2626 replies to this topic

[kai2]

When [Tesla] was engineering he could imagine entire machines operating, take them apart and inspect them in his head. He also had superhuman hearing and could hear thunder 200 miles away in his Colorado lab. He even had fits where his senses would get so profoundly strong that sounds so faint so as to be inaudible to humans would disturb him.

This is eerily close to Dr. Temple Grandin's description of her personal experience with autism
http://www.grandin.c...l.thinking.html

[chung_pao]

Could someone please explain this to me:

Why the heck is Forskolin sometimes causing acute drowsiness (feels like adenosine), and sometimes having extremely stimulatory effects? (acutely)
Is this the interaction between CILTEP and caffeine? Or have I developed a tolerance to it?

I'm thoroughly confused and couldn't find clarification by searching the thread.

Side note:
I've ordered Morus Alba (mulberry) and it'll be arriving shortly. A PDE-4 inhibitor, supposedly stronger than luteolin.
Although, it may be specific to PDE-4D2 and PDE-4B4. It's still worth a try!

Edited by chung_pao, 29 December 2013 - 04:05 AM.

[hephaestus]

cAMP isn't specifically stimulatory, increasing it potentiates all kinds of different chemical pathways. As I mentioned in some earlier posts, it upregulates DA synthesis as well as ACh synthesis, along with a bunch of other stuff we haven't even explored. I'm guessing it has something to do with the balance of nutrients available when you take it, but I haven't been able to discern any pattern. I don't think it is related to tolerance as I haven't been taking it that much lately but it still sometimes makes me sleepy. Anecdotally, people have reported that Phe as well as ALCAR alleviate the drowsiness. It seems like I have noticed less drowsiness since starting to supplement 50mg of CDP, but I'm not entirely sure. Wikipedia says DA inhibits NE release in blood vessels, but I don't think this applies in the CNS.

Edited by hephaestus, 29 December 2013 - 04:34 AM.

[Jeoshua]

I appreciate the help, but you're obviously parroting back some generalities you've either read or heard second-hand without looking into the specifics for yourself.

If by that you mean speaking out on information that I found from multifarious studies all over pubmed that I read as research before messing with my brain, then yes.

Just in general, that kind of things seems really irresponsible (as does taking a bunch of shit without even looking at the ingredients involved, I know). If I had a lack of critical thinking skills to go along with my chemical ignorance, though, then that woefully fallacious advice would've actually been put to use instead of politely discarded to "such is the internet" pile where it belongs. It's no wonder half of the threads in the "Brain Health" forum are some variation of "Help I really messed myself up using these things, now what do I do!?1?"This wasn't meant to incite or provoke anything, but I do think it would be awesome if people stepped back took a look at how qualified they actually were to respond before trying to help. Cheers

Thanks for blaming the problems of the entire forum on me. I appreciate your candor. I am sorry that you had a bad experience with something you obviously didn't research properly before you took it, but honestly I would recommend that, instead of insisting that I do research and stop "parroting back generalities", instead you should look into the effects of drugs that you take before you take them.

I wasn't entering into this to get into an e-fight. I was trying to understand how you can claim that amino acids and herbal extracts are "classic stimulants", which, clearly, they are not. This is not amphetamine or cocaine we are talking about, and the mechanism of effect is completely different. If it is not to your liking, then that is one thing. But nothing about this is "classic stimulants".

Targeting type 4 phosphodiesterase (PDE4) for treatment of COPD has multilevel benefits to patients by reducing inflammation, relieving bronchoconstriction, and improving pulmonary circulation. The isoenzyme-specific narrow spectrum PDE4 inhibitors such as cilomilast and roflumilast may have limited clinical efficacy in managing severe and very severe COPD. Development of dual therapy by combining PDE4 inhibition with Ca2+ channel antagonism may introduce an effective novel armory for physicians to manage patients with severe COPD.

http://www.ncbi.nlm....les/PMC2707810/

Edited by Jeoshua, 29 December 2013 - 07:07 AM.

