#1171
Posted 12 February 2013 - 05:59 PM
I've tried the stack with aniracetam, and it didn't really seem to work any differently than usual.
I tried taking 2 artichoke in the late afternoon for the booster dose, rather than one, and it's too much. A better approach would be to take the forskolin+artichoke first thing in the morning, then another artichoke at mid-day, and to bring another artichoke capsule to work and only take it if I need it.
#1172
Posted 12 February 2013 - 07:23 PM
Updates:
I've tried the stack with aniracetam, and it didn't really seem to work any differently than usual.
I tried taking 2 artichoke in the late afternoon for the booster dose, rather than one, and it's too much. A better approach would be to take the forskolin+artichoke first thing in the morning, then another artichoke at mid-day, and to bring another artichoke capsule to work and only take it if I need it.
What symptoms do you get if it is too much? Overstimulated? Headache?
#1173
Posted 12 February 2013 - 07:38 PM
Updates:
I've tried the stack with aniracetam, and it didn't really seem to work any differently than usual.
I tried taking 2 artichoke in the late afternoon for the booster dose, rather than one, and it's too much. A better approach would be to take the forskolin+artichoke first thing in the morning, then another artichoke at mid-day, and to bring another artichoke capsule to work and only take it if I need it.
What symptoms do you get if it is too much? Overstimulated? Headache?
Headache, mild euphoria followed by a mild crash, and mental tunnel-vision. I tried it several days last week, and I'd keep going in to work, sitting down at my computer, and all the sudden an hour would have passed and I'd done nothing productive. It was just like my college days of taking way too much MPH and piracetam and trying to study: I'd find myself getting hopelessly sucked in by time-wasters like facebook or reading news stories. I didn't even feel time passing, and I couldn't regulate my focus.
You could call it "overstimulated" because this sort of obsessive/compulsive information devouring is typical for me when taking too many stimulants. Interestingly, this problem definitely doesn't happen when I take the morning dose of forskolin with 2 artichoke capsules, so the artichoke must have a longer half-life than I've been giving it credit for.
#1174
Posted 12 February 2013 - 10:03 PM
Re: Jadamgo, from the sound of it your problem has more to do with habit rather than substance. I think your situation would be massively improved if you did a few basic things like drafting up a to-do list prior to dosing, and taking short breaks during study/work sessions to reduce the monotony and stay mentally fresh.
#1175
Posted 13 February 2013 - 05:16 AM
I've been using the artichoke extract more judiciously this week, and I haven't had any of the side effects listed above: no headache, euphoria/crash, nor mental tunnel vision.
#1176
Posted 13 February 2013 - 05:46 PM
Updates:
You could call it "overstimulated" because this sort of obsessive/compulsive information devouring is typical for me when taking too many stimulants. Interestingly, this problem definitely doesn't happen when I take the morning dose of forskolin with 2 artichoke capsules, so the artichoke must have a longer half-life than I've been giving it credit for.
Too much tyrosine + pram + ginseng + b vitamins minus choline made me do this. I found that taking Uridine at night h/e mediated the effect next day.
Also, it appears that modafinil/armodafinil-ltp occludes forskolin ltp by some mechanism described here. There was a thread on this, but I don't think we ever got to any conclusions. It seems for-ltp and mod-ltp work in the same area of the hypothalamus affecting same neurons to different degrees. This is interesting b/c I feel great on armodafinil and if for-ltp has similar effects then I may just increase dose of CILTEP and avoid buying armodafinil. Anyone have thoughts on the study?
#1177
Posted 15 February 2013 - 10:47 PM
However, I must admit there's a pretty clear lurking variable: I've abstained from coffee for the last 4 days, opting instead of a small amount of tea in the morning to decrease tolerance, and today I sucummbed again to the espresso urge. My measure of whether today's good effects were caused by CILTEP+piracetam or the reintroduction of espresso will be based on whether I can reproduce said effects at a later date without coffee.
#1178
Posted 16 February 2013 - 04:34 AM
Noticed a very nice synergy between combining 4 grams of piracetam with the CILTEP stack today. Mood improved, socialability enhanced, work ethic restored and mathematical reasoning improved. I'd call it a 'cleaner' Adderall.
However, I must admit there's a pretty clear lurking variable: I've abstained from coffee for the last 4 days, opting instead of a small amount of tea in the morning to decrease tolerance, and today I sucummbed again to the espresso urge. My measure of whether today's good effects were caused by CILTEP+piracetam or the reintroduction of espresso will be based on whether I can reproduce said effects at a later date without coffee.
