312 replies to this topic

[NoopMed]

This:
http://www.amazon.co...ils_o00_s00_i01

However, it looks like they're currently out of stock. :(

[deh707]

This:
http://www.amazon.co...ils_o00_s00_i01

However, it looks like they're currently out of stock. :(

Ah, I'm not surprised that you're getting positive results from the Hard Rhino brand of Piracetam. They seem to be getting plenty of good reviews recently.

Thanks.

[NoopMed]

Got a PM question asking for a summary of what I'm currently using in my stack... Which makes sense because as you can see from this thread I've been mixing and matching for the last few weeks. At this point I wouldnt claim to have found the perfect mix for me, especially since I've made changes in even the last week alone. Still this is what I'm currently using:

Breakfast:
800mg Piracetam
120mg extended release Ginkgo biloba
500mg Choline bitartrate.
Centrum multivitamin
120mg caffeine (one strong drip coffee)

Lunch:
400mg Piracetam
60mg Ginkgo biloba (prevents ginkgo crash)
250-500mg choline
120mg caffeine

Evening:
Caffeine as needed
Potentially a DMAE or a bit of Noopept if I'm feeling like I really need to cram in a lot of reading, or have a big group discussion to run.


As you can see, I've reintroduced Ginkgo, and I've stepped down the Piracetam. I felt like I was gradually losing effectiveness with Piracetam after about 3 weeks. I stopped the Piracetam for a couple days, which was a bad time... Tremors, anxiety, not fun. Went back on and tapered down more slowly (from about 3g, to 2, to ~1.5g a day, and then off for a couple days). After bringing it to a lower level, stopping, then starting back at about 800mg BID, I still felt pretty crappy- slow, spacey, not my usual self. But, then I reflected on how I felt overall, and realized it was actually how I felt all summer when I stopped Ginkgo altogether for 2 months. Started back on ginkgo this week with low dose piracetam, and feel fantastic. Basically back to where I was when I first started having the great results that resulted in a great exam week. (Ive been a long time ginkgo user, and I'm probably just an addict... Haha, fortunately it has a lot of great supposed collateral effects, like its action as an antioxidant, and is readily available everywhere.) I plan to cycle ginkgo and Piracetam in and out, I find this especially important with ginkgo, as tolerance to the stimulant effects seems to build for me, but remains useful if I take a week off here and there. I don't have a scheduled entirely worked out at the moment, and I probably never will have a strict schedule thanks to variable exam scheduling. However, I will be trying to maintain minimum therapeutic doses, and reserve the larger amounts for exam days. I'll also likely be flushing out the stack on weekends and weeks when there's no exam in sight.

Also got some modafinil... Tried a 1/4 of a 200mg pill around 2pm, definitely hyped me up, but Im not sure it really helped much focusing me. Reminded me of adderall. I may try a bit more for the upcoming exam, perhaps on test day as well, and report back; however, I'm still debating that because I'm not sure I really need anything else than what I'm already on. Poor brain can only live so much better through chemistry, I worry.

[NoopMed]

About 95% certain modafinil gave me hives, so I won't be reporting much on that one. I tend to be prone to hypersensitivity reactions. After noticing the typical reaction I get with ingestion of something I'm allergic to (deeply indurated urticaria [arthas-like reaction] on hands, palms, fingers, ankles, feet) after 2 days on modafinil, I did further reading on adverse effects. I thought I had recalled a rare hypersensitivity reaction with Moda in clinical trials, and bingo, I think I've nailed it once again. Stopped for a day now, and they're going away with no other change in meds. I've experience the same issue with Kava, Gotu Kola, Ibuprofen, Penicillin, Sulfonamides, and much more. Too bad I have all this modafinil now... I'm certain one of my colleagues will enjoy it.

[bugasman]

I tried many times to use piracetam, low/high doses, with/without choline... The first two days are great. Faster thought process, increased working memory and aesthetic appreciation of music, colors... After the honeymoon all I got is suicidal depression. I feel relieved because many users got the same response as mine. My hypothesis is that it increases choline or its use. Many articles confirms that increased acethylcholine is associated with depression.

[NoopMed]

I haven't run into the issue of depression. In fact, if anything I was pretty depressed before I started on this recent foray. I did have a number of days there where I was feeling very slow, and had anxiety as well, but that was resolved once I started back on Ginkgo Biloba and started ramping up my choline supplementation.

Anyways. I'm also currently using Alpha-GPC now, in place of DMAE. I use it 300mg BID, sometimes I take an additional 500mg choline bitartrate as well.

To summarize my recent nootropic Stack:
Breakfast:
800mg Piracetam
500mg Choline bitartrate
120mg Extended Release Ginkgo Biloba
300mg Alpha GPC
150-300mg Caffeine


After Lunch:
800mg Piracetam
300mg Alpha GPC
(A second Ginkgo if planning to study very late into the night, but usually not.)
120-200mg Caffeine



To look at my current exam scores...
Exam 1: 2 weeks in to start of Piracetam usage -- Top 10% with Honors
Exam 2: One month into supplementation of Piracetam, stopped ginkgo, started DMAE. -- Score dropped a bit, still good, but definitely feeling slow in general and in studies.
Exam 3: Resumed Ginkgo, brought Piracetam to a lower dosage 800mg BID, started Alpha GPC and more frequent choline bitartrate -- Top 2% with High Honors and a letter of merit.

I never scored this high in the past with Gingko alone, but it appears to be essential to the benefit I've been gaining from Piracetam. Choline seems to help the situation and provide some balance. I feel better when I'm taking it, I perform well, and I'm not depressed. However, I also occasionally use Cannabis. Sometimes I also use SAM-e supplements when I'm feeling blue, but again, my general mood and tendencies towards melancholy have not changed with nooptropics... In fact, they seem to be alleviated by them in most cases.

[Flavius Bologh]

Can you explain the thought process behind your learning?

How much time do you usually spend learning and what methods do you use? It seems to me you are doing something right

[alecnevsky]

This seems very pertinent to my target goals. NoopMed, thank you for providing a coherent account! I do have some questions if you have the time.

I haven't run into the issue of depression. In fact, if anything I was pretty depressed before I started on this recent foray. I did have a number of days there where I was feeling very slow, and had anxiety as well, but that was resolved once I started back on Ginkgo Biloba and started ramping up my choline supplementation.

Are you attributing this resolution to slowness to Ginko's "stimulation of choline uptake in the hippocampus" or your addiction to it or something else? Does Ginkgo really improve studying performance in terms of time?

To summarize my recent nootropic Stack:
Breakfast:
800mg Piracetam
500mg Choline bitartrate
120mg Extended Release Ginkgo Biloba
300mg Alpha GPC
150-300mg Caffeine

Is there a synergistic effect in taking Alpha GPC with Choline bitartrate or are you just putting left-over Choline bitartrate to use and/or experimenting?

Exam 3: Resumed Ginkgo, brought Piracetam to a lower dosage 800mg BID, started Alpha GPC and more frequent choline bitartrate -- Top 2% with High Honors and a letter of merit.

Right on!

I never scored this high in the past with Gingko alone, but it appears to be essential to the benefit I've been gaining from Piracetam. Choline seems to help the situation and provide some balance.

Again, I believe you mentioned taking Ginko for more than 2 years, no? Couldn't a caffeine addict say something similar for instance?




Overall, your posts have been of tremendous help. Thank you again! I am also in school atm functioning, more or less, on adderall (in a way, like your peers, and unlike an ADHD person ) so I am looking into maximizing output without the neurotoxic, cardio-arrhythmic effects of adderall but I am unsure whether I should take Ginko our Sulbutiamine for consistency on top of whatever racetam+choline I choose.

I should mention that I'm planning on taking Multi, Vit C, Vit D, Lion's Mane, Omegas, along with maybe some Picamilon (terrible idea?) everyday as my "general stack' and then stack "performance' on top of those.

For the latter, I came up with the following:

Theoretically, (I'm not a med/chem/neuro/bio student,) I'd like to try stacking Aniracetam (AMPA supposedly good otherwise why would they be developing its derivative right?) + Alpha GPC choline (highest bioavailability) + Sulbuitamine(consistent energy, stamina to avoid crash) for less demanding days then add on Modafinil or Phenotropyl on intense (18-24hr) study sessions. I will also soon have some Noopept but I am more than sure it's not going to be good for systematic memory encoding, but rather originality/creativity/sociability faculties with which I am more than content right now.

Does anyone have any suggestions for an effective daily studying stack (more so than anti-anxiety or "pro-creativity" effects.)

Edited by alecnevsky, 12 October 2012 - 12:35 PM.

[NoopMed]

This seems very pertinent to my target goals. NoopMed, thank you for providing a coherent account! I do have some questions if you have the time.

I haven't run into the issue of depression. In fact, if anything I was pretty depressed before I started on this recent foray. I did have a number of days there where I was feeling very slow, and had anxiety as well, but that was resolved once I started back on Ginkgo Biloba and started ramping up my choline supplementation.