[Sholrak]

cAMP isn't specifically stimulatory, increasing it potentiates all kinds of different chemical pathways. As I mentioned in some earlier posts, it upregulates DA synthesis as well as ACh synthesis, along with a bunch of other stuff we haven't even explored. I'm guessing it has something to do with the balance of nutrients available when you take it, but I haven't been able to discern any pattern. I don't think it is related to tolerance as I haven't been taking it that much lately but it still sometimes makes me sleepy. Anecdotally, people have reported that Phe as well as ALCAR alleviate the drowsiness. It seems like I have noticed less drowsiness since starting to supplement 50mg of CDP, but I'm not entirely sure. Wikipedia says DA inhibits NE release in blood vessels, but I don't think this applies in the CNS.

Maybe, that metabolic acceleration, or at least the referring to the long term potentiation chemical pathways taking place would exhaust more an organism. That big grade of LTP would naturally be impossible in any way without some induction (like here), and that just could be a hacking on our system so that will require some rest following. I will do it 3-4 days weekly, as the close to one week taking it daily almost caused me to get kranky and and feel pissed off. Big somnolience is always something tells us we are overdoing. With all this, I want to say, it's pretty potent stuff. I had understimated the power of this stack, now I see it's one of the most amazing nootropics I've tried..It's juts, it sometimes needs some crapy regulation, up and down moments. Maybe I'm doing bad on supplementation.

Edited by Sholrak, 29 December 2013 - 07:47 AM.

[machete234]

....

Edited by machete234, 29 December 2013 - 09:52 AM.

[Potent]

Similar to Abelard, I do get depressed from the CILTEP + Mr. Happy stack combo, which is unfortunate. I will try alternating days on either stack.

MHS for synaptogenesis (?) on 1 day, ciltep for LTP the next.

Again hats off to Abelard for noticing depression with the combo. I didn't notice it before, perhaps due less awareness, or concurrent adrafinil use.

Edited by Potent, 29 December 2013 - 01:52 PM.

[Jeoshua]

Maybe, that metabolic acceleration, or at least the referring to the long term potentiation chemical pathways taking place would exhaust more an organism.
...
Big somnolience is always something tells us we are overdoing
...
Maybe I'm doing bad on supplementation.

The body certainly wants more rest when being put through stressors, and LTP would qualify as one.

You bring up metabolic acceleration, and that's a good point. That's why when I ordered my set of supplements to test this with, I included Activated B Complex and Krebs Cycle Chelates. I figure by supplementing the system that the mitochondria use to create Adenosine Triphosphate (ATP), I can counterbalance the stress that must come from the inhibition of the process that turns cyclic Adenosine Monophosphate (cAMP) into Adenosine Monophosphate (AMP), which would then be used to create more ATP. I am also looking into other ways to increase the amount of ATP, as well.

I think that this is a good idea, in general, and have noticed that many people in this thread seem to be recommending B vitamins, as they have helped them achieve better results. My hypothesis for why this is, I just stated.

This would have effects much broader than increasing LTP or alleviating the somnolescence that people talk about.

-----------------

I also came across a very interesting chemical just now. It's effects mimicing cAMP and also being a PDE4 inhibitor. It's called Bucladesine.

The effects of bucladesine (10(-4) and 3 x 10(-4) M) on cardiac function and energy metabolism were investigated in comparison with those of dopamine (3 x 10(-6) and 10(-5) M) in the working rat heart preparation. Bucladesine dose-dependently increased systolic pressure, cardiac work and coronary flow, but scarcely changed heart rate or cardiac output at 78 cm H2O perfusion pressure. Dopamine increased systolic pressure to a similar extent as bucladesine and also increased heart rate, cardiac work and coronary flow, but did not change cardiac output. Neither drug caused any changes in energy metabolites. At reduced perfusion pressure (15 cm H2O), bucladesine increased systolic pressure, coronary flow and cardiac output, but caused a decrease (at 10(-4) M) or a negligible change (at 3 x 10(-4) M) in heart rate. At 10(-4) M, there was only a slight change in energy metabolism, but at 3 x 10(-4) M, anaerobic metabolism was enhanced. Dopamine decreased systolic pressure and coronary flow and increased heart rate and cardiac work. Cardiac output increased transiently and, thereafter, decreased. Dopamine also enhanced anaerobic metabolism at both doses. The results suggest that both drugs exert similar effects at normal perfusion pressure, but after reduction of perfusion pressure, some differences occur between the two drugs, presumably due to acceleration of the heart rate and subsequent increase in cardiac work by dopamine.

