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Rol82's Regimen


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#1 Rational Madman

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Posted 10 August 2010 - 01:41 AM


However, there is one Russian drug in development that might be worthy of our enthusiasm---even though it has failed in recent Alzheimer's clinical trials. That drug is Latrepiridine, or more popularly known by the trade name of Dimebon. This drug has attracted my interest because I---like many of us---endeavor to optimize my cognitive abilities through diet, lifestyle, and supplementation. And am willing to sometimes undertake risks---that deter the average person---in pursuit of that goal. Although I have no cognitive complaints that would trouble the average person, this drug has a certain captivating allure; and because I've found a reputable source, I'm interested in incurring the financial and potential health costs of experimentation next month. The source is Life Extension Drugs, which is a company that I used for procuring some Ondansetron, which is another drug with considerable potential for cognitive enhancement, but has greater personal appeal as an antiemetic. Based on previous positions I've taken on this forum, I realize that my actions might render me a hypocrite, but I care little, since my thinking on the importation of drugs has evolved somewhat. Indeed, my previous strident stance has been replaced by a more ardent desire to maximize my earning potential, and out-perform my colleagues by as much as possible---even though there is no real animus between any of us. Anybody familiar with organizational behavior and politics, and the power of the human ego, though, may share my sentiments. The price, unfortunately, may be too prohibitive for most to contemplate---and I would take no solace from anybody else incurring the same costs---but since this drug possesses the real potential to provide significant benefits to many that have been on fruitless searches for a panacea drug or supplement, I thought I might as well mention it in a thread devoted to another noteworthy drug of Russian origin.


Thanks for an eloquent and interesting post in which you mention two substances I've never heard of before. What makes you think Latrepirdine is so promising when it comes to improving cognitive processes in healthy people? I couldn't find much about it and I'm quite unfamiliar with its mechanisms.

The same goes for Ondansetron, what was your experience with that?

The mechanism of Dimebon remains unclear, but it's believed to modulate NMDA and AMPA receptors, increase catechloamine volume in the prefrontal and dorsolateral cortexes, inhibit the build up of beta amyloid proteins, and possibly inhibit acetylcholinesterase. In addition, it has a mysterious cellular cleansing mechanism, and appears to increase mitochondrial energy through a yet to be completely understood mechanism. I believe it might also reduce inflammation through its affinity for histamine receptors,but this hasn't been documented to my knowledge. Due to its multiple mechanisms--which seems to address the most important independent variables for the progression of neurodegeneration---and because of its excellent safety profile, I became quite intrigued with its potential. But given its suspicious failure in the latest clinical trial, which seems to be at odds with user experiences and other empirical evidence, I've become somewhat cautious. Because of the positive results in a well controlled Huntington's Disease study, Dimebon does appear to attenuate neurodegeneration, but I think the dosages used in recent studies are probably too low. And until more evidence emerges on the correct dosage for healthy individuals, I think I'll wait, and try other drugs in the meantime, because if I were to administer the prescribed dosage used for recent studies, a month's supply would cost approximately $1500. However, I've found an alternative supplier that's based in Ukraine, but I get the feeling that he's comfortable with supplying institutional clients in bulk----rather than individuals.

As far as Ondansetron goes, the most attractive property is its anti-emetic mechanism---which is my primary motivation for procuring the drug, since I suffer from subclinical, but recurrent bouts with nausea. Through its modulation of the 5-ht3 receptors, though---which is critical for learning and memory formation---it seems to have some value for cognitive enhancement and anxiolysis. But, I think it must have some affinity for other receptors as well, because it appears to be more effective than other 5-ht3 antagonists in these regards.

