isn't affected.

[chung_pao]

Phenylpiractam is not a dopamine precursor. In my experience, it goes very well with the stack.

Hey Abelard, Opaque and I have been experimenting recently (with extremely promising results) with PQQ + CoQ10 + 808nm laser and we were wondering about a CILTEP-ish stack with this. What would you recommend here? I'm just gonna copy and paste Opaque's recent post on my thread because it was so good. Hopefully, that will give you some context. Thanks again for all your work on this and your Linux-like approach. Respect.

" lostfalco, on 09 July 2013 - 11:18 PM, said:

This brings me to my last point. I don't see any reason why this wouldn't stack amazingly well many of the traditional nootropics. Does anyone see any possible problems combining this with CILTEP? Anybody want to try it and report back?

OpaqueMind
I tried combining it with CILTEP and got a minor headache. Nothing too severe, but definitely out of the ordinary as I never get them. I have however used it on days inbetween laserings to good effect. I have a vague, potential hypothesis - cAMP overload

According to the PQQ wiki page -

• PQQ triggers the CREB signaling protein (cAMP-response element-binding protein), which plays a pivotal role in embryonic development and growth. It also beneficially interacts withhistones, proteins involved in the packaging and nuclear organization of cell DNA.^[14] CREB also stimulates the growth of new mitochondria.

It also seems that Low-level laser therapy (LLLT) acts as cAMP-elevating agent in acute respiratory distress syndrome. [source] Since the mechanism of action on the mitochondrial metabolic level is universal, and cAMP is an aspect of the metabolic process, then cAMP is elevated in the brain also. [see diagram on page 10 of this pdf for confirmation].

Two parts of the CILTEP stack also raise cAMP (forskolin) and inhibit it's degradation(PDE4 inhibitor of choice).

I think this four-fold action causes just way too much cAMP for the brain to deal with, causing headaches and other unpleasantries."

Very interesting Lostfalco! You are considering a lot of aspects that most noot-explorers don't.
I already use the full CILTEP-stack with CoQ10, with excellent results.
I'd definitely be interested in adding PQQ to the combination. What source have you used successfully?

The laser should also synergize with this. If excessive cAMP is experienced (perceived as headaches and inhibited internal dialogue), just reduce forskolin. Forskolin stimulates systemic cAMP-activation, including in areas where it's undesired for our nootropic purposes.

I think LLLT, PQQ, CoQ10, Zembrin, Forskolin (absolute minimal effective dose!), and perhaps ALCAR and Piracetam would make an incredible combination... Requiring a lot of sleep afterwards
However, hypotheses useless unless proven through experiment!

FYI, Zembrin has produced complete PDE-4 inhibition in studies.

Edited by chung_pao, 11 July 2013 - 03:09 AM.

[chung_pao]

Doublepost. Remove, please.

Edited by chung_pao, 11 July 2013 - 03:16 AM.

[abelard lindsay]

This brings me to my last point. I don't see any reason why this wouldn't stack amazingly well many of the traditional nootropics. Does anyone see any possible problems combining this with CILTEP? Anybody want to try it and report back?

OpaqueMind
I tried combining it with CILTEP and got a minor headache. Nothing too severe, but definitely out of the ordinary as I never get them. I have however used it on days inbetween laserings to good effect. I have a vague, potential hypothesis - cAMP overload

According to the PQQ wiki page -

• PQQ triggers the CREB signaling protein (cAMP-response element-binding protein), which plays a pivotal role in embryonic development and growth. It also beneficially interacts withhistones, proteins involved in the packaging and nuclear organization of cell DNA.^[14] CREB also stimulates the growth of new mitochondria.

It also seems that Low-level laser therapy (LLLT) acts as cAMP-elevating agent in acute respiratory distress syndrome. [source] Since the mechanism of action on the mitochondrial metabolic level is universal, and cAMP is an aspect of the metabolic process, then cAMP is elevated in the brain also. [see diagram on page 10 of this pdf for confirmation].

Two parts of the CILTEP stack also raise cAMP (forskolin) and inhibit it's degradation(PDE4 inhibitor of choice).

I think this four-fold action causes just way too much cAMP for the brain to deal with, causing headaches and other unpleasantries."

With regards to LLLT, if it raises cAMP I'd imagine that the increase is localized to where the laser is applied. As I've explained before, cAMP signaling is compartmentalized and so it has different effects depending on where cAMP is elevated in the body and it does not circulate from one part of the body to the other. The obvious example is that PDE5 inhibitors like viagra raise cAMP in the male anatomy while PDE4 inhibitors raise it in the brain around CREB nearby where LTP is occuring. Therefore, the spot you stimulate on the brain is probably important. Some people were talking about how elevated cAMP in the pre-frontal cortex was closing HCN channels and this is what guanfacine counteracted, so you might want to avoid those spots when stimulating and focus on the hippocampus and other areas where memory formation is taking place.

