2626 replies to this topic

[abelard lindsay]

I have two questions currently:

1) Does anyone have short lived motivational effects? (1-3 hours)

2) Will taking Guanfacine to counteract the working memory issues also weaken positive benefits?

I would get short lived effects from Luteolin. Artichoke lasted longer. Quercetin lasted too long and caused sleep problems.

As for 2, we already got into this way back in the debate with Unbeatable King a few pages ago. Guanfacine may seem attractive because it lowers cAMP inthe pre-frontal cortex improving working memory. However cAMP is not necessarily affected in the PFC (Pre-Frontal Cortext) by our PDE4 inhibitor. cAMP signaling is highly compartmentalized. cAMP does not flow around the body like water. It is in particular areas in the body being regulated by particular PDE enzyme subtypes that are each only found in particular parts of the anatomy. That's why there are all the PDE variants PDE1-10 and then further subvariants such as PDE4A1 PDE4A5, etc. which regulate cAMP in the particular parts of the body where they are localized.

Rolipram had the problem of inhibiting the PDE4 variants that improved memory but also the ones that caused vomiting. Some PDE4 variants, when inhibited, weaken memory, some improve it. At least in my and others experience, Luteolin doesn't seem to have the vomiting or short-term memory problems probably because the mix of PDE variants it affects seems to be limited to ones that are tolerable and beneficial. In my and others experience, Quercetin seems to cause undesirable effects when inhibited (bad sleep, working memory degration) with the stack at least at dosages that most pills come in probably because it is inhibiting PDE variants that lead to these issues, for instance in the PFC. Some people have had success at 100mg of Quercetin though.

[Nootropic Cat]

Just to update my previous posts...

Some further reading has served to allay most of my concerns. First of all the study about DNA damage due to endoreduplication was dealing with very high doses: the amounts of luteolin in artichoke supplements certainly wouldn't be a problem, and to get into dangerous territory with quercetin would probably involve gram+ doses (though I think I'd keep it down to around 200mg to be on the safe side). Also having looked further into mesembrine/kanna, it's actually a very strong serotonin uptake inhibitor, so that's out, unless that's something you're looking for.

I'm still a little confused about the intraocular pressure issue. According to wiki, forskolin is used to reduce intraocular pressure; is that a bad thing? Does it have any noticeable effect at small doses anyway?

Wanted as well to reiterate my question about hesperidin, just out of curiosity. What were the problems people had with that?

Cheers

Edited by TripleHelix, 11 January 2013 - 09:51 AM.

[sparkk51]

I have two questions currently:

1) Does anyone have short lived motivational effects? (1-3 hours)

2) Will taking Guanfacine to counteract the working memory issues also weaken positive benefits?

I would get short lived effects from Luteolin. Artichoke lasted longer. Quercetin lasted too long and caused sleep problems.

As for 2, we already got into this way back in the debate with Unbeatable King a few pages ago. Guanfacine may seem attractive because it lowers cAMP inthe pre-frontal cortex improving working memory. However cAMP is not necessarily affected in the PFC (Pre-Frontal Cortext) by our PDE4 inhibitor. cAMP signaling is highly compartmentalized. cAMP does not flow around the body like water. It is in particular areas in the body being regulated by particular PDE enzyme subtypes that are each only found in particular parts of the anatomy. That's why there are all the PDE variants PDE1-10 and then further subvariants such as PDE4A1 PDE4A5, etc. which regulate cAMP in the particular parts of the body where they are localized.

Rolipram had the problem of inhibiting the PDE4 variants that improved memory but also the ones that caused vomiting. Some PDE4 variants, when inhibited, weaken memory, some improve it. At least in my and others experience, Luteolin doesn't seem to have the vomiting or short-term memory problems probably because the mix of PDE variants it affects seems to be limited to ones that are tolerable and beneficial. In my and others experience, Quercetin seems to cause undesirable effects when inhibited (bad sleep, working memory degration) with the stack at least at dosages that most pills come in probably because it is inhibiting PDE variants that lead to these issues, for instance in the PFC. Some people have had success at 100mg of Quercetin though.