http://www.ncbi.nlm..../pubmed/9712000

Bath application of dibutyryl cyclic AMP, 8-bromo cyclic AMP or forskolin to hippocampal slices caused a short-lasting decrease, followed after washout by a long-lasting increase in the amplitude of population spikes recorded in area CA1 in response to 0.05 Hz stimulation of the Schaffer collateral/commissural pathway. Population spike depression lasted only as long as the cyclic AMP analogues were present in the bath, while the potentiation lasted for at least 2 h after they were washed out. Population excitatory postsynaptic potential amplitude was depressed while dibutyryl cyclic AMP was present in the bath, but after washout it was not significantly different from baseline amplitude. The population spike depression caused by dibutyryl cyclic AMP was prevented by the adenosine antagonist 8-p-sulfophenyltheophylline, but the long-lasting potentiation was not. Thus the transient depression induced by dibutyryl cyclic AMP was probably caused by an action of the drug or its breakdown products as adenosine agonists. The long-lasting potentiation is caused by a different mechanism. Occlusion experiments were performed to examine the relationship of the long-lasting population spike potentiation caused by dibutyryl cyclic AMP to the population spike long-term potentiation caused by high-frequency stimulation. High-frequency stimulation delivered after the population spike potentiation caused by dibutyryl cyclic AMP was established did cause a further potentiation, but only up to the level caused by high-frequency stimulation alone. Dibutyryl cyclic AMP administered after high frequency stimulation-induced long-term potentiation was established had no further potentiating effect.(ABSTRACT TRUNCATED AT 250 WORDS)

http://www.ncbi.nlm.nih.gov/pubmed/8383817

This seems to show that, when narrowed down to just cAMP increase and PDE4 inhibition, there is a bit of hypertension associated with that, and an increased heart beat. This could be what DaCurrent was referring to as "classic stimulant effects" and "vasoconstriction", as vasoconstriction would cause similar effects even tho they are caused by different mechanisms. Also, it shows that LTP in these circumstances did not occur when on the substances, but rather after a washout period, actually inhibiting its formation while the drugs were in effect.

I posit, therefore, that the tiredness people feel is likely caused by LTP, itself, once the other parts of the cocktail begin wearing off. The LTP may actually be being caused by a process that is inhibited by one or more of the ingredients of the CILTEP stack, damming up the natual flow of things and then, once they wear off, causing a flood of activity that could lead to LTP.

At the very least, this suggests that cycling is a very, very highly recommended strategy.

Edited by Jeoshua, 29 December 2013 - 03:37 PM.

[Droplet33]

Similar to Abelard, I do get depressed from the CILTEP + Mr. Happy stack combo, which is unfortunate. I will try alternating days on either stack.

MHS for synaptogenesis (?) on 1 day, ciltep for LTP the next.

Again hats off to Abelard for noticing depression with the combo. I didn't notice it before, perhaps due less awareness, or concurrent adrafinil use.

Small word of warning, english isn't my first language, so bear with me.

I used CILTEP with Zembrin along Mr Happy, but NOT going full bore/dosage with the Happy stack.

Something like, after a period a couple of weeks, where i slowly increased my intake of UMP (starting from 60mg of sublingual UMP, adding 30-40mg each week) to what it is right now :

Morning
CILTEP with 25mg Zembrin (the rest is the recommended alcar, folskolin ratio)
560DHA ( i take 2x Kircland super concentrate omega 3 from Costco : 420 EPA/280 DHA each)
180-200mg UMP sublingual in the morning

Afternoon (often, but sometimes forget to take it)
180mg UMP sub

After Supper
1x kirkland super concentratre omega 3 (so 280mg DHA) OR 2x another brand of less concentrate omega 3 pills

With this, i still get quite of bit of the Happy Stack (good mental clarity, don't feel the need for coffee WHATSOEVER!) benefits, without side effects, probably due to lots of omega 3 and the slight mood effect coming with Zembrin. MIND YOU, I'VE BEEN ON STRONG OMEGA 3 INTAKE FOR YEARS, so i'm not sure someone that didn't take them before starting would not feel depressed right away, before the omega 3 balance in the brain is set.