Are you attributing this resolution to slowness to Ginko's "stimulation of choline uptake in the hippocampus" or your addiction to it or something else? Does Ginkgo really improve studying performance in terms of time?

To summarize my recent nootropic Stack:
Breakfast:
800mg Piracetam
500mg Choline bitartrate
120mg Extended Release Ginkgo Biloba
300mg Alpha GPC
150-300mg Caffeine

Is there a synergistic effect in taking Alpha GPC with Choline bitartrate or are you just putting left-over Choline bitartrate to use and/or experimenting?

Exam 3: Resumed Ginkgo, brought Piracetam to a lower dosage 800mg BID, started Alpha GPC and more frequent choline bitartrate -- Top 2% with High Honors and a letter of merit.

Right on!

I never scored this high in the past with Gingko alone, but it appears to be essential to the benefit I've been gaining from Piracetam. Choline seems to help the situation and provide some balance.

Again, I believe you mentioned taking Ginko for more than 2 years, no? Couldn't a caffeine addict say something similar for instance?




Overall, your posts have been of tremendous help. Thank you again! I am also in school atm functioning, more or less, on adderall (in a way, like your peers, and unlike an ADHD person ) so I am looking into maximizing output without the neurotoxic, cardio-arrhythmic effects of adderall but I am unsure whether I should take Ginko our Sulbutiamine for consistency on top of whatever racetam+choline I choose.

I should mention that I'm planning on taking Multi, Vit C, Vit D, Lion's Mane, Omegas, along with maybe some Picamilon (terrible idea?) everyday as my "general stack' and then stack "performance' on top of those.

For the latter, I came up with the following:

Theoretically, (I'm not a med/chem/neuro/bio student,) I'd like to try stacking Aniracetam (AMPA supposedly good otherwise why would they be developing its derivative right?) + Alpha GPC choline (highest bioavailability) + Sulbuitamine(consistent energy, stamina to avoid crash) for less demanding days then add on Modafinil or Phenotropyl on intense (18-24hr) study sessions. I will also soon have some Noopept but I am more than sure it's not going to be good for systematic memory encoding, but rather originality/creativity/sociability faculties with which I am more than content right now.

Does anyone have any suggestions for an effective daily studying stack (more so than anti-anxiety or "pro-creativity" effects.)

Well in regard to the first question, I hadn't actually noted the increased uptake of acetylcholine by the hippocampus with Ginkgo. I probably read that once before, but disregarded it at the time. Thanks for bringing that to my attention! That's probably a large part of what I experience when I include Ginkgo in my stack. In regard to "Addiction," that statement was half-joke, half-serious speculation. Ginkgo is a mild, nonspecific MAOI, and increases synapse quantities of epinephrine, norepinephrine, dopamine, and other catecholamines by inhibiting their breakdown after they've been released by the presynaptic neuron. This should provide a stimulant effect that gradually becomes attenuated by the downregulation of receptors for these neurotransmitters on the postsynaptic neurons. This downregulation results in less excitatory effect, and once those neurotransmitters return to normal levels (upon removal of the oxidase inhibitor [MAOI/Ginkgo]), this could result in inadequate stimulation of these neuronal pathways. This could be seen as a biochemical pathway supporting some level of addiction, however; "withdrawal" would be seen more as a dullness and lack of excitability for however long it takes the body to reestablish post-synaptic receptors. This takes a few months from what I understand, it is not considered an irreversible downregulation of receptors. The same thing happens with many adrenergic pathway agonists/antagonists. I took Ginkgo for basically 10 months, every day, while I was first year medical student. It helped me substantially in maintaining motivation and focus, and I performed well, but not dramatically above average. I also found benefit from Rhodiola rosea and Bacopa monneiri, and it turns out they are also MAOIs, but have some other side effects and less overall benefit, so I stopped with those. (I discuss them in other posts) I stopped taking Ginkgo for 3 months over summer before starting year two, and felt no "withdrawal," but I was also relaxing on the beach and drinking beer for a lot of the time... not cramming the collective knowledge of healthcare into my mind. Upon return to classes I felt quite slow, and began to fall behind immediately. I started back on Ginkgo and things returned to normal. I started on the rest of the supplements I've discussed here and I've climbed to the top.

I don't believe there is a synergistic effect between Alpha GPC and Choline bitartrate (nor DMAE for that matter) -- they should all be heading to the same desired end product: Acetylcholine. However, I find a great sustained and balanced experience with Ginkgo and Piracetam when I take at least 1-1.5g of Choline bitartrate per day. The Alpha GPC benefit seems more short term, and when I remove Choline bitartrate and try just Alpha GPC, I begin to feel some ups and downs in performance that correlate to dose-timing of Alpha GPC. I have no evidence for this, but I speculate that because Choline bitartrate is not directly blood brain barrier soluble, it is filling up a systemic choline pool in my body and gradually being eliminated. Alpha GPC on the other hand can easily cross the BBB and begin it's journey to becoming acetylcholine in my brain. I theorize that high levels of systemic choline inhibit the catabolism of Alpha GPC in my periphery, allowing more to stay in circulation longer and more to reach my brain. Without choline bitartrate, the Alpha GPC is more quickly eliminated and excreted and I reach a brain choline deficit from the piracetam/ginkgo combo more quickly. Again, I've never read any of this, it's just a guess. Either way, the combo seems to work better than either alone--- which I guess you could call synergy, but it seems more like Le Chatelier's principle than a direct interaction between the two supplements.

I also take a multivitamin with high C and D and a Omega 3/6 fish oil pill. I discussed Noopept earlier. I like the stuff when I'm out with friends and playing/listening to music, but I find it diluting my concentration when I'm studying. Sounds like that's what you're looking for.

Sulbutiamine makes me crash pretty hard after a few hours, and seems to leave me with a bit of a deficit the following day. I discussed that in an earlier posting. Some of my peers that have tried it have also experience the same problem. Some people reportedly benefit from it, but I couldn't seem to find the right regimen.

I haven't tried any of the other stuff you've mentioned. I would like to try aniracetam, however.

[health_nutty]

I recommend giving Pramiracetam a try.

[alecnevsky]

I recommend giving Pramiracetam a try.

Thanks. I don't want to hijack this but seeing that OP has not tried either Ani or Pram, I think it would be relevant to know whether the AMPA(kite) "connection" (I apologize for my non-tech terminology here) of Aniracetam is substantial in delivering better performance increases as opposed to Pram?

[NoopMed]

I recommend giving Pramiracetam a try.

Thanks. I don't want to hijack this but seeing that OP has not tried either Ani or Pram, I think it would be relevant to know whether the AMPA(kite) "connection" (I apologize for my non-tech terminology here) of Aniracetam is substantial in delivering better performance increases as opposed to Pram?

I'd definitely like to try both, so it's no hijack. Would be interested in any input people have on these.

[alecnevsky]

I'd definitely like to try both, so it's no hijack. Would be interested in any input people have on these.

Alright, well according to a study referenced to in this very useful discussion, "Aniracetam modifies chemical reactions at the AMPA receptor, which is associated with short term memory. The process of LTP (which CILTEP enhances) causes the nature of the modification of the AMPA receptor's chemical reactions by Aniracetam to change." Aberald Lindsey (Post 13)

So, seeing that I would like to couple my racetam+choline stack with CILTEP (Artichoke extract + Forksolin +L-Phenylanine/Tyrosin) I think I may go with Pram first, after all. This is all very speculative. Designing a stack based on meta analysis of different responders/studies is annoyingly difficult, to say the least. Anyway, I highly recommend Cephalon's thread (linked above) just in virtue of his method of organization. I think I am going to rely on his schema and tune his stack particularly for categories of "generic learning environment" and the"intense study bender emergencies."

Also, when I finish tuning my "generic" stack. I will come back and detail my "intense study" add-ons: Noopept, Phenotropyl, Picamilon (strong Russian noops.) along with Modafinil. So stay tuned!

Cheers!

Edited by alecnevsky, 12 October 2012 - 07:51 PM.

[NoopMed]

I've been trying the CILTEP stack a bit myself, specifically Artichoke extract + forskolin. (In addition to my Piracetam, Ginkgo, various acetylcholine derivatives/precursors and occasional Noopept.) I've found the forskolin to be pretty distressful to my gut, and coupled to the liver load it represents, I've decided not to use it any more. I'm not so sure it's entirely essential, as the PDE4 inhibitor Luteolin in Artichoke extract along with the NMDA (and AMPA) channel modification from Piracetam should still offer LTP effects.

That study Lindsey linked seems very relevant, but also highly specific to AMPA channels and Aniracetam (which is supposed to act specifically on these channels and not so much on NMDA like Piracetam does, from my understanding). It seems to me (in my admittedly limited knowledge of LTP kinetics and nootropics) that enhancement of NMDA channels would be more important for establishing the kind of long term memories and learning that I'm looking to improve with my stacks-- making Piracetam a superior supplement. However, the combination of both may still be very useful, which is what I've read in various people's accounts. (IE, combo aniracetam or oxiracetam or pramiracetam WITH piracetam).