With regards to PQQ and CREB/cAMP, I saw this study

http://www.ncbi.nlm....pubmed/19861415

Therefore, we hypothesized that PQQ can induce mitochondrial biogenesis in mouse hepatocytes.
...
. The induction of this process occurred through the activation of cAMP response element-binding protein (CREB) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha), a pathway known to regulate mitochondrial biogenesis. PQQ exposure stimulated phosphorylation of CREB at serine 133, activated the promoter of PGC-1alpha, and increased PGC-1alpha mRNA and protein expression.

So it improved mitochondrial biogenisis in liver cells (hepatocytes) in mice via PGC1-alpha

Let's see if this is the same thing that goes on in the brain...

http://www.ncbi.nlm....pubmed/20926834

Activation of PGC-1α results in increased expression of nuclear-encoded subunits of the mitochondrial respiratory chain and blocks the dopaminergic neuron loss induced by mutant α-synuclein or the pesticide rotenone in cellular disease models. Our systems biology analysis of Parkinson's disease identifies PGC-1α as a potential therapeutic target for early intervention.

http://www.ncbi.nlm....pubmed/22097319

When treated with PQQ at concentration of 10-100 nmol/L, the proliferation of Schwann cells increased and the expression of c-fos,c-jun, CREB and PCNA was up-regulated.

So Schwann cells being located in the brain, this is a good sign for possible CILTEP synergy.

Very interesting Lostfalco! You are considering a lot of aspects that most noot-explorers don't.
I already use the full CILTEP-stack with CoQ10, with excellent results.
I'd definitely be interested in adding PQQ to the combination. What source have you used successfully?

The laser should also synergize with this. If excessive cAMP is experienced (perceived as headaches and inhibited internal dialogue), just reduce forskolin. Forskolin stimulates systemic cAMP-activation, including in areas where it's undesired for our nootropic purposes.

I think LLLT, PQQ, CoQ10, Zembrin, Forskolin (absolute minimal effective dose!), and perhaps ALCAR and Piracetam would make an incredible combination... Requiring a lot of sleep afterwards
However, hypotheses useless unless proven through experiment!

FYI, Zembrin has produced complete PDE-4 inhibition in studies.

I tried ALCAR today when I started to get my usual 2pm tiredness. It was great. It seems that the increased ACHE transcription from Forskolin, which is what probably made me sleepy, combined with more acetylcholine from ALCAR gave me a feeling of enhanced physical coordination and better reflexes. In my study of fluid intelligence I came across a general pattern that faster brain metabolism was associated with increased performance so I think this is a good direction to go in. I wouldn't pile on the ALCAR until the afternoon tiredness showed up though as this might result in excessive ACH. Thanks Chung for the ALCAR suggestion.

Edited by abelard lindsay, 12 July 2013 - 03:12 PM.

[KoolK3n]

With regards to LLLT, if it raises cAMP I'd imagine that the increase is localized to where the laser is applied. As I've explained before, cAMP signaling is compartmentalized and so it has different effects depending on where cAMP is elevated in the body and it does not circulate from one part of the body to the other. The obvious example is that PDE5 inhibitors like viagra raise cAMP in the male anatomy while PDE4 inhibitors raise it in the brain around CREB nearby where LTP is occuring. Therefore, the spot you stimulate on the brain is probably important. Some people were talking about how elevated cAMP in the pre-frontal cortex was closing HCN channels and this is what guanfacine counteracted, so you might want to avoid those spots when stimulating and focus on the hippocampus and other areas where memory formation is taking place.

That's what I'm saying. Why not combine CILTEP stack with either Guanfacine or Clonidine because won't Kanna (Zembrin), Forskolin, Artichoke, etc raise cAMP in the PFC also? This is why Guanfacine or Clonidine are important. Would it lessen some of the side effects from an overload of cAMP? In the brain, A2 agonists primarily affect the PFC. So that could mean the two would synergize. Increased cAMP in hippocampus and stronger connections in the PFC.

Edited by KoolK3n, 12 July 2013 - 06:26 PM.

[abelard lindsay]

Won't Kanna (Zembrin), Forskolin, Artichoke, etc raise cAMP in the PFC also? This is why Guanfacine or Clonidine are important. Would it lessen some of the side effects from an overload of cAMP? In the brain, A2 agonists primarily affect the PFC. So that could mean the two would synergize. Increased cAMP in hippocampus and stronger connections in the PFC.

cAMP signalling is compartmentalized. What that means is that there are many PDE isoforms and each isoform only exist in very specific parts of the body. They do very different things based on where in the body they are expressed by cells. There are many PDE4 isoforms PDE4A-PDE4D for example and then isoforms variants among those such as PDE4A1, PDE4B5, etc. PDE4 inhibition is just a simpler thing to test for than testing for each isoform so they usually do studies on broad PDE4 inhibition. That's why some PDE4 inhibitors cause vomiting and gastrointestinal distress (e.g Rolipram,Rofulimast), while others are more benign (Kanna, Artichoke, etc). It's because these substances have different interactions with different PDE4 isoforms. There are even some PDE4B isoforms that impair memory (http://www.ncbi.nlm....pubmed/21458469, "Our findings support the view that various PDE4 isoforms are non-redundant and have distinct neurological roles.". While PD4D inhibition significantly enhances memory (http://www.ncbi.nlm....pubmed/21209202). This is because these two are regulating cAMP signaling in different parts of the brain anatomy because they are expressed differently in different regions and cell types of the brain.