NOW, I must say that i TRIED going full dose (250mg+ of sublingual UMP), ONCE, in the afternoon (so CILTEP was probably past its peak effects), WITH 1g of tryptophan (2x 500mg caps from "Doctor's Best) and at the time, i felt my brain was running a bit *racy* for a while (took some time to get used to it, but not too uncomfortable).

I can't for the life of me remember if i have taken my usual 180mg of UMP sublingual the same morning and still kicking myself for not doing so, a couple of days ago. Next morning, i felt a bit cranky for a while, until i took the combo i described at the top.

As Abelard said, more experimentation are necessary, tryptophan is important to have under your hands to even consider "playing" with this stuff and Mr Happy said himself in another thread that the timing/quantity of the tryptophan intake might be important to consider.

Small note, i also started to take 5-7mg of sunifiram once or twice a day, in the last few days, i'll have to stop to make accurate tests. I might give it another shot in the next days, as i have nothing planned.

Hope this info will help someone, i'm just a amateur toddler starting to crawl around, so take what i've said with a grain of salt .

Edited by Droplet33, 29 December 2013 - 05:37 PM.

[machete234]

Does anybody get random boners from this? Its a serious question.
I suspect its the artichoke extract because thats somehow viagra like.

Spontanious erection again, this time Im sure it happens after ingesting the forskolin.
I took the artichoke extract 1h before and then the forskolin and thats when it happened.
Maybe its the combination I dont know but probably not the artichoke alone.

[BioFreak]

I don't know if this has been discussed before, but here I go...

luteolin seems to be a dopamine reuptake enhancer as well.
http://www.ncbi.nlm....pubmed/19815045

Maybe thats why a dopamine increasing compound is needed, and another comt inhibitor would be better for people with already low levels of dopamine. And maybe thats the reason why many people prefer artichoke over other supplements, because they already got normal / high levels of dopamine?

Some people have been reporting that quercetin was too much, maybe it is because it is also inhibiting dopamine metabolism through mao and comt, not by being a stronger pde4 inhibitor.
http://www.ncbi.nlm....pubmed/12711835

This would also make sense since forskolin increases d2 receptor densities, maybe its too much for dopamine personalities?
http://www.ncbi.nlm..../pubmed/9353595

So in theory, forskolin + quercetin would require less to none phenylalanine compared to artichoke+forskolin, depending on individual baseline dopamine levels, or would still be not a good choice for dopamine dominant natures.

Maybe we need different stacks, based on individual baseline dopamine levels?

I will test forskolin + quercetin next, and play with adding dopamine increasing compounds.

[chung_pao]

I do not recommend MORUS ALBA to anyone.
Ugh, horrible, depressing experience.

It's supposedly a strong PDE-4 inhibitor. Which might be true - there seemed to be some vasodilation or occurring in the brain while on it.
But, I didn't expect it to be such a strong dopamine antagonist. Hence the very depressing effect.

It did significantly lower blood glucose however, and it was a very potent anxiolytic.
Resultant effect: Wakefulness, depression, a weird "vasodilation" effect occurring in the brain, anxiolysis.
Studies indicate that the wakefulness was partially due to H3 (histamine) agonism.

I tried some tests at cambridgebrainsciences but gave up pretty quickly.

Edited by chung_pao, 01 January 2014 - 12:00 AM.

[abelard lindsay]

I do not recommend MORUS ALBA to anyone.
Ugh, horrible, depressing experience.

I tried that a while ago but it wasn't any good. Hesperidin was worse though as it gave me this weird tunnel vision thing and made me extremely irritable. Zembrin or Artichoke is really where it's at unless you wanted to try to make Ginger work. Taking 1650mg with 4mg of forskolin made things pretty swimmy though. Same thing happened a while ago with Rosmarinic acid. At some point I'll have to try ginger again with lower dosages.