From what I understand of LTP (long term potentiation), it requires the action of BOTH AMPA and NMDA channels, and can rest in kind of a tricky balance. Basically AMPA channels open in response to glutamate (or other excitatory neurotransmitters) and allow Sodium to pass into the cell. Once enough of them open this will provide enough Na to depolarize the membrane of the neuron allowing for the Magnesium that is stuck, blocking the NMDA channel in its resting state, to leave. This allows BOTH Sodium and Calcium to pass through that NMDA channel. *(It's basically like, a team of foot soldiers open the maintenance door to the castle, and once enough of them are inside to help pull open the big ass gate, the Calcium knights can ride across the mote and take over the castle.) Once Calcium (specifically) begins entering the neuron, a series of enzymatic processes are triggered that results in the enhancement of existing AMPA receptor activity and placement of new AMPA receptors at the cell surface allowing future excitatory stimulii to generate a stronger post synaptic response in the potentiated neuron. This aspect of LTP is a singular, albeit important, component of learning. What the paper specifically says about Aniracetam and AMPA is this: "LTP reduced the effect of aniracetam on the amplitude but increased its effect on the decay time constant of field EPSPs recorded under conditions in which local spiking and inhibitory responses were blocked." I'm not really sure what increased duration of excitatory post synaptic potentials means for learning and memory, but the reduction of the (already artificially increased) amplitude of AMPA channel response seems to suggest that as one learns, the effect of Aniracetam on that matured neuron will be lessened-- which doesn't seem like a problem to me, as long as this doesn't indicate a decrease in the utilization of that neuron.

The reason I describe LTP as a tricky balance above is because excessive induction of Calcium through NMDA channels is the mechanism by which Excitotoxicity occurs. Excess Ca will result in neuron caspase activation and proteolytic enzyme overexpression-- eventually leading to neuron apoptosis (controlled suicide of the cell). This is a very bad thing, and is now one of the main theories behind the patholophysiology of brain deficits observed in stroke, head trauma, and even Alzheimer's. I do like the Artichoke heart extract for this reason, as it's a potent antioxidant that could reduce the chances of cell damage through reactive oxygen and nitrogen species, which is another pathway potentially leading to apoptosis...but this is a different avenue of cell management that does not counter excitotoxicity.

[alecnevsky]

I theorize that high levels of systemic choline inhibit the catabolism of Alpha GPC in my periphery, allowing more to stay in circulation longer and more to reach my brain. Without choline bitartrate, the Alpha GPC is more quickly eliminated and excreted and I reach a brain choline deficit from the piracetam/ginkgo combo more quickly.

I think I understand -- can anyone confirm/deny this line of reasoning? I just got some Alpha GPC (amongst everything else) and, seeing that it is relatively more expensive, I think I may get some citicoline or bitartrate (after I try GPC+TAU+DHA) to avoid the potential cliff you're talking about.

It seems to me (in my admittedly limited knowledge of LTP kinetics and nootropics) that enhancement of NMDA channels would be more important for establishing the kind of long term memories and learning that I'm looking to improve with my stacks-- making Piracetam a superior supplement.

I just read this abstract from some med consulting group doing a meta-analysis in 2010 (strangely, is it not possible to download these studies? I can log into pubmed via my school id but I do not see any pdf links?) and it seems that they're suggesting that Pram has "improved cognitive deficits associated with traumatic brain injuries." While piracetam "exhibited no long-term benefits for the treatment of mild cognitive impairments, recent studies demonstrated its neuroprotective effect when used during coronary bypass surgery. It was also effective in the treatment of cognitive disorders of cerebrovascular and traumatic origins;"

My question then is what is the difference between "traumatic brain injuries" and "cognitive disorders of traumatic origins" ? How can we translate these findings into benefits in learning environments?

I also saw on pubmed this study from Australia that says piracetam acts also as an AMPA?

Admittedly, I am not entirely sure I understand what's going on. I may just avoid doing any more research and focus on my actual field of study while gauging effects subjectively as this seems like a pursuit that is more in your path than mine.

So far I've had positive yet mild effects of CILTEP + caffeine(haven't tried with gingko/l-tyrosine yet!) I believe (since the effects are much less pronounced than adderall) I can make this a routine morning dose along with CDP/bitartrate choline, with perhaps, and afternoon add-on of GPC+TAU+DHA to anticipate the afternoon crash and an evening boost of Pram + GPC + Sulbuitamine to get work done before 2am. That's 2 doses of Alpha GPC and one CDP in the morning which should keep my choline bank full.

It's slowly coming together Thanks for you input NoopMed!

Edited by alecnevsky, 19 October 2012 - 02:15 AM.

[somerandomnotuscitizen]

Can you explain the thought process behind your learning?

How much time do you usually spend learning and what methods do you use? It seems to me you are doing something right

Could you answer this question?

[icey]

Side effects...bleh. Have had a significant blepharospasm (eye lid twitching) for about a week that worsens in the hours after taking piracetam. I also seem to be having something like a diffuse myoclonus (twitching/spasm) of many axial and peripheral muscle groups of my thorax and arms. This is interesting because I've never had this before, and these symptoms are actually along the lines of the indicated conditions for medical use of piracetam. Stopped piracetam for 2 days now, which initially increased the spasms significantly, but then resolved all spasms. Stopping left me feeling pretty exhausted and depressed in the washout period as well, but it was temporary. Feeling fine now, after two days off and some time out with friends on the town and relaxing. Reflecting on the last few weeks, I'm starting to realize I've probably been pushing myself too hard. Unfortunately, med school doesn't leave much time for R&R. As tempting as it is to be functioning at 200% all the time, it seems to be best to cycle off this stuff completely after about 2-3 weeks.

I know you're a med student and all, so this is your speciality, and this is an old post. However the eye and muscle twitching is just from lack of sleep. And then at the end when I read you were pushing yourself too hard, I knew that was it. I've seen it a million times. Glad you were able to get some rest, that will always fix it.

[NoopMed]

Can you explain the thought process behind your learning?

How much time do you usually spend learning and what methods do you use? It seems to me you are doing something right

Could you answer this question?

I did address this issue pretty briefly in a previous post: "Depends a lot on the structure of your schools curriculum. Mine is organ based, and I'm currently in second year. Last year most of our tests were written in house by professors. This year almost all of them are retired NBME questions, intended to simulate the boards. Last year I studied lectures, lectures are also recorded. I would read my notes. If they confused me I would rewatch lectures. After becoming comfortable with the material I would begin practice questions and talk through concepts with friends. This year I watch all the lectures, but I do much of my studying with Pathoma, Gunner Training, Kaplan, and First Aid for Step One. I make flash cards on StudyBlue (mostly use other people's). Then I go through Qbanks from Kaplan and USMLEWorld."

I purposely avoided further elaboration because the intention of this forum (I believe) is to discuss nootropics, healthy living, and mental/physical longevity. Student Doctor Network (http://studentdoctor.net/) has a plethora of discussions geared towards study habits. However, I'll give another basically to reiteration-- I attend every lecture. I often re-watch lectures that I do not feel immediately comfortable with in downloadable video format. I read and reread the admittedly very brief notes I take. I watch Pathoma, I watch Dr. Najeeb to review (or learn) 1st year material, I study First Aid, Kaplan, USMLE World, and Gunner Training to tackle boards-oriented material. I do not read text books, unless I have spare time or a class specifically assigns a chapter for reading. I do PRACTICE QUESTIONS. These are the key element. I literally try to do hundreds for every exam, and I try to organize a highly motivated group that has ALREADY PREPARED substantially for the exam. We embrace verbal discussion of answers with a conscious effort to tie in other related material and concepts to each question for a consolidated, unifying approach to the material. I generally lead discussion. I ask the group the question (usually a clinical scenario) and present possible answers. We come to a collective decision, and then check the answer. Then we discuss absolutely anything we can think of that relates to the answer. Then I try to ask brief related followup questions that come to mind for a couple minutes. (ie. Patient comes in vomiting blood, with a month long history of epigastric pain that is relieved by eating food. Is this: A. Liver Cirrhosis B. Gastric Ulcer C. Duodenal Ulcer D. Esophageal varices. ?? Then we answer (Likely C, but I just pulled this out of my ass for example sake.) We discuss the explanation of the answer, and explanations for the alternative, wrong answers. (A good set of questions will have thorough explanations for each possible answer... ie. Kaplan review questions, Robbins and Coltrane Pathology Review, etc.) Then I will ask to my group: Which bacterial species is commonly involved here? (H. pylori) What antibiotics should be used? (Ampicillin and clarythromycin) Is there a risk of malignancy here? (Yes. MALT lymphoma.) What diagnostic tests should we run? (Urea breath test, endoscopy, fecal occult blood test, Iron labs, etc.) ) Then we move on to the next question. That's basically my plan every test, and it works very well for me. Especially with the addition of these nootropics.