Anyway, with regards to guanfacine, In studies, Rolipram and Guanfacine cancel each other's effects but although Rolipram cancels Guanfacine's effects, it does not lower performance below baseline levels. Has anybody taken Guanfacine and found it beneficial? I haven't seen a lot of good reviews around the net that it actually works. It also seems to have some side effects. Here's two threads I found on it: http://www.addforums...ead.php?t=54053 , http://www.drugs-for...ad.php?t=126697. It seems to decrease hyperactivity/impulsivity but otherwise the results appear somewhat mixed.

Edited by abelard lindsay, 12 July 2013 - 07:39 PM.

[KoolK3n]

Anyway, with regards to guanfacine, In studies, Rolipram and Guanfacine cancel each other's effects but although Rolipram cancels Guanfacine's effects, it does not lower performance below baseline levels. Has anybody taken Guanfacine and found it beneficial? I haven't seen a lot of good reviews around the net that it actually works. It also seems to have some side effects. Here's two threads I found on it: http://www.addforums...ead.php?t=54053 , http://www.drugs-for...ad.php?t=126697. It seems to decrease hyperactivity/impulsivity but otherwise the results appear somewhat mixed.

I don't know if you read the whole study from this link: http://www.ncbi.nlm....?report=classic. It's definitely worth reading. The review still concludes that a2a agonists could benefit those with ADHD. It looks like "they" "chose" STM over LTM.

Check this out: http://books.google....ocampus&f=false. On page 372, it said PDE4A, PDE4B, and PDE8B are primarily expressed in the hippocampus while PDE4D represents the majority of the soluble PDE4 in the brain. I don't know what the second half of the sentence meant. Does it mean it's unbound to any specific part of the brain?

I think we should group buy $35 to buy this article, http://www.nature.co...s/nbt.1598.html lol.

Yeah I agree the jury is still out with a2(a) agonists. Again, maybe the side effects from Guanfacine/Clonidine like dizziness, somnolence, decreased dopamine (my hypothesis from this link: http://www.ingentaco...58?crawler=true), etc that come from it's insane antihypertensive action masks any perceived improvement in working memory. I mean it does shut down NE production (at least in the PFC). Taking preventative steps such as those outlined in this artcle: http://www.ncbi.nlm....les/PMC2888469/ could allow for a higher dose of a2(a) agonists. Completely off topic, but it could also be taken with a low-dose of Amisulpride: http://forums.phoeni...r-me-cfs.20964/, Selegiline, or any long term DA enhancement in the deep parts of the brain (i.e. mesolimbic and nigrostriatal pathway).

Edited by KoolK3n, 13 July 2013 - 05:08 PM.

[stephen_b]

Anyone else have issues with Solaray forskohlii? I had fast onset loose stools (about 2 hours after taking on an empty stomach) and a hive reaction.

[Babychris]

is the CILTEP stack worth a try ?

[Suirsuss]

is the CILTEP stack worth a try ?

absolutely after first using ciltp and then trying the ampakines and now back to ciltp I have to hand it to the extracts.

Anyone else have issues with Solaray forskohlii? I had fast onset loose stools (about 2 hours after taking on an empty stomach) and a hive reaction.

idk about the hives but depending on dosage+diet loose poops common with forskolin

[stephen_b]

Some herbals besides forskolin that are reported to raise cAMP are geranium, lavender, and jasmine (PMID 12203263). It appears that the chemical in the herbals that cause the cAMP increase is 1,3-dimethylamylamine (DMAA; longecity thread). DMAA looks to have been banned by the FDA as unsafe. I wonder if dendrobium extract, used in supplements advertised as a DMAA replacement might also have cAMP raising properties.

[abelard lindsay]

Anyone else have issues with Solaray forskohlii? I had fast onset loose stools (about 2 hours after taking on an empty stomach) and a hive reaction.

You could try taking small amounts of pure forskolin by measuring out small amounts of the uncapped C-Bolic product by Better Body Sports. This is what I do. There is also good evidence that Sesamin, which is derived from sesame seeds, is a potent cAMP increaser:

http://www.ncbi.nlm....pubmed/22293035

Sesamin at 20-100 μM rapidly increased the intracellular levels of cyclic AMP (cAMP) to 158.3%-270.3% of control levels at 30 min

[stephen_b]

I have sesamin and dendrobium extract on order. I'll give them separate trials.

[xsiv1]

I'm kind of surprised at the gastrointestinal issues some are having with forskolin at the doses recommended in CILTEP but I guess everyone is different. I'm wondering how those guys deal with the real issues related to higher dose use. They must be walking gas machines. :-)

[stephen_b]

Well a 3.85% forskolin product is 96.15% other stuff that can potentially mess with your digestive system.