Since I'm probably not going purchase Dimebon in the near future, there are other candidates that I'm considering, which include Amineptine, Cerebrolysin, Donepezil, Tolcapone, and Rasagiline. For Rasagiline, I've found a great source---with an incredible price---that offers a month's supply in the 0.5 mg dose, which would be ideal for life extension purposes, and for coadministration with the other drugs that I'm using if taken at .125 mg/day. As a tricyclic with dopamine reuptake inhibitor properties, the use of Amineptine would require that I make adjustments in my drug regimen---which I'm loath to do because of its efficacy---and the lone supplier that I've discovered is demanding a price that far exceeds the drug's relative worth. However, the drug is highly praised by David Pearce---whom I highly regard. Tolcapone also seems promising, but potentially very dangerous, and would certainly require significant adjustments be made to my current regimen. Donepezil has some appeal because its half life is considerably greater than the supplement grade of Galantamine that I currently use, but its effects on healthy adults doesn't seem to be profound, and in the absence of enzymatic dysfunction, may be a bit too risky. This leaves Cerebrolysin, which may be the most tolerable and safest addition, and could potentially yield the best results if used at an effective dose of 10ml per day. This source seems to be the best at the moment http://www.rxpharmac...rebrolysin.html, unless anyone can offer any alternatives that I've overlooked.

Anyway, although this thread might be the inappropriate place to post my regimen, some people have made inquiries in the past, and since this thread is devoted to the use of a drug with mood and cognitive enhancing properties---and as I imagine the previous content of my post has aroused some curiousity---I think I might as well provide a list of drugs and supplements that I've found to be immensely helpful in pulling myself out of my post-graduate state of dysthymia---which interested users may consider as an alternative to ordering Cerebrolysin. While expensive, my regimen is designed to aggressively address all of the important variables of ageing: enzymatic dysfunction, inflammation, enhanced monoamine reuptake, neuronal death, mitochondrial dysfunction, altered gene expression, etc.

Drugs
Vyvanse--30 mg---Debatably safe, tolerable, effective, and for me, inseparable.
Strattera--80 mg---At higher doses, it increases the cortical volume of acetylcholine, reduces the volume of glutamate, and increases frontocortical catechloamine volume.
Mirtazapine--30 mg--One of the few antidepressants that has been noted for its distinctive memory enhancing properties, which becomes more appreciable at higher doses.
Luvox 150 mg--An underrated antidepressant that is free of stupefying effects when administered at low doses, and is especially effective for controlling obsessive-compulsive behavior. I was previously a long term user of Zoloft, but I prefer the serenity that Luvox provides---which is considerably less activating.
Minocycline--100 mg---Used for neuroprotective purposes---it mechanistically inhibits 5-lox, and appears to reduce the volume of glutamate---in addition to other virtues. Due to potential complications, though, it's best administered at low doses.
Cycloserine--250 mg---Used for its anxiolytic properties, but the drug has multiple applications, and has gained considerable appeal as a novel cognitive enhancer.
Hydergine---20 mg---Since I've become somewhat dubious about the strength of its causal relationship with the onset of fibrosis, and because a long-term, high dose study conducted by Cucinotta, et al. seems to lend credence to past claims about its safety and enhanced efficaciousness at higher doses, I consequentially started a high dose trial. Although it would be premature to report its effects, I believe the drug has some potential as a mood stabilizer, or an anxiolytic when administered at higher doses. Presently, I'm taking 20 mg a day in two divided doses, but I may titrate to 40 mg/day---in accordance with the long term study that I cited.
Nystatin--500,000 units---Used to reduce the likely fungal proliferation that occurs with long term antibiotic use.
Ondansetron: Still in transit.

Drugs that I've used in the past, which might have some appeal to users:
Low Dose Amisulpride: This drug loses its effectiveness relatively quickly---probably due to a change in affinity.
Low Dose Naltrexone: At the risk of incurring the wrath of its indefatigable advocates, I believe that its utility is greatly exaggerated, and seems effective only as a mood enhancer and possible analgesic. I found its effects to be somewhat noticeable, but not enough to justify continued use, and until more evidence emerges, I have no intention of resuming use. Minocycline is a much more palatable alternative, and is supported by far more convincing empirical evidence. However, there is some evidence that naltrexone may have cognitive enhancing properties at higher doses.
Buspirone: I tried this for a week, but in all honesty, I didn't have the patience to wait for its effects to become appreciable---which in any case, seems to be rather mild. For better results, users should stick with SSRIs, which have the advantage of not having an antagonistic affinity for D2 receptors---a mechanism that may lead to problems for some users at higher doses.