Thank you, you helped clear up alot of things for me as well as gave me more hope for this stack. Judging from your response to question 2, it's most likely fine to take Guanfacine as it will only affect cAMP in the prefrontal cortex, which isnt an area being targeted for LTP? If so, would this be a beneficial addition to the stack if a favorable pde4 inhibitor is discovered that also, unfortunately, reduces working memory through raising cAMP in the prefrontal cortex?

[PigeonParty]

I've been trying this stack for a few days now. Everything seemed good at first, especially boosts to mood and sociability. Can't say for sure if I experienced any boosts in long term memory that weren't placebo. Today, however, I'm still getting the mood improvements, but I'm stuck under a pretty thick brain fog. It's feeling like my working memory is at a significant deficit.

Right now I'm taking:

• 6.5 mg Forskolii
• 450 mg Artichoke
• 1000 mg L-Phenylalanine

I'm thinking of abandoning this stack for now, but am curious if anyone else has experienced this and found a way to get around it?

[chziime]

I started this stack today... 1x NOW Artichoke and 1x Solaray Forskolii. I took it with about 100mg of 1-carboxy (the L-DOPA + COMT inhibitor extract of Mucuna). I suddenly got a little bit anxious and nauseous, a bit too much to be able to gauge effects. Would 1-carboxy be a bad idea daily because of COMT inhibition leading to the effects lasting too long?

Really, you just need any dopaminergic, right? Most make me anxious... I take 1-carboxy at bedtime for better sleep, but it can backfire sometimes by causing insomnia. So, something mildly dopaminergic like ginkgo or theanine would work well with the stack?

I also take 450mg of Kira St. Johns Wort every morning (might lower the dosage, as more than 300mg causes a bit of hypomania), would its MAOI-A activity exacerbate anxiety even more? Isn't ginkgo a mild MAOI-A as well?

Sorry for all the questions, I would appreciate any help. As a video editor, I need to spend long hours working on the computer. Maybe the stack is working, after all. This is the most detailed post I ever made on this forum!

[owtsgmi]

I've been trying this stack for a few days now. Everything seemed good at first, especially boosts to mood and sociability. Can't say for sure if I experienced any boosts in long term memory that weren't placebo. Today, however, I'm still getting the mood improvements, but I'm stuck under a pretty thick brain fog. It's feeling like my working memory is at a significant deficit.

Right now I'm taking:

• 6.5 mg Forskolii
• 450 mg Artichoke
• 1000 mg L-Phenylalanine

I'm thinking of abandoning this stack for now, but am curious if anyone else has experienced this and found a way to get around it?

Maybe too much dopamine. I would cut down to 200mg LPA and see if you have an improvement. The other dosages seem good to me.

I started this stack today... 1x NOW Artichoke and 1x Solaray Forskolii. I took it with about 100mg of 1-carboxy (the L-DOPA + COMT inhibitor extract of Mucuna). I suddenly got a little bit anxious and nauseous, a bit too much to be able to gauge effects. Would 1-carboxy be a bad idea daily because of COMT inhibition leading to the effects lasting too long?

Really, you just need any dopaminergic, right? Most make me anxious... I take 1-carboxy at bedtime for better sleep, but it can backfire sometimes by causing insomnia. So, something mildly dopaminergic like ginkgo or theanine would work well with the stack?

I also take 450mg of Kira St. Johns Wort every morning (might lower the dosage, as more than 300mg causes a bit of hypomania), would its MAOI-A activity exacerbate anxiety even more? Isn't ginkgo a mild MAOI-A as well?

Sorry for all the questions, I would appreciate any help. As a video editor, I need to spend long hours working on the computer. Maybe the stack is working, after all. This is the most detailed post I ever made on this forum!

Mildly dopaminergic? I would try LPA or uridine 250mg (w/ DHA). Or, just drink some strong coffee.