A key thing about noots in medical school, and perhaps any situation, is that they can only provide a mind that is potentially better suited to the challenges of learning. They do not provide knowledge de novo, they will not make you "Limitless," as the movies convey. The only thing they do is enhance one's ability to sustain focus and retain knowledge while putting in as much effort as possible to learn. You will still have to work your ass off (if you're a med student, for example), and they will just make that endeavor easier, with more rewards.

Another point (if you're not a medical student, in particular) is this: If you take nootropics and feel that you have no effects, you're probably not stimulating your mind enough to notice the difference.

Side effects...bleh. Have had a significant blepharospasm (eye lid twitching) for about a week that worsens in the hours after taking piracetam. I also seem to be having something like a diffuse myoclonus (twitching/spasm) of many axial and peripheral muscle groups of my thorax and arms. This is interesting because I've never had this before, and these symptoms are actually along the lines of the indicated conditions for medical use of piracetam. Stopped piracetam for 2 days now, which initially increased the spasms significantly, but then resolved all spasms. Stopping left me feeling pretty exhausted and depressed in the washout period as well, but it was temporary. Feeling fine now, after two days off and some time out with friends on the town and relaxing. Reflecting on the last few weeks, I'm starting to realize I've probably been pushing myself too hard. Unfortunately, med school doesn't leave much time for R&R. As tempting as it is to be functioning at 200% all the time, it seems to be best to cycle off this stuff completely after about 2-3 weeks.

I know you're a med student and all, so this is your speciality, and this is an old post. However the eye and muscle twitching is just from lack of sleep. And then at the end when I read you were pushing yourself too hard, I knew that was it. I've seen it a million times. Glad you were able to get some rest, that will always fix it.

Yes you're right. This is called a blepharospasm. I've had it before, simply from lacking sleep and drinking too much coffee. My point in discussing it here, was that I believe taking many of these nootropics lowers the threshold for this to occur. Additionally, as MORE sleep and LESS caffeine are not really an option for me, I sought another solution, and had success. Adding more sources of Choline and Tyrosine to my diet, and simply eating healthier, smaller meals more frequently has prevented the reoccurrence of this problem.

[NoopMed]

I theorize that high levels of systemic choline inhibit the catabolism of Alpha GPC in my periphery, allowing more to stay in circulation longer and more to reach my brain. Without choline bitartrate, the Alpha GPC is more quickly eliminated and excreted and I reach a brain choline deficit from the piracetam/ginkgo combo more quickly.

I think I understand -- can anyone confirm/deny this line of reasoning? I just got some Alpha GPC (amongst everything else) and, seeing that it is relatively more expensive, I think I may get some citicoline or bitartrate (after I try GPC+TAU+DHA) to avoid the potential cliff you're talking about.

It seems to me (in my admittedly limited knowledge of LTP kinetics and nootropics) that enhancement of NMDA channels would be more important for establishing the kind of long term memories and learning that I'm looking to improve with my stacks-- making Piracetam a superior supplement.

I just read this abstract from some med consulting group doing a meta-analysis in 2010 (strangely, is it not possible to download these studies? I can log into pubmed via my school id but I do not see any pdf links?) and it seems that they're suggesting that Pram has "improved cognitive deficits associated with traumatic brain injuries." While piracetam "exhibited no long-term benefits for the treatment of mild cognitive impairments, recent studies demonstrated its neuroprotective effect when used during coronary bypass surgery. It was also effective in the treatment of cognitive disorders of cerebrovascular and traumatic origins;"

My question then is what is the difference between "traumatic brain injuries" and "cognitive disorders of traumatic origins" ? How can we translate these findings into benefits in learning environments?

I also saw on pubmed this study from Australia that says piracetam acts also as an AMPA?

Admittedly, I am not entirely sure I understand what's going on. I may just avoid doing any more research and focus on my actual field of study while gauging effects subjectively as this seems like a pursuit that is more in your path than mine.

So far I've had positive yet mild effects of CILTEP + caffeine(haven't tried with gingko/l-tyrosine yet!) I believe (since the effects are much less pronounced than adderall) I can make this a routine morning dose along with CDP/bitartrate choline, with perhaps, and afternoon add-on of GPC+TAU+DHA to anticipate the afternoon crash and an evening boost of Pram + GPC + Sulbuitamine to get work done before 2am. That's 2 doses of Alpha GPC and one CDP in the morning which should keep my choline bank full.

It's slowly coming together Thanks for you input NoopMed!

Your stack sounds pretty great. I want to mention that I have been trying that CILTEP stack, and I'm not sure if it's because my LTP pathways are working perfectly fine or are different than those of other people, but I find that CILTEP (Artichoke extract, foreskolin) actually decreases my learning efficiency and long term retention. I tried it for 2 weeks, and actually performed worse in that time frame. I will be sticking to my tried and true nootropics -- Ginkgo, Spark Energy Drink from Advocare (which you should probably review, as it contains many vitamins and neurotransmitter precursors we've discussed elsewhere here), Choline bitartrate, Alpha GPC, and Piracetam.

You mention wanting to try Choline AND Bitartrate, I want to clarify that "Choline bitartrate" is one chemical: it's a salt of Choline and the neutral, non-nootropic chemical bitartrate that stabilizes the choline for packaging, distribution, and shelf life. This supplement is the most basic form you can buy of Choline which is the precursor to Acetylcholine, an important neurotransmitter in memory, learning, muscle action, and many autonomic actions of the nervous system. Choline is depleted by piracetam, and other racetams. Various substances classified as "Acetylcholine esterase inhibitors" like Huperzine A, Galantamine, Donezpil, etc prevent the normal breakdown of acetylcholine in an attempt to increase it's levels.

You asked about traumatic brain injuries and cognitive disorders from traumatic origins, in regard to nootropics. This brings up an interesting issue. First, as far as we're concerned here, these issues are one in the same. Various decreases in cognitive function can occur with traumatic injury to the brain (ie. impact to the skull, rupture of arteries causing brain bleeds, and the following issue of widespread neuron ischemia (from lack of blood supply), excitotoxicity in healthy neurons from the dump of Calcium released by dying cells, and further death of neurons in the effected area.) These kind of injuries lead to major loss of brain function. Another avenue of disease effecting the brain that is important to nootropics is the study of degenerative disease: ie. Alzheimer's, Parkinsons, and various dementias. The reason these issues are almost always present in the literature regarding nootropics is because Medicine is most often thought of as the fight against human disease, and not the enhancement of healthy human beings. Nearly all the research that has resulted in the advancement of brain enhancing drugs has stemmed from the efforts to heal damaged brains, not make people smarter. (Consider the human history of scientific and industrial advancement in the context of human wars... do you think we would have explored and developed atomic power, weapons and other nuclear sciences if we didn't have a fear of the Nazis doing it first and an equal desire to blow the shit out of our other enemies? Likely not, or at least, not so quickly.) Nootropics come from the fight against disease of the human mind, and it's always important to remember that our use of these drugs in studying enhancement for our own reasons or in an attempt to just become smarter is piggy-backing on this effort to heal disease. Equally important is consideration for the context of the "Evidence" of nootropic effectiveness. Nearly all the supportive literature showing success with various supplements/drugs is "Success" shown in context of catastrophically damaged brains, not healthy subjects. It should all be "taken with a grain of salt." A few studies do employ "young healthy adults," but most of these are in Russia, Italy, and China. The United States has classically avoided the use of medicine for the purpose of enhancement of healthy humans beings. Obviously, I find this disappointing, but I also definitely respect the ethical dilemma presented in this situation. The future will likely hold aggressive expansion of the research supporting nootropics, and there will likely be many ethical and moral issues that bubble to the surface.

[alecnevsky]

I will be sticking to my tried and true nootropics -- Ginkgo, Spark Energy Drink from Advocare (which you should probably review, as it contains many vitamins and neurotransmitter precursors we've discussed elsewhere here), Choline bitartrate, Alpha GPC, and Piracetam.

Yeah I did look through the ingredients:
B-vitamin complex (thiamine, riboflavin, niacin, vitamin B-6, vitamin B-12 and pantothenic acid), taurine, L-tyrosine, choline, caffeine, GABA (gamma-aminobutyric acid), citrus flavonoids, inositol

I italicized everything I already have either in my multi (optimum nutrition) or in bulk powders. I am however theorizing that huge multis in pill form do not get digested/absorbed as much as shakes like this one. Do you have any information on this?

You mention wanting to try Choline AND Bitartrate

Sorry, no, I meant either CDP Choline (Citicoline) OR Choline Bitartrate. Which would you recommend for daily dosing?

You asked about traumatic brain injuries and cognitive disorders from traumatic origins, in regard to nootropics. This brings up an interesting issue. First, as far as we're concerned here, these issues are one in the same. Various decreases in cognitive function can occur with traumatic injury to the brain (ie. impact to the skull, rupture of arteries causing brain bleeds, and the following issue of widespread neuron ischemia (from lack of blood supply), excitotoxicity in healthy neurons from the dump of Calcium released by dying cells, and further death of neurons in the effected area.) These kind of injuries lead to major loss of brain function. Another avenue of disease effecting the brain that is important to nootropics is the study of degenerative disease: ie. Alzheimer's, Parkinsons, and various dementias.