Supplements
1. Cerebral Health's Memeron: 2 capsules per day: Probably the best memory enhancer in the supplemental marketplace, and far superior to the garbage product that Life Enhancement produces.
2. AOR's Orthocore: 6 capsules per day: Deserving of its reputation as the best multivitamin on the market, and when taken religiously, a subjective improvement can definitely be felt. Although I would prefer a greater quantity of flavonoids in the formula, I think this product exceeds most in addressing the health needs of the average individual, and should therefore be an indispensable component of any regimen.
3. Cerebral Health's Synaptine Excel: 2 capsules per day, but not every day: Although it's debatable, I think Oxiracetam is probably the best overall -racetam in terms of half-life, potency, subjective enhancement, and effectiveness with healthy individuals.
4. Life Extension's Mitochondrial Energy Optimizer: 4 capsules per day: Covers most of the basics of enhancing mitochondrial function, but is not without its deficits: Coenzyme Q-10, and because of its inclusion of luteolin and carnosine, it's marginally better than AOR's Mito-Charger.
5. Nordic Natural's Ultimate Omega: 6 capsules per day: I haven't decided on the relative superiority of EPA or DHA, since there is evidence supporting both of their supplemental use. If forced to choose, I would opt for EPA, but until the controversy becomes satisfactorily decided, I'll stick with a balanced formula that favors EPA. Once it's picked up by vendors, I think AOR's Omega 3 Vegan is worth a trial, though.
6. AOR's Methylcobalamin Ultra: 2 lozenges per day: An underappreciated neuroprotector that can be safely administered in doses larger than what is suggested in the dosage guideline---even the 30 mg that I take daily.
7. Revgenetic's NitroMx: 2 capsules daily: Sure, resveratrol has been oversold, but it still remains an effective broad spectrum supplement that is worth including in any regimen.
8. AOR's Curecumin: 2 capsules daily: Another panacea supplement, and it appears that AOR has solved the bioavailability problem that renders many Curcumin supplements next to useless.
9. AOR's EGCG Max: 3 capsules daily: The evidence supporting the use of green tea is quite compelling, and since I dislike caffeine, I decided to include this supplement.
10. Revgenetic's Master Cleanse P-16: 1 capsule daily for a week, and resumed a week later: I'm a bit intrigued by the mechanism of this supplement, which may be a powerful enhancer of cellular health---among other interesting attributes.
11. AOR's Benagene: 1 capsule daily: Although I was initially skeptical, there is increasing evidence that validates some of the mechanistic claims of the inventor and manufacturers, which I believe warrants the price.
12. Bluebonnet's Super Quercetin: 8 capsules daily: Used primarily for its utility in the degradation of histamine, but the constituents of this formula possess multiple properties that don't require reiteration.
13. Nicoderm Patch: Although many use the patch for enhancing focus, I find the use of a single patch to be highly motivating, and quite useful as a learning aid and for supplementing my neuroprotectective firewall.
14. Life Extension's Timed Release Melatonin: 1 capsule: An effective sleep aid when administered at 3 mg, which I believe to be the most effective dose.
15. AOR's Ortho Mind: 3-6 capsules when needed: This formula includes ingredients that broadly covers the needs for optimal neurological health, and is far superior to the formulas of competitors that either choose the wrong ingredients or fail to provide sufficient quantities in each serving.
16. Healthy Origin's Ubiquinol: 1 capsule daily: In healthy individuals, the use of Coenyme Q10 is highly debatable, but using its reduced form should be less problematic, and the degree of the markdown on this product made it irresistible.
17. Revgenetic's Astral Fruit C: 2 capsules daily for a one week on and one week off cycle: Even if you're not completely convinced by the rationale for the product, Revgenetics offers a highly concentrated form of astragalus, which has a great deal of use for producing a healthy immune response.
18. My morning concoction, which contains kefir, thawed goji berries, goat's milk whey, brown rice protein powder, cinnamon, ginger, and cocoa powder. Of course, this shouldn't be classified as a supplement, but I thought it was worthy of inclusion.