I've found that Phenylpiracetam and CILTEP together make a great stack. I have yet to try 4 grams of Piracetam, but I'll give it a go soon. 'Racetams (except Aniracetam) are a good thing to stack since they work on the AMPA receptor part of the memory encoding process which is upstream from cAMP and CREB.
Speaking on interesting additions to the stack. Rhodiola by itself gives me random flashbacks of old memories. It's kind of interesting with CILTEP because of the emotional blunting and such it lets me reprocess them and reexamine them in a more objective light. I find I get these deep insights when analyzing my own personal history that provide an almost spiritual experience. I wonder if CILTEP could help people who are struggling with negative memories.
#1179
Posted 16 February 2013 - 04:56 AM
For me, rhodiola provides a mild mood boost without really blunting my emotions.
#1180
Posted 16 February 2013 - 04:56 AM
Headache, mild euphoria followed by a mild crash, and mental tunnel-vision. I tried it several days last week, and I'd keep going in to work, sitting down at my computer, and all the sudden an hour would have passed and I'd done nothing productive. It was just like my college days of taking way too much MPH and piracetam and trying to study: I'd find myself getting hopelessly sucked in by time-wasters like facebook or reading news stories. I didn't even feel time passing, and I couldn't regulate my focus.
You could call it "overstimulated" because this sort of obsessive/compulsive information devouring is typical for me when taking too many stimulants. Interestingly, this problem definitely doesn't happen when I take the morning dose of forskolin with 2 artichoke capsules, so the artichoke must have a longer half-life than I've been giving it credit for.
This is likely caused by too much cAMP. One of the suspected mechanisms of ADHD is elevated cAMP in the Prefrontal-Cortex, which causes overstimulation of hyperpolarization-activated cyclic nucleotide-gated channels, resulting in affected neurons being unable to communicate. On the large scale, this results in spotty communication between the PFC and the rest of the brain, resulting in difficulties with executive function (regulating attention, planning, initiating tasks that have delayed rewards, regulating mood, etc). One novel ADHD drug, Guanfacine (marketed as Intuniv for ADHD) works by reducing cAMP in the PFC, which in some ADHD individuals, results in a dramatic improvement in attention-regulation, impulsiveness and mood fluctuations.
So perhaps slicing your doses of the CILTEP stack in half. If that still doesn't help, it might just not be for you. Perhaps you naturally have more cAMP than average individuals, but not enough to be pathological on it's own, in which case something like a PDE4 inhibitor could cause issues.
Noticed a very nice synergy between combining 4 grams of piracetam with the CILTEP stack today. Mood improved, socialability enhanced, work ethic restored and mathematical reasoning improved. I'd call it a 'cleaner' Adderall.
However, I must admit there's a pretty clear lurking variable: I've abstained from coffee for the last 4 days, opting instead of a small amount of tea in the morning to decrease tolerance, and today I sucummbed again to the espresso urge. My measure of whether today's good effects were caused by CILTEP+piracetam or the reintroduction of espresso will be based on whether I can reproduce said effects at a later date without coffee.
It was almost definitely the coffee, with more "behind the curtain" effects from the CILTEP (coffee would strongly impact mood and overall energy, CILTEP would assist with logical cognition). Especially considering that you had been abstaining for the last 4 days. It takes around 2 weeks usually for the brain to return to homeostasis after prolonged regular caffeine usage (2 weeks at about 50+ mg a day is sufficient to cause noticeable tolerance/mild addiction). So during the 4 days you had abstained, your cognition would have gone downhill, as well as your mood and energy. So getting more caffeine would bring you back to "normal" which would feel great.
Edited by GetOutOfBox, 16 February 2013 - 04:57 AM.
#1181
Posted 16 February 2013 - 05:47 AM
This is likely caused by too much cAMP. One of the suspected mechanisms of ADHD is elevated cAMP in the Prefrontal-Cortex, which causes overstimulation of hyperpolarization-activated cyclic nucleotide-gated channels, resulting in affected neurons being unable to communicate. On the large scale, this results in spotty communication between the PFC and the rest of the brain, resulting in difficulties with executive function (regulating attention, planning, initiating tasks that have delayed rewards, regulating mood, etc). One novel ADHD drug, Guanfacine (marketed as Intuniv for ADHD) works by reducing cAMP in the PFC, which in some ADHD individuals, results in a dramatic improvement in attention-regulation, impulsiveness and mood fluctuations.