Right, I think you explained earlier different mechanisms of Pram versus Piracetam. But how do we know whether Pram + Piracetam combo is more efficacious for learning/memory, as you say, than Pram alone, when we're not concerned with the discrepancy of "traumatic brain injuries" (Pram) and "cognitive disorder from traumatic origins"(Piracetam). You see what I'm saying?

The future will likely hold aggressive expansion of the research supporting nootropics, and there will likely be many ethical and moral issues that bubble to the surface.

First come, first served!

[optic]

I have been taking Piracetam for about 15 days and I cannot notice any difference. My stabilised regimen can be found below. This could be to the fact that I have been taking during that time Modafinil (about 150-200mg) a day 5 times a week, as I do not sleep more than 4 hours a day. I am a software engineer.

Morning stack:

• 1x800mg Piracetam
• 1x250mg CDP Choline
• 1x300mg Alpha GPC
• 1000mg Omega-3 Fish Oil - 1x pill (with food)
• 1000mg Glucosamine, 1x pill (with food)
• 1xCoffee

Afternoon stack:

• 1x800mg Piracetam
• 1x250mg CDP Choline
• 1000mg Glucosamine, 1x pill (with food)

Evening stack:

• 50mg Modafinil

Please note that my choline intake is high as I am currently on diet, therefore, do not take much choline from food - I eat meat (chicken, beef) during weekends only. I recently limit Alpha GPC to 300mg as my hands started sweating and my body started heating up easily after minimal physical effect.

My plan is to keep low amount of Modafinil (evenings only - 50mg) and to introduce ALCAR 500mg a day. First time I took Piracetam 1600mg with ALCAR 1000mg I had kick straight away. Unfortunately that lead to headaches in the following days - due to lack of choline as it appeared. Since I stabilised my stack I am thinking on introducing ALCAR back, only 500mg. People say that it works greatly with Piracetam and Choline. Could you advise on that please?

[NoopMed]

I will be sticking to my tried and true nootropics -- Ginkgo, Spark Energy Drink from Advocare (which you should probably review, as it contains many vitamins and neurotransmitter precursors we've discussed elsewhere here), Choline bitartrate, Alpha GPC, and Piracetam.

Yeah I did look through the ingredients:
B-vitamin complex (thiamine, riboflavin, niacin, vitamin B-6, vitamin B-12 and pantothenic acid), taurine, L-tyrosine, choline, caffeine, GABA (gamma-aminobutyric acid), citrus flavonoids, inositol

I italicized everything I already have either in my multi (optimum nutrition) or in bulk powders. I am however theorizing that huge multis in pill form do not get digested/absorbed as much as shakes like this one. Do you have any information on this?

You mention wanting to try Choline AND Bitartrate

Sorry, no, I meant either CDP Choline (Citicoline) OR Choline Bitartrate. Which would you recommend for daily dosing?

You asked about traumatic brain injuries and cognitive disorders from traumatic origins, in regard to nootropics. This brings up an interesting issue. First, as far as we're concerned here, these issues are one in the same. Various decreases in cognitive function can occur with traumatic injury to the brain (ie. impact to the skull, rupture of arteries causing brain bleeds, and the following issue of widespread neuron ischemia (from lack of blood supply), excitotoxicity in healthy neurons from the dump of Calcium released by dying cells, and further death of neurons in the effected area.) These kind of injuries lead to major loss of brain function. Another avenue of disease effecting the brain that is important to nootropics is the study of degenerative disease: ie. Alzheimer's, Parkinsons, and various dementias.

Right, I think you explained earlier different mechanisms of Pram versus Piracetam. But how do we know whether Pram + Piracetam combo is more efficacious for learning/memory, as you say, than Pram alone, when we're not concerned with the discrepancy of "traumatic brain injuries" (Pram) and "cognitive disorder from traumatic origins"(Piracetam). You see what I'm saying?

The future will likely hold aggressive expansion of the research supporting nootropics, and there will likely be many ethical and moral issues that bubble to the surface.

First come, first served!

As far as CDP-Choline (Citicoline) vs Choline bitartrate. I'm actually currently been taking both. 300mg BID of Citicoline and 500mg Choline bitartrate TID. CDP Choline is actually a somewhat active molecule in its own regard in addition to being a acetylcholine precursor. I hadn't mentioned it before because I just started it this week. From what I understand, it will be beneficial to take both. Previously I have tried the combo of Choline bitartrate WITH either DMAE or Alpha-GPC (but never all 3). I have now been trying CDP Choline in place of either of those two. (I like Alpha GPC better for studying, and DMAE better for exercising. some literature has shown a correlated improvement in physical activity with DMAE, showing it also has intrinsic activity of it's own--outside being another precursor for acetylcholine.) So far I like the CDP-Choline, but haven't noticed a big difference in acute mental performance. Which I will outline below--- The following citation is from Natural Med Supplement Database, which is basically a gold standard tool for physicians researching supplements that lie outside the realm of traditional pharmacology reference material:


Citicoline (CDP-Choline) is an intermediate compound that is formed endogenously in the process of synthesizing phosphatidylcholine from choline (12129,12140).
When taken orally, citicoline is metabolized in the gut to cytidine and choline. Both compounds are absorbed independently and taken up by brain cells. Within the brain cell cytidine is converted to cytidine monophosphate, cytidine diphosphate, and cytidine triphosphate. Choline is phosphorylated to form phosphocholine. Phosphocholine combines with cytidine triphosphate to reform citicoline. Citicoline then rapidly combines with diacylglycerol to from phosphatidylcholine (12129,12140,12195).
In animal models, orally administered citicoline increases brain phosphatidylcholine levels by 23% after 42 days and 30% after 90 days. In humans, a single dose of citicoline increases brain choline levels by about 18% in younger adults. But in older adults, brain choline levels don't seem to increase significantly. It's thought that choline uptake in the brain decreases with age, but cytidine uptake does not decrease (12129).
Age-related cognitive dysfunction, dementia, and other brain disorders have been linked to decreases in cholinergic neurons, decreases in acetylcholine, and alterations in cell membrane composition, including decreases in choline-containing phospholipids (12129). During episodes of cerebral ischemia and brain trauma, phosphatidylcholine is degraded to free radicals and free fatty acids (12131,12194).
Citicoline is thought to be beneficial for cerebral ischemia by decreasing generation of reactive oxygen species and stabilizing cell membranes (12134,12194,12195).
Citicoline's potential benefits for central nervous system disorders such as dementia, brain trauma, and other conditions is thought to be related to citicoline's effects on brain acetylcholine and phosphatidylcholine levels (12129,12130,12195).
In animal models, citicoline seems to protect against age-related decline in spatial memory (12196).
Citicoline might also affect dopamine levels. In animal models, citicoline increases retinal dopamine levels. Therefore, there is interest in using citicoline for glaucoma and Parkinson's disease (12132).
Citicoline might also help for Parkinson's disease by improving dopaminergic cell survival. Patients with Parkinson's disease tend to have a degeneration of dopaminergic cells over time. Citicoline also seems to increase levels of reduced glutathione, a potent antioxidant. Glutathione levels are found to be decreased in the substantia nigra of Parkinson's patients (12133,12140).
In animal models of brain trauma, citicoline reduces neuronal death, cortical contusion volume, and improves neurological recovery (12137).
In animal models of ischemic stroke, citicoline seems to help reduce neuronal damage, possibly by decreasing neuronal apoptosis (12138).
Citicoline seems to have a pressor effect. In animal models of hemorrhagic shock, intravenous administration of citicoline reverses hypotension. In normotensive rats, intravenous administration of citicoline increases blood pressure (12136). It's not known if therapeutic doses of citicoline affect blood pressure in humans.
Citicoline is readily absorbed when taken orally. Less than 1% is excreted unchanged in the feces. Citicoline has a biphasic peak. The first peak occurs at 1 hour after administration, followed by a higher peak 24-hours post-dose. Citicoline is primarily eliminated through the kidneys. Its half-life is 71 hours (12132).

Shown to be effective in:
Age-related cognitive impairment. People aged 50 to 85 years with poor memory, taking citicoline 1000-2000 mg daily, seem to have improved verbal memory (12130).
Cerebrovascular disease. There is some evidence that citicoline taken orally or given intramuscularly or by intravenous infusion might improve memory and behavior in patients with chronic cerebrovascular diseases, such as stroke (12131).
Ischemic stroke. Stroke patients who receive citicoline 500-2000 mg/day orally within 24 hours of acute ischemic stroke are more likely to have a complete recovery within 3 months compared to placebo (12139).