[Bateau]

I do not recommend MORUS ALBA to anyone.
Ugh, horrible, depressing experience.

I tried that a while ago but it wasn't any good... Zembrin or Artichoke is really where it's at unless you wanted to try to make Ginger work.

That's really too bad to hear. Aside from Luteolin, Morus alba is the only potent natural PDE4 inhibitor that I'm aware of that's actually shown significant nootropic potential in animal studies by itself. Some, like quercetin for example, impair cognitive function instead of improve it.

Abelard, can you please elaborate on mulberry not being any good? Was it unremarkable or were there negative aspects to the experience?

What form of Morus did each of you take and how much did you each experiment with it?

Anyone else have some White Mulberry experiences worth mentioning?

Edited by Bateau, 04 January 2014 - 04:46 AM.

[abelard lindsay]

Abelard, can you please elaborate on mulberry not being any good? Was it unremarkable or were there negative aspects to the experience?

What form of Morus did each of you take and how much did you each experiment with it?

Anyone else have some White Mulberry experiences worth mentioning?

This is the one I took:

http://www.amazon.co...ords=morus alba

I'd say it was unremarkable, maybe slightly negative. I ordered it back in April, 2012 so it's been a while since I tried it.

[Jeoshua]

Luteolin is actually a very common chemical, so it should be possible with very little effort to find many different sources for it. Swanson's Ultra Luteolin Complex, for example, gives like 50 mg of Luteolin per pill, and 50 mg of Rutin, a supposed co-factor for absorption.

Today, I have received my shipment:
Enzymatic Coleus Forskolii Extract, 50mg (9mg Forskolin)
Planetary Herbals Holy Basil Extract, 450mg (Taking 2x, roughly 5mg Luteolin, 10mg co-factors, 50mg mixed flavinoids)
Source Naturals Chocolift, 500mg (60 mg Theobromine, 40 mg Caffeine, some L-Tyrosine and L-Phenylalanine)

That's the base of my experimental CILTEP Herbal stack. I will also be supplementing with a Multivitamin, Fully Active B Complex, and Krebs Cycle Precursors w/ Minerals.

In the interest of non-pollution of results, I also vape 12mg/ml Nicotine e-cig fluid every few hours (one of the most potent and well studied nootropics)

Edited by Jeoshua, 04 January 2014 - 02:06 PM.

[chung_pao]

I'm ordering some pure Luteolin from a Chinese manufacturer.
What's a common dose? Somewhere in the 25-100 mg-range?

Aside from simple curiosity, I'm testing pure Luteolin in order to see if we can get the benefits of Artichoke Extract, with less side-effects.

I'm hoping that without the Apigenin (GABA-ergic component of Artichoke), we might get a cleaner effect.

Edited by chung_pao, 04 January 2014 - 06:43 PM.

[kai2]

In the interest of non-pollution of results, I also vape 12mg/ml Nicotine e-cig fluid every few hours (one of the most potent and well studied nootropics)

Isn't nicotine specifically contraindicated for use with CILTEP?

Edited by kai2, 05 January 2014 - 01:23 AM.

[abelard lindsay]

In the interest of non-pollution of results, I also vape 12mg/ml Nicotine e-cig fluid every few hours (one of the most potent and well studied nootropics)

Isn't nicotine specifically contraindicated for use with CILTEP?

Nicotine and CILTEP have a particularly strong interaction that I haven't fully tested so by default I recommend against it. Search back through the thread for anecdotes written by others who have tried it.

[abelard lindsay]

A buddy of mine talked to me about using Forskolin + artichoke extract + vitex as a way to reduce prolactin and even increase libido. He said it was a combo that worked well for him.

Dug up this post from a while ago. Vitex is a d2 antagonist. D2 is a g-protein coupled receptor that inhibits adenylyl cyclase, which forskolin activates....So this could do something synergistic perhaps. It also decreases prolactin so it will probably increase libido.