So perhaps slicing your doses of the CILTEP stack in half. If that still doesn't help, it might just not be for you. Perhaps you naturally have more cAMP than average individuals, but not enough to be pathological on it's own, in which case something like a PDE4 inhibitor could cause issues.
Rolipram, which is a LOT stronger than Artichoke Extract as a PDE4 inhibitor, did not make working memory tasks any worse than baseline in a study I've referenced several times. It did cancel Guanfacine's effects though. Taking too much Forskolin however could cause excess cAMP in the wrong places. Maybe a lower dosage of Forskolin while keeping the pde4 inhibitor component the same is what would help? Seems 10mg or less seems to work pretty well.
Edit: I think "paired associates" on cambridgebrainsciences.com is as good a test of working memory as I've seen. I think I'll do a test where I get a few baseline readings without forskolin and then add it back, 5/10/15/20 mg (splitting up 25mg c-bolic tablets) and see when my working memory starts to degrade. I'll then add in the artichoke extract and see how far I get before working memory is affected. I know this isn't double blind or anything but it's better than nothing. BTW, I find my paired associates scores are usually increased the most by galantamine.
Edited by abelard lindsay, 16 February 2013 - 06:30 AM.
#1182
Posted 16 February 2013 - 05:57 AM
For me, rhodiola provides a mild mood boost without really blunting my emotions.
Actually, for me, CILTEP provides the emotional blunting. Rhodiola brings back the memories.
#1183
Posted 16 February 2013 - 04:00 PM
http://www.ncbi.nlm....pubmed/10923759
Psychopharmacology (Berl). 2000 Jun;150(3):311-6.
Effects of rolipram on scopolamine-induced impairment of working and reference memory in the radial-arm maze tests in rats.
Zhang HT, O'Donnell JM.
Source Department of Pharmacology and Therapeutics, Louisiana State University Medical Center, Shreveport 71130, USA. hzhang@lsumc.edu
Abstract
RATIONALE:
Rolipram, a selective inhibitor of cyclic AMP-specific phosphodiesterase (PDE4), has been shown to enhance scopolamine-induced impairment of working memory. However, its effect on reference memory, which appears to be related to the level of cyclic AMP (cAMP), has not been investigated yet; in addition, the mechanism involved in its effects on memory remains to be elucidated.
OBJECTIVES:
To investigate the effects of rolipram on working and reference memories impaired by scopolamine and the involvement of cAMP.
METHODS:
By administration (IP) of rolipram and forskolin, an activator of adenylyl cyclase (AC), the effects of both drugs on the number of correct choices and errors in experiment 1 and, the frequency of both working memory errors and reference memory errors in experiment 2 were observed in two eight-arm radial maze tasks in rats.
RESULTS:
In experiment 1, rolipram (0.01-1.0 mg/kg) attenuated the scopolamine-induced (0.5 mg/kg) increase in the total number of errors in dose- and time-dependent manners. The minimum effective dose of rolipram was 0.05 mg/kg and the effects lasted nearly 60 min. By contrast, forskolin(1.0-10.0 mg/kg) failed significantly to affect any of the above indices altered by scopolamine. In experiment 2, rolipram (0.05 and 0.1 mg/kg) decreased the frequencies of both working and reference memory errors that were elevated by scopolamine. Forskolin did not alter either type of error at a dose that increased the exploration time.
CONCLUSION:
Rolipram may exert its effects of reversing both working and reference memory impairments via increased cyclic AMP concentrations in certain signal transduction pathways, rather than by a generalized increase in cAMP.
My reading of this study is that raising cAMP everywhere in the brain is not really helpful. However, increasing it substantially in the areas of the brain where PDE4 is active is helpful. This would lend credibility to the strategy of lowering the dose of forskolin to the minimum amount necessary to get an effect. I imagine this strategy would help to avoid possible problems with excess cAMP in other areas of the brain besides those regulated by PDE4.
Edited by abelard lindsay, 16 February 2013 - 04:06 PM.
#1184
Posted 16 February 2013 - 05:18 PM
#1185
Posted 17 February 2013 - 09:25 PM
This is likely caused by too much cAMP. One of the suspected mechanisms of ADHD is elevated cAMP in the Prefrontal-Cortex, which causes overstimulation of hyperpolarization-activated cyclic nucleotide-gated channels, resulting in affected neurons being unable to communicate. On the large scale, this results in spotty communication between the PFC and the rest of the brain, resulting in difficulties with executive function (regulating attention, planning, initiating tasks that have delayed rewards, regulating mood, etc). One novel ADHD drug, Guanfacine (marketed as Intuniv for ADHD) works by reducing cAMP in the PFC, which in some ADHD individuals, results in a dramatic improvement in attention-regulation, impulsiveness and mood fluctuations.