[chziime]

I can't tolerate caffeine. Why is DLPA recommended over L-DOPA? Earlier on in this thread, the OP said that ginkgo or theanine can be used as the dopamine agent in the stack, right?

[owtsgmi]

I can't tolerate caffeine. Why is DLPA recommended over L-DOPA? Earlier on in this thread, the OP said that ginkgo or theanine can be used as the dopamine agent in the stack, right?

Sounds like you are sensitive to dopaminergics like me. I also get very amped on caffeine. I do drink coffee, but only a cup in the morning. Have you just tried smaller dosages of your chosen dopaminergic? DLPA is not the same as LPA (I think it is one of the racetams?). I recommend the LPA. I have tried L-DOPA (mucuna) and found it too stimulating. Gingko messes with GABA so I don't use that either. Theanine is actually not bad. I used it for awhile as the dopamine in this stack, but eventually found it lacking. From theanine, I switched to LPA. Then, i finally discovered uridine. Uridine modulates dopamine, so I think it utilizes the caffiene in the most optimal way.

[abelard lindsay]

Are any of you who are getting good results at first that don't last taking a b vitamin supplement? B6 is an essential parts of dopamine metabolism. Vitamin B6, like l-phenylalanine, may get depleted by CILTEP and thus need to be supplemented. I would advise to not take more b vitamins than the amount recommended by the instructions on the supplement bottle. This is not a case where more is better, especially with b6.

Edited by abelard lindsay, 16 January 2013 - 02:42 PM.

[health_nutty]

Are any of you who are getting good results at first that don't last taking a b vitamin supplement? B6 is an essential parts of dopamine metabolism. Vitamin B6, like l-phenylalanine, may get depleted by CILTEP and thus need to be supplemented. I would advise to not take more b vitamins than the amount recommended by the instructions on the supplement bottle. This is not a case where more is better, especially with b6.

Is a simple multivitamin enough?

[fenra]

Are any of you who are getting good results at first that don't last taking a b vitamin supplement? B6 is an essential parts of dopamine metabolism. Vitamin B6, like l-phenylalanine, may get depleted by CILTEP and thus need to be supplemented. I would advise to not take more b vitamins than the amount recommended by the instructions on the supplement bottle. This is not a case where more is better, especially with b6.

Is a simple multivitamin enough?

I took this multivitamin with 100% of the daily dosage of all the b vitamins... then again, it might be a fraction of what someone on CILTEP really needs.

[abelard lindsay]

Here's some B6/Dopamine Metabolism research. I just thought of this as being a possible reason why ZRBarnes and I did not have diminished effects as we are both taking B-Complex Supplements as part of our regular stacks.

http://www.ncbi.nlm..../pubmed/2761676

Effect of vitamin B-6 nutrition on the levels of dopamine, dopamine metabolites, dopa decarboxylase activity, tyrosine, and GABA in the developing rat corpus striatum.

....

The concentration of striatal DA in rats fed vitamin B-6 inadequate diets was significantly lower than rats fed optimal diets at 28 and 56 days of age. The differences in striatal DA concentrations among vitamin B-6 dietary groups was more evident with age. Measurements of the major metabolites of DA, homovanillic acid (HVA), and 3,4-dihydroxyphenylacetic acid (DOPAC) in rat corpus striatum showed a significant decrease in HVA level in B-6 restricted rats compared to B-6 sufficient groups. Striatal DOPAC levels were not significantly different among any of the groups at any age. The activity of dopa decarboxylase holoenzyme was found to be significantly lower in the corpus striatum of rats fed suboptimal B-6 diets. Whether this finding has a significant effect on DA levels has yet to be determined since dopa decarboxylase is not the rate-limiting enzyme in the synthesis of DA. In an effort to determine the underlying mechanism for the loss of striatal DA, the concentration of its precursor tyrosine (TYR) was measured. Vitamin B-6 undernutrition had no significant effect on the levels of TYR in rat corpus striatum. The concentration of the inhibitory neurotransmitter GABA was also measured. The results indicate that as expected the levels of striatal GABA were significantly lower than controls at 14 and 28 days of age. On the other hand, striatal GABA levels in B-6 restricted rats did not differ from controls at 56 days of age