[machete234]

If theres one effect that forskolin and artichoke has on me then its a hightened libido.
Becoming smarter is a lot harder to measure or notice than having a higher libido of course.
With the accute effects Im not sure if it makes it easier to concentrate sometimes yes and sometimes its the opposite and I might even feel slightly drunk.
The wakefulness could be there when I take a lot of artichoke so in the combo this is what could make that effect stronger.

I also tried Alcar for the tiredness after a few hours but alcar itself seems to give me a runny nose and other allergy symptoms which is a bit strange.

[Jeoshua]

With all due respect, I had absolutely no untoward effects from Nicotine. It could be that the previous anecdotes were based on the usage of cigarettes, and not vaporized nicotine. At any rate, Nicotine is part of my base chemistry at this point, and I will ignore all data points surrounding it by more than 15-20 minutes.

The Coleus + Tulsi + Cocoa combination worked very well. I had a nice, clear headed feeling for half the day, and I've tried all these substances alone, before. They definitely synergize in some way. I got none of the stimulant pushiness some people have described, which may be due to the usage of Tulsi, which has approximately 2x the Luteolin of Artichoke (still looking for a full chemical breakdown of Holy Basil that I don't have to pay $50 just to look at) and some other chemicals which help manage stress. As far as affordability goes, Tulsi ranks up there with the basic Artichoke Extract. I am considering a buy of Ultra Luteolin and Supercritical Holy Basil extract, so I can compare the two.

[kai2]

In the interest of non-pollution of results, I also vape 12mg/ml Nicotine e-cig fluid every few hours (one of the most potent and well studied nootropics)

Isn't nicotine specifically contraindicated for use with CILTEP?

Nicotine and CILTEP have a particularly strong interaction that I haven't fully tested so by default I recommend against it. Search back through the thread for anecdotes written by others who have tried it.

With all due respect, I had absolutely no untoward effects from Nicotine. It could be that the previous anecdotes were based on the usage of cigarettes, and not vaporized nicotine.

Hi Jeoshua,
Yes, the chemistry of cigarettes is very, very different from that of vaporized nicotine. Anyone that is so far behind the science that they would attribute cigarette-CILTEP interactions to nicotine loses all credibility. That said, this is the first I've seen here on longecity about nicotine being a nootropic (but then, I haven't searched for that yet, either). Could you send me a link to a thread on this topic that you recommend?

[Jeoshua]

I don't want to derail this discussion, as the Nicotinic Acetylcholine Receptors (nAChR) don't seem to have much to do with LTP, so are sort of a different topic, altogether, but:

Nicotinic receptor agonists as neuroprotective/neurotrophic drugs. Progress in molecular mechanisms. http://www.ncbi.nlm....pubmed/16906354
Nootropic effect of nicotine on carbon monoxide (CO)-induced delayed amnesia in mice. http://www.ncbi.nlm..../pubmed/7862928
The Effects of Nicotine on Memory and Learning http://digitalcommon....edu/psychhp/5/

The Motherload: http://www.gwern.net/Nicotine

[abelard lindsay]

In the interest of continuously improving on the CILTEP concept I did some more research and came up with another idea for manipulating cAMP levels in the CNS in a beneficial manner:

The idea is to find a herbal D1 agonist and a D2 antagonist with a good safety profile. D2 antagonists and D1 agonists raise cAMP in the CNS and I'm pretty sure nowhere else. This would help focus CILTEP in the CNS.

http://en.wikipedia....iki/D1_receptor

The D₁ subtype is the most abundant dopamine receptor in the central nervous system. This G protein-coupled receptor stimulates adenylate cyclase and indirectly activates cyclic AMP-dependent protein kinases

http://en.wikipedia....iki/D2_receptor

This gene encodes the D₂ subtype of the dopamine receptor. This G protein-coupled receptor inhibits adenylyl cyclase activity.

Now let's see what's in the herb cabinet for this:

http://informahealth...i.41.1.45.14695

Aw crap $43 dollars. Oh well.. Anyway after using google a bit we find that Schinus molle leaf extract with its combined D1/D2 activity increases cAMP in cells that express D1/D2 to 130% of that of forskolin when combined with forskolin.