Diet, Exercise, and Lifestyle
Although many enjoy the narcotic quality of exercise, I think an alternating brisk walk/ light jog in the park for an hour each day is more than sufficient---unless, of course, you need to reduce your weight, improve insulin sensitivity, etc.. This is supplemented by a few days of light anaerobic exercise, with an added emphasis on light. As for my diet, there is some caloric restriction---but not to an extreme degree. More importantly, its rich in flavonoid dense foods, seafood, nuts, spices, and seeds, but in addition, small quantities of meat and grains are consumed. Although I have my occasional reclusive periods, I force myself to remain socially active, and exposed to diverse environments of stimuli. This can be highly elevating, even if it's sometimes accompanied by moments of agony---boring dates, facile people, etc. Although I have no philosophical objection, I've never used illicit narcotics, but my alcohol consumption probably fits the operational definition of moderate----mostly including wine and cognac. To shield my body from stress, I rely heavily on Mozart, meditative exercises, and the occasional therapeutic massage. Even though my current stress level is not problematic, I'm also considering investing in a cranial electric therapy device, but I've found the supporting evidence to be underwhelming.

Anyway, I apologize for my narcissistic deviation from the topic, but once I started typing, I decided to finish what I originally intended to compose.

Edited by Rol82, 10 August 2010 - 03:33 PM.

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#2 aLurker

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Posted 10 August 2010 - 02:01 AM

Very interesting. Please consider reposting your regimen in the regimen forum so that I and others may comment on it. I'll just PM you later otherwise. I'm intrigued by a few things about your regimen and I don't want to derail the thread any further than I've already done.

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#3 stillwater

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Posted 10 August 2010 - 03:57 AM

Incredible. I picture several users wetting their pants upon viewing your stated regimen. I'm amazed there's no conflicts, negative interactions or side effects with that kind of volume. With my constitution I'd probably be a yellow, frothing at the mouth raging insomniac with facial tics sampling only a quarter of that.

Thank you for posting and sharing, it's given me some new ideas, I look forward to your analysis of Cerebrolysin if you decide to move forward with it.

#4 Animal

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Posted 17 August 2010 - 03:28 PM

Incredible. I picture several users wetting their pants upon viewing your stated regimen. I'm amazed there's no conflicts, negative interactions or side effects with that kind of volume. With my constitution I'd probably be a yellow, frothing at the mouth raging insomniac with facial tics sampling only a quarter of that.

Thank you for posting and sharing, it's given me some new ideas, I look forward to your analysis of Cerebrolysin if you decide to move forward with it.


There probably are many conflicts and side effects. But he's not really going to feel them when he's phetted up on Vyvanse potentiated by the NERI effects of Strattera (which in itself produces effects indistinguishable from low doses of cocaine or methamphetamine). Take those two out and I bet he would feel like shit. But that's going to happen anyway since insensitivity develops to both medications over time so they can't be taken indefinitely. Combined with multiple antidepressants and anxiolytic psychoactives I doubt there is much of his original personality left. Obviously he is just trying to medicate away some perceived inadequacy or psychological deficit. A bit sad, but meh, if he's happy for the moment then so be it.
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#5 Rational Madman

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Posted 18 August 2010 - 05:23 AM

Incredible. I picture several users wetting their pants upon viewing your stated regimen. I'm amazed there's no conflicts, negative interactions or side effects with that kind of volume. With my constitution I'd probably be a yellow, frothing at the mouth raging insomniac with facial tics sampling only a quarter of that.

Thank you for posting and sharing, it's given me some new ideas, I look forward to your analysis of Cerebrolysin if you decide to move forward with it.