So perhaps slicing your doses of the CILTEP stack in half. If that still doesn't help, it might just not be for you. Perhaps you naturally have more cAMP than average individuals, but not enough to be pathological on it's own, in which case something like a PDE4 inhibitor could cause issues.
Rolipram, which is a LOT stronger than Artichoke Extract as a PDE4 inhibitor, did not make working memory tasks any worse than baseline in a study I've referenced several times. It did cancel Guanfacine's effects though. Taking too much Forskolin however could cause excess cAMP in the wrong places. Maybe a lower dosage of Forskolin while keeping the pde4 inhibitor component the same is what would help? Seems 10mg or less seems to work pretty well.
I do have ADHD, but the interesting thing is that the executive dysfunction does not scale linearly with dose of artichoke. (I've been holding the dose of forskolin steady at one 6.25mg capsule every morning.) Rather, it seems to suddenly appear when I escalate dose of artichoke extract too high. Somewhere earlier in the thread, someone mentioned that luteolin (which seems to be the main active PDE inhibitor in artichoke extract) is somewhat selective for PDE4, but not nearly as selective as rolipram.
So one working hypothesis is that low to moderate doses of artichoke extract are selective enough for PDE4 that they don't impair PFC function, but above a certain threshold executive dysfunction becomes a problem. Especially in people like me who are already vulnerable to disruptions of executive functions.
For now, I'm sticking with one forskolin + 2 artichoke in the morning, with another 1 artichoke in the afternoon. This is my sweet spot. It provides a highly effective boost to energy, reminiscent of a cleaner modafinil. Bright light therapy and CBT mostly take care of my seasonal affective disorder, but I'm still pretty tired much of the time. CILTEP fixes that.
Though I don't notice any improvements to memory, which seems to have been the original purpose of the CILTEP stack. Either it doesn't improve my memory encoding, or the effect is too small and I'm too spoiled by the effectiveness of good study techniques and racetams.
#1186
Posted 18 February 2013 - 05:03 AM
I do have ADHD, but the interesting thing is that the executive dysfunction does not scale linearly with dose of artichoke. (I've been holding the dose of forskolin steady at one 6.25mg capsule every morning.) Rather, it seems to suddenly appear when I escalate dose of artichoke extract too high. Somewhere earlier in the thread, someone mentioned that luteolin (which seems to be the main active PDE inhibitor in artichoke extract) is somewhat selective for PDE4, but not nearly as selective as rolipram.
So one working hypothesis is that low to moderate doses of artichoke extract are selective enough for PDE4 that they don't impair PFC function, but above a certain threshold executive dysfunction becomes a problem. Especially in people like me who are already vulnerable to disruptions of executive functions.
For now, I'm sticking with one forskolin + 2 artichoke in the morning, with another 1 artichoke in the afternoon. This is my sweet spot. It provides a highly effective boost to energy, reminiscent of a cleaner modafinil. Bright light therapy and CBT mostly take care of my seasonal affective disorder, but I'm still pretty tired much of the time. CILTEP fixes that.
Though I don't notice any improvements to memory, which seems to have been the original purpose of the CILTEP stack. Either it doesn't improve my memory encoding, or the effect is too small and I'm too spoiled by the effectiveness of good study techniques and racetams.
I'm the same as you, I don't really notice any literal memory improvements (by that I mean, my visual memories seem clearer, or it's easier to remember specific things), however my hypothesis is that this stack more improves learning in a general sense. Perhaps by increasing synaptic plasticity one improves one's ability to adapt to/adopt new behaviors or an overall grasp of something. So rather than helping to study for a test, perhaps it just increases the effectiveness of one's learning in an overall sense. This is based on my understanding that there are various forms of memory, and two distinct types, memories that are encoded data (like images, concepts, people, events, etc), and behaviors which manifest as large-scale changes in the neural network. An example of what I mean is the difference between studying (and memorizing concepts to be recalled later) and learning to be more social (through say, Cognitive Behavioral Therapy). With one, you store memories that you recall precisely as you stored them, whereas the other is more of a change in how you think, rather than specific memories. So in a nutshell, learning vs memorization.