Studies that are still in progress or deemed in need of further review and research showed:
Alzheimer's disease. Preliminary evidence suggests that taking citicoline 1000 mg/day orally might improve cognitive function in patients with mild to moderate Alzheimer's disease (12131).
Glaucoma. Preliminary evidence suggests that citicoline 1000 mg/day intramuscularly might improve vision in patients with open-angle glaucoma (12132). Taking 1000 mg/day orally also seems to improve visual evoked potentials in patients with glaucoma (12173).
Parkinson's disease. Preliminary evidence suggests that patients who receive citicoline 500 mg/day intramuscularly in conjunction with conventional treatment might have improved rigidity and bradykinesia. But citicoline does not seem to improve tremor (12132).
Vascular dementia. Preliminary evidence indicates that citicoline 500 mg twice daily (1000 mg/day) does not seem to improve symptoms in patients with vascular dementia (12135).
More evidence is needed to rate citicoline for these uses.

If you'd like the link/PDF to the supporting literature for those statements, please reply with the citation number.

As far as the Spark Drink is concerned... VS large pill versions of the vitamins in it...

I don't really have much specific information, but I wouldn't be surprised of the powder form was potentially better and more quickly absorbed. I mostly use it because it includes many great support supplements for the overdrive these noots and my schedule all in one thing, and it's very easy to consume at once. Pills are harder to manage, and I already tote around enough of them with the other stuff.

Caffeine and Taurine, and especially synergistically combined, have been proven time and again to enhance cognitive performance, they're definitely essential for me... caffeine more so than taurine, obviously. I didn't see italics on those, but you should definitely go for those. GABA is an inhibitor neurotransmitter, some people find it beneficial, I don't really notice it as the amount is pretty low. Citrus flavinoids? Didn't even notice, haha, I'll read into them. Probably antioxidants or something.



I have not used Pramiracetam if that's what you're asking about with Pram? I've read it has stronger and longer lasting stimulant effects, but I've also read that it generates excess NO in the brain at high doses which can lead to neuron apoptosis (death). I prefer to avoid that side effect. I do have some right now, and I'll likely sample a small amount, but do not plan to take long term at all and have not tried it. Aniracetam looks promising to combine with Piracetam, as does Noopept. I also have Noopept and enjoyed that. I found it helped with long term memory retention and studying, but not so much with testable performance or discussion of material with peers. It does make me very social, but very distractable.

Edited by NoopMed, 22 October 2012 - 02:08 AM.

[NoopMed]

I have been taking Piracetam for about 15 days and I cannot notice any difference. My stabilised regimen can be found below. This could be to the fact that I have been taking during that time Modafinil (about 150-200mg) a day 5 times a week, as I do not sleep more than 4 hours a day. I am a software engineer.

Morning stack:

• 1x800mg Piracetam
• 1x250mg CDP Choline
• 1x300mg Alpha GPC
• 1000mg Omega-3 Fish Oil - 1x pill (with food)
• 1000mg Glucosamine, 1x pill (with food)
• 1xCoffee

Afternoon stack:

• 1x800mg Piracetam
• 1x250mg CDP Choline
• 1000mg Glucosamine, 1x pill (with food)

Evening stack:

• 50mg Modafinil

Please note that my choline intake is high as I am currently on diet, therefore, do not take much choline from food - I eat meat (chicken, beef) during weekends only. I recently limit Alpha GPC to 300mg as my hands started sweating and my body started heating up easily after minimal physical effect.

My plan is to keep low amount of Modafinil (evenings only - 50mg) and to introduce ALCAR 500mg a day. First time I took Piracetam 1600mg with ALCAR 1000mg I had kick straight away. Unfortunately that lead to headaches in the following days - due to lack of choline as it appeared. Since I stabilised my stack I am thinking on introducing ALCAR back, only 500mg. People say that it works greatly with Piracetam and Choline. Could you advise on that please?

I could never take Modafinil at night like that, even low dose. When I tried it, I was awake for many, many hours. Sleep is very important to brain function.

The rest of the stack looks great, I just like more choline sources... like choline bitartrate in addition. I try to total around 1500-2000mg of various acetylcholine sources total. Sometimes I throw in a SAM-e to give me a boost in energy and mood, as I've read elsewhere in this forum that excess choline is associated with depression.

I once tried ALCAR for quite a long period of time, about 3 months. I liked the boost it gave me in my libido, haha. And it made me feel pretty good overall. However, I found it made me gain weight and gave me acne (which I typically never get to any noticeable excess-- maybe a zit every few months.). It also seemed to reduce by attention span, and I did not experience any improvement in memory or LTP. It was NOW brand ALCAR. Maybe I'll try it again someday, but not at this point. Many people seem to find benefit with it and studies do support its use:


Here's some more data from Nat Med on ALCAR:

POSSIBLY EFFECTIVE
Age-related cognitive impairment. Taking acetyl-L-carnitine orally seems to improve some measures of cognitive function and memory in elderly people with age-related mental impairment (42,3600,3601).
Age-related testosterone deficiency. Taking acetyl-L-carnitine orally, in combination with propionyl-L-carnitine, seems to help symptoms of androgen decline in older men. The combination taken for 6 months seems to be similar to testosterone for improving sexual dysfunction, depression, and fatigue (12353).
Alzheimer's disease. Acetyl-L-carnitine might slow the rate of disease progression, improve memory, and improve some measures of cognitive function and behavioral performance in some patients with Alzheimer's disease. It is more likely to show some effect in those with early-onset Alzheimer's disease who are less than 66 years of age and have a faster rate of disease progression and mental decline (1594,1595,1596,1597,1598,1599,9105,10391). Acetyl-L-carnitine has not been compared with cholinesterase inhibitors such as donepezil (Aricept).
Chronic cerebral ischemia. Administering a single dose of acetyl-L-carnitine intravenously seems to produce short-term improvements in cerebral blood flow in people with chronic cerebral ischemia (1591,1592).
Cognitive impairment. Taking acetyl-L-carnitine orally seems to improve memory and visuospatial capacity in 30-60 year-old chronic alcoholics with cognitive impairment (1589).
Diabetic neuropathy. Patients with neuropathy related to type 1 or type 2 diabetes seem to have improved symptoms after taking acetyl-L-carnitine 1500-3000 mg daily in divided doses for a year. Acetyl-L-carnitine seems to increase nerve fibers, regenerate nerve fiber clusters, and improve vibratory sensations. However, research is conflicting on whether it can modestly improve nerve conduction velocity. In patients who have neuropathic pain as the most significant symptoms, taking acetyl-L-carnitine 1000 mg two to three times daily also decreases neuropathy-related pain within six months of beginning treatment. Doses of 500 mg three times daily do not seem to reduce pain. Acetyl-L-carnitine also seems more likely to be effective for reducing pain in patients with a shorter duration of diabetes and patients with poorly-controlled type 2 diabetes (1593,12743,12753,13007).
Infertility. Taking acetyl-L-carnitine orally, in combination with L-carnitine for 6 months, seems to increase sperm motility in men with infertility (12352). Some pregnancies occurred after taking these carnitines, but not enough to be statistically significant (12352). Taking acetyl-L-carnitine orally, in combination with L-carnitine and nonsteroidal anti-inflammatory drugs (NSAIDs), seems to improve male infertility caused by abacterial prostatovesiculoepididymitis, an inflammation of the prostate gland, seminal vesicles, and epididymis. The carnitines increase sperm count and motility. The carnitines are used following 2 months of treatment with NSAIDs (9791).
Peyronie's disease. Taking acetyl-L-carnitine orally seems to help treat acute and early chronic Peyronie's disease (10076). Acetyl-L-carnitine appears to be more effective than tamoxifen for reducing pain and inhibiting disease progression.

Mechanism of Action:

Acetyl-L-carnitine occurs naturally in the body. Endogenous carnitines exist as a "carnitine pool" consisting of L-carnitine and several acetyl-carnitine esters. Intracellular enzymes and cell membrane transporters can rapidly interconvert the carnitines to the needed form and transport them between the tissues and extracellular space. Acetyl-L-carnitine, the most important carnitine ester, is converted to L-carnitine in the body by carnitine acetyltransferase (10395,12744). The body obtains some carnitine from the diet, primarily from red meats and dairy products. The body can also synthesize carnitines from the amino acids, lysine and methionine. The kidney aids in keeping carnitine levels stable. Normally, greater than 90% of filtered carnitine is reabsorbed. If dietary intake of carnitines decreases, carnitine reabsorption becomes even more efficient (12744). Carnitines play an important role in lipid metabolism and energy production. They are essential for normal mitochondrial function, acting as a transporter of long-chain fatty acids into the mitochondria for beta-oxidation (12745,12748,12756,13007). Carnitine deficiency from inborn disorders of carnitine metabolism most often presents with symptoms of progressive cardiomyopathy and skeletal muscle weakness, and less frequently with fasting hypoglycemic coma (12748).
Acetyl-L-carnitine is structurally related to acetylcholine. It also serves as a precursor to acetyl coenzyme A, and contributes acetyl groups to acetylcholine (10395). It also seems to promote acetylcholine release and increases choline acetyltransferase activity (44). These effects have lead to the study of acetyl-L-carnitine in Alzheimer's disease, in which there is substantial cholinergic neuronal loss and acetylcholine depletion (1594). It may also lessen oxidative stress and prevent oxidative damage in the brain better than L-carnitine (12688).
Carnitine levels are lower in people with complications of diabetes (12746). In diabetic neuropathy, there is damage to sensory neuronal membranes. This causes an increase in sodium channels and therefore an increase in spontaneous neuronal firing. Acetyl-L-carnitine is thought to slow neuronal degeneration or help in the regeneration and repair of neurons and therefore decrease excessive excitability and firing. Acetyl-L-carnitine might improve peripheral as well as autonomic neuropathy (12749,12750,12751,12752,13007). Additionally, preliminary clinical research suggests that acetyl-L-carnitine might also improve glucose utilization, possibly by increasing expression of glycolytic and gluconeogenic enzymes (12754).
In HIV patients, acetyl-L-carnitine might slow the loss of CD4 lymphocytes by reducing apoptosis and increasing the serum level of insulin-like growth factor 1 which protects against apoptosis (3605). Lower plasma levels of acetyl-L-carnitine are also associated with neuropathy in people who take HIV drugs (3606). Preliminary research suggests it might increase the activity of nerve growth factor and promote peripheral nerve regeneration. It might also have analgesic properties. However, it doesn't seem to affect viral load or CD4 or CD8 cell counts (12745).
Preliminary research suggests acetyl-L-carnitine might also prevent cisplatin (Platinol) and paclitaxel (Taxol)-induced neuropathy (12755).
Acetyl-L-carnitine and L-carnitine are present in human sperm and seminal fluid (3607). Their levels increase in sperm during the maturation process in the epididymis and coincide with the acquisition of progressive motility (3608,3609). Levels of acetyl-L-carnitine, and the ratio of acetyl-L-carnitine to L-carnitine, have been reported to be lower in infertile semen and sperm samples with low motility (3610,3611), and an increase in sperm motility is seen in vitro when acetyl-L-carnitine or L-carnitine is added to the sample (3612). Preliminary research also suggests acetyl-L-carnitine may increase testosterone production and improve testicular function (12686,12687).
In patients with alcohol-induced cirrhosis, serum levels of L-carnitine and its esters are sometimes increased, possibly due to increased L-carnitine biosynthesis (1931,1948).

Edited by NoopMed, 22 October 2012 - 02:21 AM.

[Luminosity]

NoopMed,

I'm glad there will be a doctor who is open to natural medicines but I think you need to know that life is not a chemistry experiment. Manipulating your body with chemicals to bring it up and down will hurt you. Specifically, I think you should eliminate the marijuana, the "energy drink" and any large amount of caffeine. That may be causing the the problems you seem to blame on other things. I've taken Gingko and large amounts of many supplements regularly but not had the ill effects you've had. Marijuana can be very addictive for people these days. Don't be afraid to seek help if you need it. Needing substances to sleep or function everyday when you are young and and healthy is symptomatic of addiction.

It's best to eat well and have a steamed green vegetable every day. If it agrees with you, moderate amounts of hot plain green tea help some people to think. Exercising in fresh air helps too. I've enclosed a link to my thread on Chinese medicine because I think that it is very wise.

http://www.longecity...inese-medicine/


I've also enclosed a link to some poems and quotations I've assembled. Some of them deal with health.

http://www.longecity...and-quotations/


Good luck.

Edited by Luminosity, 22 October 2012 - 02:30 AM.

[NoopMed]

Also people have previously asked about LTP with foreskolin and Artichoke extract. As I've mentioned, I'm skeptical about this phenomenon. I have seem some research on it, but currently it's not really discussed in Nat Med, or in the sphere of medical treatment or basic medical sciences I've learned about elsewhere.

I do however have the following info from Nat Med about each:

Foreskolin:

Effectiveness:

POSSIBLY EFFECTIVE
Asthma. There is some evidence that a single-dose inhalation of forskolin powder 10 mg from a Spinhaler inhaler can significantly increase forced expiratory volume in 1 second (FEV1) in patients with asthma (7281).
Idiopathic congestive cardiomyopathy. There is some evidence that intravenous forskolin, starting at 0.5 mcg/kg/minute, increasing at 15 minute intervals to 1.0, 2.0, and 3.0 mcg/kg/minute, is effective in improving cardiac output and pulmonary vascular pressures in patients with idiopathic congestive cardiomyopathy (7278).

Mechanism of Action:

Forskolin is a diterpene and the major active constituent found in the roots of the plant Plectranthus barbatus (Coleus forskohlii) (7277). Forskolin stimulates and activates the enzyme adenylate cyclase in the heart and smooth muscle. This causes increased production of cyclic AMP (cAMP), which causes calcium channels to open and intracellular calcium concentrations to increase, resulting in increased contractility of heart muscle and relaxation of smooth muscle (7277,7406,7407,7408,7409). Researchers speculate that forskolin might also activate adenylate cyclase in other cells of the body such as platelet cells and cells in the thyroid, pancreas, adrenal, or pituitary glands (7277). There is preliminary evidence that forskolin prevents platelet aggregation and adhesion (7410,7411); and may also block tumor cell-induced human platelet aggregation, prevent tumor cell growth, and prevent cancer metastasis (7412,7413).


Artichoke Extract:


POSSIBLY EFFECTIVE
Dyspepsia. Artichoke leaf extract seems to significantly reduce symptoms such as nausea, vomiting, flatulence, and abdominal pain in functional dyspepsia and dyspepsia associated with biliary disease. Improvement can take up to 2 to 8 weeks of treatment (2056,11429,12208). Artichoke leaf extract needs to be given to 11.5 patients for 6 weeks in order for one patient to have markedly or completely improved symptoms (12208). Some studies have used a specific extract called ALE LI 220 (Hepar-SL forte, Serturner Arzneimittel GmbH) (2056,12208). Another study has used a different specific artichoke leaf extract (Cynara SL, Lichtwer Pharma) (11429).
Hyperlipidemia. Taking a specific artichoke extract (Valverde Artischocke, Novartis Consumer Health) seems to modestly reduce total and low-density lipoprotein (LDL) cholesterol, and the LDL/high density lipoprotein (HDL) ratio over 6 to 12 weeks of treatment. Artichoke extract may work better in people with higher cholesterol levels (6282,11773); however, studies using the isolated cynarin constituent have been contradictory (1423,1424).
POSSIBLY INEFFECTIVE
Hangover. Some evidence shows that taking an artichoke extract does not prevent alcohol-induced hangover (11774).

Mechanism of Action:
The applicable parts of artichoke are the leaf, stem, and root. The primary constituents include up to 2% phenolic acids, primarily chlorogenic acid, cynarin, and caffeic acid. Artichoke also contains up to 4% sesquiterpene lactones, and 1% flavonoids including scolymoside, cynaroside, and luteolin (2056). Artichoke's therapeutic benefit in dyspepsia has centered around its choleretic effects, or ability to stimulate bile flow, which has been demonstrated in several studies (2056). This might explain its use as a hangover remedy (11774). Constituents responsible for this effect are thought to be cynarin, chlorogenic acid, and scolymoside (2056).
Antiemetic, spasmolytic, and carminative effects of artichoke have also been described. These effects may be responsible for the potential beneficial effects in patients with irritable bowel syndrome (IBS) (2562). Cynarin and chlorogenic acid may also have cholesterol-lowering effects, although studies with cynarin for hyperlipidemia have produced mixed results (1423,1424).
Artichoke might reduce cholesterol synthesis (11773). Cynaroside and its derivative, luteolin, might also indirectly inhibit HMG-CoA reductase (1425,1426,2056). Several constituents are reported to have antioxidant activity (1422). Preliminary research suggests that artichoke leaf extract might also protect liver cells from damage (1421,1422,2056,3269). A mixture of polyphenols and flavonoids including caffeic acid, chlorogenic acid, cynarin, luteolin-7-O-glycoside (cynaroside), and luteolin might contribute to hepatoprotective activity (3269,2056).


From what I've seen, there's nothing exceptionally Nootropic going on here, and I didn't enjoy the subjective experience.

[NoopMed]

NoopMed,

I'm glad there will be a doctor who is open to natural medicines but I think you need to know that life is not a chemistry experiment. Manipulating your body with chemicals to bring it up and down will hurt you. Specifically, I think you should eliminate the marijuana, the "energy drink" and any large amount of caffeine. That may be causing the the problems you seem to blame on other things. I've taken Gingko and large amounts of many supplements regularly but not had the ill effects you've had. Marijuana can be very addictive for people these days. Don't be afraid to seek help if you need it. Needing substances to sleep or function everyday when you are young and and healthy is symptomatic of addiction.