http://www.ncbi.nlm....ov/pubmed/18422

Levels of neurotransmitters in brain of vitamin B12 deficient rats.
Deana R, Vincenti E, Deana AD.
Abstract
The levels of norepinephrine, dopamine and 5-hydroxytryptamine in brain homogenates of vitamin B12-deficient rats have been investigated. The norepinephrine levels were significantly decreased in the deficient animals compared to controls. The two major catabolic pathways of norepinephrine e.g. monoamine oxidase and catechol-O-methyl transferase did not show significant variations. Both acetyl cholinesterase and butiryl-cholinesterase markedly decreased in the plasma of the vitamin B12-deficient rats.

[norepinephrine]

Abelard - I've been supplementing with SN's coenzymated B-complex daily over the entire run of my CILTEP trial. I consider the B vitamins to be a pretty core component to my daily stack.

I've actually been having better luck with quercetin after halving the dosage to 500mg, first thing in the morning. Doing that along with liquid melatonin and proper sleep hygeine seemed to alleviate my onset-related insomnia. The quercetin supplement I take also contains 800mg vitamin C, so along with the B complex and L-tyrosine, that should be enough co-factors to ensure catecholamine synthesis. (Should note - I also take zinc and magnesium daily.)

What I'm interested in, and what seems to have slipped under the radar thus far - is the MAO-inhibiting properties of the various PDE4 inhibitors proposed for the stack. Luteolin, quercetin and resveratrol all have various MAO-A and B inhibition qualities, as does curcumin (which also inhibits PDE4). Thus, the genius of this stack seems to be, at least in my mind, how it mimics an Adderall-like effect with a more sustainable mode of action.

I'm still trying to perfect my own personal stack, but needless to say it'll be a variant of CILTEP. Rhodiola, curcumin and (if I can ever find a reasonable source) Chinese Cat's Claw are all on my list of MAO-inhibiting herbs/phytonutrients. Green tea inhibits COMT and has always stacked well for me on CILTEP or otherwise. Ginkgo and gotu as well have proven synergistic for me, though I cycle them to avoid tolerance.

[trip96]

Hey norepineherine! I too have been trying to source a reliable Chinese cats claw vendor. However, I have access to other MAOI herbs. I know the Chinese cats claw is MAOI-B but perhaps you can exchange (for the meantime) with harmaline containing herbs. The smoothest I have found is passionflower. I make a tea daily and noticed a better feeling of well being as well as synergism with all kinds of mind altering foods, nootropics, drugs; whatever you want to label it. Also, check out tony wright's book "left in the dark" if you haven't already. It's an short read and very interesting.

[peakplasma]

Abelard - I've been supplementing with SN's coenzymated B-complex daily over the entire run of my CILTEP trial. I consider the B vitamins to be a pretty core component to my daily stack.

I've actually been having better luck with quercetin after halving the dosage to 500mg, first thing in the morning. Doing that along with liquid melatonin and proper sleep hygeine seemed to alleviate my onset-related insomnia. The quercetin supplement I take also contains 800mg vitamin C, so along with the B complex and L-tyrosine, that should be enough co-factors to ensure catecholamine synthesis. (Should note - I also take zinc and magnesium daily.)

What I'm interested in, and what seems to have slipped under the radar thus far - is the MAO-inhibiting properties of the various PDE4 inhibitors proposed for the stack. Luteolin, quercetin and resveratrol all have various MAO-A and B inhibition qualities, as does curcumin (which also inhibits PDE4). Thus, the genius of this stack seems to be, at least in my mind, how it mimics an Adderall-like effect with a more sustainable mode of action.