#1187
Posted 19 February 2013 - 11:32 AM
#1188
Posted 19 February 2013 - 04:35 PM
#1189
Posted 19 February 2013 - 05:03 PM
If I overdo the coffee/espresso, insomnia becomes an inevitable consequence. Using high quality green tea as your caffeine source should help. I've also found ashwagandha and magnesium to provide some nice balance from the stimulation, though I actually prefer that tunneled-in effect.
I've got some Ashwagandha in stock maybe I should go with that and also limit my caffeine. thanks for the anecdote.
maybe we can create Chilltep stack lol
Edited by Galaxyshock, 19 February 2013 - 05:48 PM.
#1190
Posted 19 February 2013 - 10:00 PM
God yes. I hate this 2.5mg bi-hourly microdosing crap. But it costs one twentieth of what Concerta costs...I found concerta to be a lot more convenient than taking small doses of IR all day long.
I got generic 18mg XR and I think it was around $18 for 30.
#1191
Posted 19 February 2013 - 10:34 PM
#1192
Posted 20 February 2013 - 12:16 AM
I've got some Ashwagandha in stock maybe I should go with that and also limit my caffeine. thanks for the anecdote.
maybe we can create Chilltep stack lol
I generally turn to theanine if I'm overstimulated. I prefer to just get my caffeine dosage right - for me, a few cups of tea or two quarters of a 200 mg caffeine pill. But if I overdo it, then theanine.
I also like melatonin to fall asleep when I have some lingering stimulant effects. 750 mcg seems to be able to overcome some residual armodafinil effects.
#1193
Posted 20 February 2013 - 07:40 PM
#1194
Posted 20 February 2013 - 10:10 PM
#1195
Posted 21 February 2013 - 07:04 AM
Also wondering if people have seen success without a stim?(might need a high dopa producing brain)
Edited by bobz1lla, 21 February 2013 - 07:05 AM.
#1196
Posted 21 February 2013 - 10:10 PM
Mostly, I think CILTEP's dopamine boosting/stimulant/mood improving properties are distinct from any effect it has on LTP, and when people here say it works well with a stimulant they mostly mean the former.
#1197
Posted 21 February 2013 - 11:34 PM
Thinking of taking the plunge into ciltep, but leery of throwing in a stim as I don't respond too well. I'm thinking of substituting uridine, as this is a dopa regulator, and a few others have had success earlier in the thread. Anyone care to elaborate why or why not this might work?
Also wondering if people have seen success without a stim?(might need a high dopa producing brain)
Well, LTP is partially contingent on dopamine, but I'm not sure you need high levels necessarily. LTP should be going on in people even with ordinary dopamine levels, so uridine probably won't break the stack.
Mostly, I think CILTEP's dopamine boosting/stimulant/mood improving properties are distinct from any effect it has on LTP, and when people here say it works well with a stimulant they mostly mean the former.
To build on that response, tyrosine hydroxylase (TH) is the rate-limiting enzyme in dopamine (& other catecholamine) synthesis. cAMP plays a role in TH transcription and therefore, can significantly increase DA in the long-term (without downregulation via homeostasis). CILTEP already comes with a built-in dopamine increase via an increase in phosphorylation of TH.
I have a secret.
I haven't posted about it thus far, since I'm extremely concerned a silly individual might kill themselves but it is honestly better I tell you and warn you about the dangers.
This is not medical advice. Use at your own risk.
Here is my secret: nicotine gum.
If you need a stimulant boost for the CILTEP, try some nicotine gum BUT BEWARE IT IS DANGEROUSLY STRONG!
The study below suggests nicotine has very powerful effects in combination since it can sustain the TH phosphorylation increase for up to 48 hours from mere minutes!
Sustained phosphorylation of tyrosine hydroxylase at serine 40: a novel mechanism for maintenance of catecholamine synthesis.
Abstract
Tyrosine hydroxylase (TH) is the rate-limiting enzyme in catecholamine synthesis. Its activity is known to be controlled acutely (minutes) by phosphorylation and chronically (days) by protein synthesis. Using bovine adrenal chromaffin cells we found that nicotine, acting via nicotinic receptors, sustained the phosphorylation of TH at Ser40 for up to 48 h. Nicotine also induced sustained activation of TH, which for the first 24 h was completely independent of TH protein synthesis, and the phosphorylation of TH at Ser31. Imipramine did not inhibit the acute phosphorylation of TH at Ser40 or TH activation induced by nicotine, but did inhibit the sustained responses to nicotine seen at 24 h. The protein kinase(s) responsible for TH phosphorylation at Ser40 switched from being protein kinase C (PKC) independent in the acute phase to PKC dependent in the sustained phase. Sustained phosphorylation and activation of TH were also observed with histamine and angiotensin II. Sustained phosphorylation of TH at Ser40 provides a novel mechanism for increasing TH activity and this leads to increased catecholamine synthesis. Sustained phosphorylation of TH may be a selective target for drugs or pathology in neurons that contain TH and synthesize dopamine, noradrenaline or adrenaline.