It's best to eat well and have a steamed green vegetable every day. If it agrees with you, moderate amounts of hot plain green tea help some people to think. Exercising in fresh air helps too. I've enclosed a link to my thread on Chinese medicine because I think that it is very wise.


I've also enclosed a link to some poems and quotations I've assembled. Some of them deal with health.


Good luck.

Thank you very much for your input. Ginkgo has been used for many centuries in Chinese medicine, as you likely know. I enjoy using it regularly, and I'm currently not experiencing any ill effects. In the past, I have however, and I believe that was in great part due to poor management and insufficient balance of other nutrients and many of the other things you mention. I frequently drink Green Tea. I also regularly exercise, and love the outdoors. I camp, hike, and cycle on a regular basis. I eat many green vegetables, generally a full, very diverse spinach salad at least once every day. Marijuana can be quite habituating, you are correct there. However, I use it very moderately, and rarely ever combust it-- preferring vaporization. It's a very relaxing experience for me, and I enjoy the experience with many friends, all of which in present company are other medical students. As for caffeine... It's a rare thing to find a medical student that doesn't use some sort of energy drink or coffee.

As a final note, I don't need supplements to function or sleep-- you're right I am relatively young (but not so much as my classmates, at 32) and healthy. However, I have functioned and slept moderately well before the quest into nootropics, and I've taken breaks from absolutely everything (while away from school) and been perfectly fine. My sleep in the present "chemistry experiment" has actually been very good, better than when taking nothing at all. The point you're missing. The point of this entire discussion, is to improve upon functioning "perfectly fine." I functioned at or below the class average when I began medical school. I am now in the very top of my class in terms of performance, I still manage a busier social life and other hobbies than most of my peers, and my sleep, diet, and health maintenance are relatively superb compared with most medical students.

I do thank you for your concern, but as of now and the last month or so, I have reached a place of greater balance and performance in my life as a medical student than I have here had before. I want to be a doctor, I want to dedicate my life to the care of people who need my help. What I have done is found, in a bit of chemistry, a way to improve the obligatory training I must complete to become the best doctor I can possible be. Throughout this experience, I have emphasized a focus on lowest minimum dosage and the avoidance of long term sequelae. I experiment to find what works for me after doing thorough research, and safety is always a top priority.

I think we may differ in opinions on many things, but I respect your opinion, and I appreciate your input. I look forward to reading the poetry you've attached. I sometimes write poetry as well, though more often to accompany music that I write.







Also, here's some info from Nat Med. on L-Theanine, the active ingredient in Green Tea:

Effectiveness:

Anxiety. Preliminary evidence suggests that taking theanine 200 mg might induce subjective feelings of tranquility in healthy people. But theanine does not seem to reduce experimentally induced anticipatory anxiety (12188). More evidence is needed to rate theanine for this use.


Mechanism of Action:

Theanine is the major amino acid found in green tea. Green tea contains 1% to 3% theanine (7685,7690). Theanine is also found in some mushrooms (12188).
Theanine has historically been used for it's relaxing and anti-anxiety effects. It's thought that theanine might work for anxiety by increasing levels of GABA and serotonin (12188).
There is interest in using theanine for dementia. Theanine is an analog of glutamate, which is an excitatory neurotransmitter. Levels of glutamate increase and cause neuronal death during periods of cerebral ischemia. Theanine demonstrates a protective effect by decreasing ischemic neuronal death in the forebrains of animal models (7685). The antagonistic effects of theanine on glutamate and N-methyl-D-aspartate (NMDA) receptors might provide neuroprotection (7685).
There is also interest in using theanine for hypertension. Theanine affects catecholamines that can cause vasoconstriction and lead to elevations in blood pressure. In animal models, theanine decreases norepinephrine levels (7686), decreases systolic and diastolic blood pressure (7687), and suppresses the stimulatory effects of caffeine (7685,8665). However, there is also some evidence theanine might induce an excitatory effect when used in very small doses, suggesting the effects of theanine are dose dependent (8665).
Green tea might prevent atherosclerosis by inhibiting the proliferation of smooth muscle cells in blood vessel walls, but theanine doesn't seem to affect smooth muscle (8666). Additionally, there is evidence that suggests theanine might prevent the development of atherosclerosis by inhibiting lipid peroxidation of low-density lipoproteins (LDL) (8667).
There is also interest in using theanine adjunctively for cancer. In studies involving doxorubicin, theanine increases the concentration of doxorubicin and adriamycin in tumors by blocking efflux of the drug from tumor cells (7688,7690,8668,8669). Theanine seems to enhance the effects of doxorubicin and adriamycin on drug sensitive and multi-drug resistant tumors (7688,8668,8669). Theanine may also enhance the suppressive action of doxorubicin on metastatic tumors (8312). Theanine also inhibits the efflux of idarubicin from leukemia cells in animal models (7689). Additionally, theanine seems to decrease the toxicity of idarubicin by reversing adverse effects on leukocytes and bone marrow cells (7689).
There is also some evidence that theanine might decrease serotonin and 5-hydroxyindole acetic acid (5HIAA) concentrations in the brain. Theanine might enhance the degradation of serotonin, and it might also directly inhibit the enzyme responsible for serotonin synthesis (8670).
Animal research suggests theanine may act synergistically with caffeine and other constituents in green tea to cause weight loss (11960).

Edited by NoopMed, 22 October 2012 - 03:06 AM.

[abelard lindsay]

Somehow I don't think your natural medicine book is going to contain information about artichoke and forskolin that was discovered and developed on the "Chemically Induced LTP" thread.

[NoopMed]

Somehow I don't think your natural medicine book is going to contain information about artichoke and forskolin that was discovered and developed on the "Chemically Induced LTP" thread.

I certainly agree with you there, Albard. If I'm correct, you were very involved with (perhaps spearheaded?) those efforts to develop CILTP. I've read a portion of your posts, and found the information very convincing, which is why I tried Forskolin and Artichoke. The source I was using in my previous post is not actually a book. That info is from the Natural Medicine and Supplement Database, which is an organization that provides thorough meta-review and analysis of published papers from thousands of sources via PubMed.gov. It is a tool used by many physicians when evaluating a patient's supplement intake, and for treating patients through natural and alternative measures. The extent of literature incorporated into Nat Med is admittedly limited to the frequently cited studies, which is why I'm not surprised the articles you cite were not included, as they are very cutting-edge and recent.

In terms of my personal experience with CILTP... I tried it as part of my current stack for nearly a month, and found it subjectively added to distractability and reduced my focus. This could easily be from a conflict with other supplements I'm using, or perhaps unique to my own physiology. I certainly don't have any evidence from my own experience that it reduced LTP or inhibited my learning, it may certainly have enhanced it. Unfortunately, the volume of material I must cover in medical school is so extensive that I cannot rely on enhanced long term memory alone: Much of the time, I simply must put my nose to the grind stone and sustain many, many long hours of uninterrupted, focused studying.

As my current stack has been working very well for me (now in the absence of CILTP), it is unlikely I will try to expand it further for the moment. However, I may have a use for it in the future.

Again, I'm not questioning the legitimacy of artichoke and forskolin in CILTP, and I'm not saying it doesn't work. I'm just not entirely on board. I'm stating that it didn't work out for me, and the resources at my disposal as a medical student (and those available to physicians) don't have much information on it.

I won't ask you to reiterate your information here, nor give me individual suggestions about CILTP, however; some readers (and myself) will likely appreciate a link to your most recent thread of info for further review.
You're an excellent contributor to this forum, and I honestly want to thank you for your efforts. The posts I've read from you are always thorough and informative. I hope it didn't seem like I was bashing on CILTP, as I certainly don't have the evidence nor experience to form a solid opinion either way.




Also, just for some context, this is my current stack... (I know I need to be more consistent about listing an updated version, as I've made frequent changes, so here's what is working very well currently):

Morning:
1 Scoop Spark Energy Drink from Advocare
800mg Piracetam
120mg Extended Release Ginkgo biloba
1000mg Fish Oil
300mg CDP Choline

Afternoon:
Large cup of coffee
800mg Piracetam
500mg Choline bitartrate
300mg CDP Choline

(If I plan to study late, I take another ginkgo in the afternoon, and potentially a Noopept or Aniracetam. If I take Aniracetam, I will take again in the evening.)

Evening: (Only taken if I plan to study late, generally I stop with afternoon on the average day.)
500mg Choline bitartrate

Large cup of coffee
800mg Piracetam

Night:
Vaporize a very small amount of Cannabis.
Small glass of Red Wine for reservatrol and vasodilatory effects.


Overall: Exercise for 45 minutes in the afternoon. Eat healthy. Drink plenty of water.

Edited by NoopMed, 22 October 2012 - 03:27 PM.

[JChief]

The moral of the story: in the end, you stick with Piracetam. Best noot out there in my opinion. subtle yet profound

[UCSBkid]

Thanks for the great writeup! I know I'm new here, but I was wondering if any of these supplements you mentioned interact with Vyvanse? I know Paracetam does, but I want to ensure I dont risk excitotoxcity with the others. Thanks!