There probably are many conflicts and side effects. But he's not really going to feel them when he's phetted up on Vyvanse potentiated by the NERI effects of Strattera (which in itself produces effects indistinguishable from low doses of cocaine or methamphetamine). Take those two out and I bet he would feel like shit. But that's going to happen anyway since insensitivity develops to both medications over time so they can't be taken indefinitely. Combined with multiple antidepressants and anxiolytic psychoactives I doubt there is much of his original personality left. Obviously he is just trying to medicate away some perceived inadequacy or psychological deficit. A bit sad, but meh, if he's happy for the moment then so be it.


Given your evident bias against supplementation in excess of the norm, your wariness of a polypharmaceutical approach, and the polarity of your unpredictable temperament, it may be futile to begin an intractable argument. However, I believe your claim about the perils of the co-administration Vyvanse and Strattera to be without merit since it's not corroborated by the literature, and even if it were, there would undoubtedly be a systemic re-evaluation of the prescription of this combination (given the frequency of this combination's application), which would have ultimately lead to action by regulatory bodies, or a sudden end to clinical use. Furthermore, there is no reported or plausible conflict with the inclusion of the two antidepressants that I listed---especially at the dosage specified. I should also note that my other dalliances with Naltrexone, Buspirone, and Amisulpride were not attempted in addition to the constituents of my cocktail, but I suppose that matters little. However, through the additional use of Minocycline, Cycloserine, Hydergine, and possible intermittent use of Ondansetron, I'm admittedly entering uncharted territory---since this combination is without precedent in the literature. With the inclusion of each, there is an increase in the chance of side effects, and because of this, I am careful to monitor markers of health through regular blood testing (either ordered by a physician or secured through an online acquired requisition form), examination, and through a diligent health diary. Beyond the use of prescribed medications, the quantity of my supplement intake is by my own admission unorthodox, but save for the exception of B-12, most of my choices are not terribly at odds with empirical findings for dosage and co-administration, and relative to the pharmacological profiles and effects of medications that were aforementioned, pose considerably less of a risk for health complications---even if consumed in the quantity specified. Although my previous post selfishly deviated from the present topic, it was simply meant to demonstrate my potential interest in adding Cerebrolysin to my already complicated cocktail, but as you have pointed out---and has long been apparent---there are potential hazards and is little need. While it shouldn't have to be stated, the protocol that I've outlined is tailored for myself, and should not be attempted in whole---or in part---without substantial reflection and research.

Finally, while a relentless desire for self-improvement (and to take great risks towards that end), life extension, and attenuating/guarding against symptoms of dysthymia can understandably be mistaken as a manifestation of insecurity or some other disturbance, I can assure you that it's not the case in this instance. Since virtual barriers prevent a validation of my claim, my word will have to suffice. However, because I'm not a porcelain doll that's liable to shatter when mishandled, feel free to ponder about my current psychological state, but others may take offense at your demonstrated interest in taking provocative positions. Anyway, since my postings are not germane to the present discussion, I ask that future inquiries and comments be communicated via private message---unless, of course, I decide in the likely event to begin a separate thread.

Edited by Rol82, 18 August 2010 - 05:29 AM.

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#6 Animal

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Posted 18 August 2010 - 11:02 AM

So how would you assess your well-being Rol82? You are obviously not satisfied with your current state of being if you feel the need to add Cerebrolysin or any of the other psychoactives you mentioned. I think you are the kind of person who will never be satisfied, being content is not a sign of weakness or defeatist acceptance.

Many individuals who take Cerebrolysin take it as the sole component of their regime. I don't see how you will be able to objectively evaluate it's effects in combination with all the other substances you are taking.

So you think I have an unpredictable temperament and a demonstrated interest in taking provocative positions? I appreciate the sentiment. :cool:

#7 aLurker

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Posted 18 August 2010 - 11:44 PM

First let me just say that I actually appreciate Animal's direct and honest comments even if some might read them as overly confrontational. I might be wrong but Animal strikes me as someone who at least tries to remain honest to himself and therefore calls out others when they might be deceiving themselves. I take what he says very seriously and what he has said to me has helped me remain honest to myself. When Animal says something I at least consider the possibility that I might be wrong and have simply rationalised an excuse to avoid the issue. The more intelligent you are the easier it is to come up with a reasonable excuse to justify bad habits. Questioning your sanity is the only way to remain sane.