I'm still trying to perfect my own personal stack, but needless to say it'll be a variant of CILTEP. Rhodiola, curcumin and (if I can ever find a reasonable source) Chinese Cat's Claw are all on my list of MAO-inhibiting herbs/phytonutrients. Green tea inhibits COMT and has always stacked well for me on CILTEP or otherwise. Ginkgo and gotu as well have proven synergistic for me, though I cycle them to avoid tolerance.

Have you seen this? http://www.sciencedi...197018609002794

We isolated luteolin and apigenin from the fruit of Perilla frutescens (L.) Britt by using an activity-guided extraction technique, and proved that the two compounds possess actions of enhancing monoamine uptake either upon monoamine-transporter transgenic Chinese hamster ovary (CHO) cells or upon wild dopaminergic cell lines, with higher specificity for dopamine (DA) uptake than for norepinephrine (NE)- and serotonin (5HT)-uptake, as well as with more potency and greater efficacy for luteolin than for apigenin. Further, in the transgenic cells, the principal NE/DA uptake activation by luteolin was significantly prevented by respective transporter inhibitor, and the transmitter-uptake-enhancing action was independent of its ligands, which is in support of the compounds as monoamine transporter activators. Furthermore, luteolin evoked a marked disinhibition of cocaine-targeted effect in CHO cells overexpressing dopamine transporter. Thus, luteolin and apigenin function as monoamine transporter activators, which would improve several hypermonoaminergic neuropsychological disorders, especially cocaine dependence, through up-regulating monoamine transporter activity.

Potent MAO-A inhibitor, Luteolin (artichoke extract), also acts as a potent monoamine transport activator (a seemingly contradictory mechanism). Wrap your head around that.

[Galaxyshock]

Hordenine may be considered as a stimulant, it's a potent selective MAOB-inhibitor AND noradrenaline-reuptake-inhibitor

Edited by Galaxyshock, 19 January 2013 - 12:17 AM.

[nupi]

Are there any decent non-prescription (I know there's Selegiline and Rasagiline but good luck getting a prescription for those, much less if you are already on an SSRI) selective MAOB-I without NRI properties (NE makes me anxious and obsessive)?

[Galaxyshock]

Are there any decent non-prescription (I know there's Selegiline and Rasagiline but good luck getting a prescription for those, much less if you are already on an SSRI) selective MAOB-I without NRI properties (NE makes me anxious and obsessive)?

Olive oil (Hydroxytyrosol)
Fo-Ti
Cat's claw (also NMDA-antagonist)
Rutin (similar to quercetin)

[nupi]

Guess I will have to look into Fo-Ti and Cat's claw - I know that hydroxytyrosol is rather weak sauce as far as MAOB-I goes.

[norepinephrine]

Fo-ti is apparently pretty estrogenic FWIW.

Doesn't hordenine come with some undesirable side effects? Been a while since I looked into it.

Rutin is included in the quercetin supplement I take (as well as a few other flavonoids and vitamin C).

Manganese is supposed to enhance MAO-inhibition whereas copper is utilized in creating MAO. The MAO-inhibiting qualities of some of the above substance "could" be due to manganese content; just an educated guess. Turmeric, for example, is high in manganese.

Cat's Claw refers to both the Peruvian and Chinese herb - in the case of MAO-inhibition, it's the Chinese one you want (and that happens to also be the one I'm having a hard time sourcing for a reasonable price on the internet; may be worth trying a TCM brick-and-mortar place).

In other news, I started trialing curcumin on it's own today. Rhodiola should arrive tonight. It's way too preliminary to talk about any real effects from curcumin (aside from markedly reducing the soreness in my back from weight lifting yesterday), but I think a nice combination for CILTEP may be curcumin, quercetin+rutin+C, B complex and forskolin.

P.S. That's actually a very interesting point about luteolin and may explain why it's been more well-tolerated than the other suspects in the mix.

Abelard, what's your stance on using a cocktail of low-dosed PDE4/MAO-inhibitors in the stack? That's what I'm looking at right now.

[abelard lindsay]

Abelard, what's your stance on using a cocktail of low-dosed PDE4/MAO-inhibitors in the stack? That's what I'm looking at right now.