I found one place that sells the leaf extract. They are in Peru:

http://www.inkanatur...ml#importanciam

This is going to take forever to ship...

[MercuryAX]

Interesting observation, Abelard. I might have to order some of this stuff myself. Have one of the other things they sell (eucalyptus oil) already, not sure what that's good for.

Regarding the mention of vitex a few posts above, shouldn't that theoretically decrease libido? After all, it is the chaste berry. Perhaps stacked with the other ingredients it has the opposite effect.

[chung_pao]

I don't know of any D2 antagonists - but I'm pretty disinclined to be the ginniepig for them, since I think Morus Alba's depressing effect was due to D2 antagonism.

D1 agonists, on the other hand, I'm all for!

Myself, I'm going to see if Forskolin's effect can be replicated by CORDYCEPS.
Studies suggest it's also an agonist at adenosine receptors (A2), while having other cool properties.

http://www.ncbi.nlm......7229422<br />

whereas the NO-sensitive guanylyl cyclase inhibitor ODQ did not alter the cordycepin-induced up-regulation of cGMP, the adenylyl cyclase inhibitor SQ22536 completely blocked the cAMP enhancement mediated by cordycepin, indicating that cordycepin had different modes of action.

http://www.ncbi.nlm......1512251<br />

Cordycepin, a pure compound of Cordyceps sinensis (CS), is known as an adenosine analog.
In addition, the protein levels of AR subtypes (A1, A2A, and A2B) were increased after the administration of cordycepin,

We further observed that cordycepin regulated the mRNA expression of the A1, A2a, A2b, and A3 adenosinereceptors in the mouse Leydig cells, and that antagonists of A1, A2a, and A3 suppressed testosterone production 20-50% testosterone production.

When the Taiwanese researchers added cordycepin and various adenosine blockers to Leydig cells, they were able to work out that cordycepin works most via adenosine receptor A2a (production increased by a maximum of factor 7), and to a lesser extent via A1 and A3.
http://www.ergo-log....cordycepin.html

I know it sounds pretty far-fetched - the last quote isn't even a study.
But I'm still testing Cordyceps + Artichoke out of curiosity. At least, it'll probably have some cool effects on fertility.

In addition, I found Artichoke had much stronger effects when combined with EGCG.
Turns out, the concentration of Luteolin is increased by COMT-inhibitors (such as egcg), because COMT metabolizes Luteolin.
It's a very strong difference, and using 900 mg artichoke extract with egcg definitely makes the stack too strong.

http://www.ncbi.nlm....pubmed/23386290
[

Luteolin was a rare substrate of human COMT favoring a para-methylation, but further demethylation by human CYP1A2 and CYP3A4/5 caused a preference of accumulation in meta-methylated luteolin in vivo.

Edited by chung_pao, 07 January 2014 - 12:14 AM.

[magta39]

That's interesting about the cordyceps increasing both cAMP and cGMP......wondering if you get get more synergy with taking PDE1 and PDE4 inhibitors together....like vinpocetine and artichoke taken together?

[hephaestus]

Wouldn't increased expression of adenosine receptors and adenosine receptor agonism make you tired? Caffeine is an antagonist.

[abelard lindsay]

I found a local source for Schinus molle Leaf extract which is also known as "California Pepper Tree" : http://healingherbsb...-tinctures.html

Not the most awesome web store in existence unfortunately. The rest of the site does not lend me a lot of confidence in their product. Seems this is a real odd ball of a supplement. Hardly anyone has it in stock.

These guys *used to* carry it and have a lot of good information on it: http://www.rain-tree...tm#.UstulmRDvFc

The berries of this plant are apparently a well known french cooking spice known as "pink peppercorns" though (http://www.pink-peppercorns.com/).

Seems to be a powerful antimicrobial:

http://www.scribd.co...T-SCHINUS-MOLLE

Anyway... Seems this one has a long history of traditional use but it's not very well known otherwise. I'm going to be careful with it and watch for any sort of adverse reaction.

Edited by abelard lindsay, 07 January 2014 - 03:41 AM.