I have been using nicotine gum with CILTEP for >3 months when I really need an energy boost. It turns CILTEP into meth; it is incredibly stimulating + don't plan on sleeping or eating.
EDIT: Sources! ONE! TWO! POW!
Also, I should give credit to the earlier discussion in this thread regarding adding nicotine to the CILTEP stack. However, I can only assume those individuals tried nicotine+CILTEP, became insanely addicted and died from a stroke shortly after. RIP hephaestus RIP nidhogg
Edited by peakplasma, 22 February 2013 - 12:25 AM.
#1198
Posted 22 February 2013 - 01:08 AM
Also, I should give credit to the earlier discussion in this thread regarding adding nicotine to the CILTEP stack. However, I can only assume those individuals tried nicotine+CILTEP, became insanely addicted and died from a stroke shortly after. RIP hephaestus RIP nidhogg
Nicotine is not too be toyed around with. It has a very low LD50 and is well known for being damaging to health even when used in "recommended dosages" and of course being extremely addictive. Trying to increase the effects of nicotine, given that it is dangerous to begin with, is a really dumb idea.
The point of this forum is to figure out how to live forever and increase our human capabilities. Nicotine is well known for decreasing human lifespan. I've been taking CILTEP for more than a year now and plan to take it for the rest of my life. That's what we should be aiming for: increasing our capabilities over the rest of a healthy lifespan and not some short-lived experience involving nicotine or other drugs that are known to be detrimental to human health.
Edited by abelard lindsay, 22 February 2013 - 01:41 AM.
#1199
Posted 22 February 2013 - 01:33 AM
Also, I should give credit to the earlier discussion in this thread regarding adding nicotine to the CILTEP stack. However, I can only assume those individuals tried nicotine+CILTEP, became insanely addicted and died from a stroke shortly after. RIP hephaestus RIP nidhogg
Nicotine is not too be toyed around with. It has a very low LD50 and is well known for being damaging to health even when used in "recommended dosages" and of course being extremely addictive. Trying to increase the effects of nicotine, given that it is dangerous to begin with, is a really dumb idea.
The point of this forum is to figure out how to live forever and increase our human capabilities. Nicotine is well known for decreasing human lifespan. I've been taking CILTEP for more than a year now and plan to take it for the rest of my life. That's what we should be aiming for: increasing our capabilities over the rest of a healthy lifespan and not some short-lived experience involving nicotine and other drugs detrimental to human health.
Nicotine does have potential health risks. Keep in mind that these are far lower than those of cigarettes, since cigarettes are creating free radicals through combustion. The addictivity is also far lower since pure nicotine lacks cigarettes' MAOIs. There are a few studies showing some mild negative health effects - possible endogenous conversion to a mild carcinogen and an inhibition of an estrogen subunit. Regardless, nicotine is extremely well-researched and only shows a few negatives. Admittedly, it's not perfectly safe, but it's not reasonable to issue a blanket statement that individuals should not use nicotine. There are many users of this forum, myself included, who've used nicotine sporadically without any dependence.
I'd also just like to note that CILTeP is not well-researched, so suggesting that nicotine is far more dangerous is very questionable. Although nicotine may be unsafe, it is certainly not immediately or dramatically harmful. In contrast, CILTeP is mostly an unknown. Again, I'm not discouraging people from taking CILTeP (I've taken it myself), just saying that nicotine should not have the negatives of cigarettes held against it.
#1200
Posted 22 February 2013 - 01:37 AM
To build on that response, tyrosine hydroxylase (TH) is the rate-limiting enzyme in dopamine (& other catecholamine) synthesis. cAMP plays a role in TH transcription and therefore, can significantly increase DA in the long-term (without downregulation via homeostasis). CILTEP already comes with a built-in dopamine increase via an increase in phosphorylation of TH.
Increased TH transcription should cease if forskolin is eliminated, right? I would hope the body would be able to return to baseline production. I'm guessing long-term dopa increase via TH would be felt whole body? Not sure if TH/cAMP's role with dopa is isolated to the brain.
There's gotta be addiction potential with the things people are mixing. Not including peak's nicotine OD.
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