With that said, back to the regimen! There are so many things I'm curious about and I haven't even had the time to look everything up yet since there is just sooo much of it. The only thing missing seems to be 50 000 mg of kitchen sink.

How did you create your stack? I'm guessing piece by piece although I find it hard to believe you would notice an effect from each added supplement.

Most people here, myself included, seem to supplement D3 and K2 separately but most people don't take a full dose of Orthocore. Is that why you don't supplement these separately or is there another reason?

What makes you think Rasagiline should have life extension effects in your regimen? Obviously it might conflict with your other meds and there have been no lifespan experiments with it. If it is because of the similarities with Selegiline I'd like to know more specifically. I think it has SOD effects not unlike Selegiline but I couldn't find anything about CAE. The mechanisms behind Selegiline's life extending effects are somewhat unclear so whether Rasagiline would have similar or better effects is up in the air IMHO. Even if it has life extending effects they are probably dose dependant and might interact with the other supplements.

Minocycline is another interesting aspect of your regimen. Never heard of this before so thank you for introducing me. I can see why you're taking it: the neuroprotective and anti-inflammatory effects look really tempting. Aren't you worried about breeding drug resistant bacteria though? From what my doctor says you shouldn't take antibiotics unless you really need to since they might lose their effectiveness for when you really need them.

What are your thoughts about potential up- or down-regulation and tolerance which might occur because of chronic use of some of these medications? Disregarding the monumental cost of the regimen do you think it is feasible long-term?

Lastly, and perhaps most importantly:
This comes to mind. Since you mention life extension as one of your goals; aren't you worried that the potential interactions will have the opposite effect?

I know that's probably a lot of questions but I am, and surely many others are, genuinely curious about your regimen and the underlying research which unquestionably has gone into its creation. Thanks for sharing it with us.

Edited by aLurker, 18 August 2010 - 11:50 PM.

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#8 Rational Madman

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Posted 24 August 2010 - 06:52 PM

First let me just say that I actually appreciate Animal's direct and honest comments even if some might read them as overly confrontational. I might be wrong but Animal strikes me as someone who at least tries to remain honest to himself and therefore calls out others when they might be deceiving themselves. I take what he says very seriously and what he has said to me has helped me remain honest to myself. When Animal says something I at least consider the possibility that I might be wrong and have simply rationalised an excuse to avoid the issue. The more intelligent you are the easier it is to come up with a reasonable excuse to justify bad habits. Questioning your sanity is the only way to remain sane.

With that said, back to the regimen! There are so many things I'm curious about and I haven't even had the time to look everything up yet since there is just sooo much of it. The only thing missing seems to be 50 000 mg of kitchen sink.

How did you create your stack? I'm guessing piece by piece although I find it hard to believe you would notice an effect from each added supplement.

Most people here, myself included, seem to supplement D3 and K2 separately but most people don't take a full dose of Orthocore. Is that why you don't supplement these separately or is there another reason?

What makes you think Rasagiline should have life extension effects in your regimen? Obviously it might conflict with your other meds and there have been no lifespan experiments with it. If it is because of the similarities with Selegiline I'd like to know more specifically. I think it has SOD effects not unlike Selegiline but I couldn't find anything about CAE. The mechanisms behind Selegiline's life extending effects are somewhat unclear so whether Rasagiline would have similar or better effects is up in the air IMHO. Even if it has life extending effects they are probably dose dependant and might interact with the other supplements.

Minocycline is another interesting aspect of your regimen. Never heard of this before so thank you for introducing me. I can see why you're taking it: the neuroprotective and anti-inflammatory effects look really tempting. Aren't you worried about breeding drug resistant bacteria though? From what my doctor says you shouldn't take antibiotics unless you really need to since they might lose their effectiveness for when you really need them.

What are your thoughts about potential up- or down-regulation and tolerance which might occur because of chronic use of some of these medications? Disregarding the monumental cost of the regimen do you think it is feasible long-term?