I don't really recommend fooling around with MAOI inhibitors if you're not depressed. In my opinion, I really think the CILTEP stack is more than strong enough by itself without throwing MAOIs into the mix.

That being said, a few words about MAOIs, at least on their own:

The thing to keep in mind with MAOI inhibition is that MAOI-A inhibition is undesirable vs MAOI-B inhibition. MAOI-A inhibition has the tyramine problem where if one eats certain foods that contain tyramine while taking an MAOI-A inhibitors it can percipitate a hypertensive crisis. At least in my experience, MAOI-A inhibition, which blocks the breakdown of epinephrine and norepinephrine, is not that pleasurable as it leads to heightened stress responses. it is also unwise to mix MAOI inhibitors and other strongly psychoactive drugs due to serotonin syndrome (MAOI-A inhibits serotonin breakdown). More stuff to scare you over here : http://en.wikipedia....drenergic_storm .

MAOI-B inhibition is a little smoother, in my experience, and people have been raving about Deprenyl for years. I'll refer you to the thread, as the pros and cons have been mulled over repeatedly in much more detail.

Edited by abelard lindsay, 20 January 2013 - 12:00 AM.

[Werper]

Do you know at what dose deprenyl turns from being a MAOI-B inhibitor to a MAOI_A inhibitor? I've read somewhere on here like 10mg or greater, but nothing concrete.

[peakplasma]

Do you know at what dose deprenyl turns from being a MAOI-B inhibitor to a MAOI_A inhibitor? I've read somewhere on here like 10mg or greater, but nothing concrete.

A loss of selectivity for MAO-B might not occur until well above 20mg with subchronic doses; however, with chronic dosing some MAO-A inhibition was observed at 10mg.

Tyramine pressor sensitivity changes during deprenyl treatment

"While only a modest (3.7-fold) increase in tyramine sensitivity was found with the 10 mg/day deprenyl dose, the increase in tyramine sensitivity at the 60 mg/day dose of deprenyl (22-fold) approached that found with tranylcypromine."

Norepinephrine, aren't you concerned that Luteolin is already a rather potent MAO-A inhibitor? I am taking low dose deprenyl (1mg p.d., >1.5 years) with my CILTEP (3 months) and I'm already cautious about increased tyramine sensitivity.

Abelard, have you been cycling your CILTEP? Or are you just abstaining on weekends?
.

[abelard lindsay]

Do you know at what dose deprenyl turns from being a MAOI-B inhibitor to a MAOI_A inhibitor? I've read somewhere on here like 10mg or greater, but nothing concrete.

Norepinephrine, aren't you concerned that Luteolin is already a rather potent MAO-A inhibitor? I am taking low dose deprenyl (1mg p.d., >1.5 years) with my CILTEP (3 months) and I'm already cautious about increased tyramine sensitivity.

Abelard, have you been cycling your CILTEP? Or are you just abstaining on weekends?

Luteolin and Quercetin have some MAO inhibiting properties, though nowhere near as strong as MAO inhibiting anti-depressants:

http://www.ncbi.nlm....pubmed/17328236

Furthermore, quercetin (7) had a more potent inhibitory effect on MAO-A (IC50 value: 2.8 microM) than MAO-B (IC50 value: 90.0 microM). Apigenin (2) and luteolin (3) also preferentially inhibited MAO-A (IC50 values: 1.7 and 4.9 microM, respectively) compared with MAO-B (IC50 values: 12.8 and 59.7 microM, respectively).

Just to put that in perspective, Methylene Blue, is a very potent MAO-A inhibitor. It also has metabolites with ic50 values for inhibiting MAO-A that are about 440 times more potent than Luteolin.

http://www.ncbi.nlm....pubmed/22197611

The results show that azure B is a potent MAO-A inhibitor (IC₅₀=11 nM), approximately 6-fold more potent than is MB (IC₅₀=70 nM) under identical conditions

We could also compare Luteolin to a common tri-cyclic anti-depressant such as Nardil (MAO-A Ic50 0.146 microM
http://pubchem.ncbi....ry.cgi?cid=3675) which is about 33 times more potent.