Lastly, and perhaps most importantly:
This comes to mind. Since you mention life extension as one of your goals; aren't you worried that the potential interactions will have the opposite effect?

I know that's probably a lot of questions but I am, and surely many others are, genuinely curious about your regimen and the underlying research which unquestionably has gone into its creation. Thanks for sharing it with us.


Well, I should say again that I'm not particularly bothered by Animal's commentary, but I do believe that his criticism is part of an odd pattern.

My regimen certainly wasn't created overnight, but began with a core of supplements that I gradually expanded upon so that the effects could be better quantified. Indeed, it would be foolish to begin with a regimen of 15 supplements. My exclusion of K2 and D3 shouldn't be mistaken for a lack of confidence in either supplement, since the amount of supporting evidence is impressive, but more of a judgment of personal need----since none of my blood tests suggest a need for their addition. However, I've been seriously considering making some adjustments, and if I ultimately decide to include either, I'll probably add AOR's Peak K2 and/or AOR's Vitamin D Liquid.

Based on its mechanism, the life extending properties of Rasagiline is based entirely on theory----so there has yet to be any evidence to substantiate that notion. But, should there really be any doubt? I know of a professor that I met at a social occasion that spoke of using Selegiline in research, and probably would know a bit more on the dosage guideline and potential of Rasagiline. Based on data about the change in its MAO-B selectivity, I suspect that 2 mg of Rasagiline is the equivalent of about 10 mg of Selegiline, so it's definitely not for everyone, and I doubt if if I'll actually order it. But, it depends on what the aforementioned professor says---who knows full well that many of his former students have experimented with the prescription drugs and nootropics.

As for Minocycline, there are indeed some potential dangers associated with usage, and I'm working on devising a strategy for minimizing the chance for potential side effects, but since I've been using the drug at a low dosage for nearly four months without incident, and because of data on its usage, the chance of hypothetical side effects aren't keeping me up at night.

Although amphetamine tolerance is often a problem with users, I believe that Minocycline and possibly Strattera--at least in theory---should help in that regard. If not, there are other adjuncts to consider. The only other risk is Strattera tolerance, and I'm still considering some options to mitigate that possibility, but it would seem to bit premature.

To answer your last question, and many of your previous questions, yes, there are many inherent risks with my current endeavor, but I've found no reason to alter my present course. Such risks are inexorable from any serious attempt to maximize life/well being.

Edited by Rol82, 24 August 2010 - 06:59 PM.


#9 aLurker

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Posted 24 August 2010 - 08:03 PM

Thank you for replying. Your firm grasp of the English language aside I still feel the concerns from my previous post are valid though.

Regarding Rasagiline, actually I insist there SHOULD be doubt since there is absolutely no research done yet regarding life extension and rough interpolations from Selegiline or appeals to authority doesn't change that. And as I said, dosage is unclear at best and it would interact with the rest of your stack. With a stack like that you probably have enough interactions as it is, whether you know it or not. If you get any noticeable side effect the troubleshooting might be hard. At least consider the possibility that maybe you can't see the forest because of all the supplements.

Mentioning nearly four months of Minocycline usage without problems doesn't really strike me as long-term thinking. It isn't that long at all, especially if you plan on keep this stack up indefinitely. Let us know how things work out or if you decide to make any changes.

I'm glad the stack is treating you good right now and I hope it continues to work well for you.

#10 Rational Madman

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Posted 24 August 2010 - 11:28 PM

Thank you for replying. Your firm grasp of the English language aside I still feel the concerns from my previous post are valid though.

Regarding Rasagiline, actually I insist there SHOULD be doubt since there is absolutely no research done yet regarding life extension and rough interpolations from Selegiline or appeals to authority doesn't change that. And as I said, dosage is unclear at best and it would interact with the rest of your stack. With a stack like that you probably have enough interactions as it is, whether you know it or not. If you get any noticeable side effect the troubleshooting might be hard. At least consider the possibility that maybe you can't see the forest because of all the supplements.