Also, anecdotally, luteolin does not feel at all like methylene blue.

With regards to cycling CILTEP, sometimes I take a day or two off when I want to relax and have a couple of lazy days. I'm not on a consistent schedule of cycling. ZRBarnes says he takes Sundays off.

Edited by abelard lindsay, 20 January 2013 - 02:24 AM.

[norepinephrine]

Indeed, the concern for me is low because of how mild most of the aforementioned herbal MAO inhibitors are (not too mention they're reversible). If I were taking pharmaceuticals (or strongly psychoactive drugs), I'd be concerned - but alas, the hardest thing I really touch is pot, and even that's on strict occassion. Correct me if I'm wrong, but the tyramine deal is mainly problematic for pharmaceutical-grade, irreversible MAO-A inhibitors, no?

Anyway, the reason I brought it up is because I started noticing a commonality over the years between all these seemingly separate things that were helping me in terms of motivation (e.g., fo-ti, ginkgo, green tea, etc.) without having any idea there was something connecting them together. Hence,

[Galaxyshock]

Yes most of the herbal MAOIs are rather mild/"moderate" and won't get you in trouble. I think harmala alkaloids are the most potent plant-based MAOa-inhibitors (in higher doses MAOb-affinity too) and even with them tyramine doesn't seem to be a big concern. I've read people combining Rhodiola and SSRI without problems but caution is of course adviced. So the bad reputation of MAOIs stems from the pharmaceutical irreversible MAO-inhibitors and -blockers. I don't really see a point of creating that type of harsh drugs when the nature provides us effective compounds with high safety profile.

[nupi]

We could also compare Luteolin to a common tri-cyclic anti-depressant such as Nardil (MAO-A Ic50 0.146 microM
http://pubchem.ncbi....ry.cgi?cid=3675) which is about 33 times more potent.

Nardil (Phenelzine) is not a TCA but rather a prototypical non-selective MAOI. And non-selective MAOIs definitely are no toys (people seem to think of Selegiline as a rather harmless substance and presumably below 10mg it is comparably benign, but above 10mg things can get nasty).

[abelard lindsay]

Nardil (Phenelzine) is not a TCA but rather a prototypical non-selective MAOI. And non-selective MAOIs definitely are no toys (people seem to think of Selegiline as a rather harmless substance and presumably below 10mg it is comparably benign, but above 10mg things can get nasty).

Thanks for the correction! It's great to have the community around to check my theorizing for any mistakes.

[norepinephrine]

Couple things:

1) What's the consensus on preferred forskolin brand? I'm about a week away from running out of my Solaray forskohlii (385mg, 1% extract). I liked it but I'm sure there could be better brands out.

2) Having pretty good luck on the following:
First thing in the morning: 385mg forskohlii, 1 sublingual B-complex, 500mg quercetin+rutin+C, 1000mg curcumin, 500mg ashwagandha, 250mg rhodiola rosea, 30mcg zinc, 1000mg omega 3's, 15 drops ginkgo/gotu/rosemary tincture, 500mg ALCAR.
15-30 minutes later: double shot espresso, food.
Keeping all of those first thing in the morning and only redosing the ginkgo later on (and if I feel like it, ashwagandha) while cutting off all caffeine around 12pm allows me to still get a good night's rest.

I noticed the focusing/stimulative effects I'd get were mainly when combining my ginkgo tincture with the regular CILTEP stack; YMMV. (FWIW I was diagnosed from ADD as a child and have had periodic episodes of depression/anxiety for most of my life.)

[medievil]

Diazepam is a PDE4 inhibitor, i take it in combination with nefiracetam but im not sure wheter benzo's inhibit the cAMP acumulation induced by nefi as with forskolin, anyone has any info behind the mechanism? May readd quercetin but kinda switched from most sups to a healthier diet and trying to take less supplements too, see what that gives.