Mentioning nearly four months of Minocycline usage without problems doesn't really strike me as long-term thinking. It isn't that long at all, especially if you plan on keep this stack up indefinitely. Let us know how things work out or if you decide to make any changes.

I'm glad the stack is treating you good right now and I hope it continues to work well for you.


If you remember, the dosage I was contemplating for Rasagiline was .125 mg/day, which shouldn't create an interaction problem if the appropriate adjustments are made, and would probably be in accordance with the dosage range that might be suggested for ostensible life extension purposes---if or when it's found to play such a role. But, like I said, I'm not seriously contemplating using Rasagiline anymore. As for Minocycline, I'm being rather cautious, and looking for ways to prevent the incidence of the more dreaded side effects. But based on the data for usage, I still have a great deal of time before I need to make some major decisions on the continuation or suspension of use.

Edited by Rol82, 25 August 2010 - 02:51 PM.


#11 medievil

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Posted 27 August 2010 - 11:41 PM

Although amphetamine tolerance is often a problem with users, I believe that Minocycline and possibly Strattera--at least in theory---should help in that regard. If not, there are other adjuncts to consider. The only other risk is Strattera tolerance, and I'm still considering some options to mitigate that possibility, but it would seem to bit premature.



Its been confirmed by numerous anecdotal reports that NMDA antagonist work against amphetamine tolerance, however there's a flaw in your regime, D-cycloserine is a NMDA agonist and has for example been shown to speed up tolerance to ethanol.

(PMID: 8545482) D-cycloserine enhances rapid tolerance to ethanol motor incoordination
The enhancement of ethanol tolerance by D-cycloserine and the antagonism of this effect by ketamine cannot be attributed to changes in pharmacokinetics of ethanol. Taken together, these results confirm the participation of the NMDA receptor system in the development of tolerance to ethanol, and reinforce earlier findings about the involvement of learning in tolerance.

Consedering NMDA antagonism has been found succesfull by many for amphetamine tolerance, it wont be suprising if this one ends up accelerating tolerance to your amphetamine.

#12 aLurker

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Posted 29 August 2010 - 12:30 AM

Cerebral Health's Memeron: 2 capsules per day: Probably the best memory enhancer in the supplemental marketplace, and far superior to the garbage product that Life Enhancement produces.


Thanks for the heads up, I've been looking into Galantamine recently. What aspects make Cerebral Health's Galantamine product Memeron that great and superior to Galantamind? Is it possible to divide the dose into two by cutting the pill or dissolving it in liquid?

#13 arvcondor

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Posted 09 September 2010 - 12:51 AM

Incredible. I picture several users wetting their pants upon viewing your stated regimen. I'm amazed there's no conflicts, negative interactions or side effects with that kind of volume. With my constitution I'd probably be a yellow, frothing at the mouth raging insomniac with facial tics sampling only a quarter of that.

Thank you for posting and sharing, it's given me some new ideas, I look forward to your analysis of Cerebrolysin if you decide to move forward with it.



I was about to ask about your post, but your last line just confirmed it: This is exactly what you wrote in the Cerebrolysin thread.

#14 medievil

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Posted 09 September 2010 - 08:13 PM

Incredible. I picture several users wetting their pants upon viewing your stated regimen. I'm amazed there's no conflicts, negative interactions or side effects with that kind of volume. With my constitution I'd probably be a yellow, frothing at the mouth raging insomniac with facial tics sampling only a quarter of that.

Thank you for posting and sharing, it's given me some new ideas, I look forward to your analysis of Cerebrolysin if you decide to move forward with it.



I was about to ask about your post, but your last line just confirmed it: This is exactly what you wrote in the Cerebrolysin thread.

This thread was taken out of the cere thread to make a new topic.

#15 Rational Madman

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Posted 11 September 2010 - 06:17 AM

Although amphetamine tolerance is often a problem with users, I believe that Minocycline and possibly Strattera--at least in theory---should help in that regard. If not, there are other adjuncts to consider. The only other risk is Strattera tolerance, and I'm still considering some options to mitigate that possibility, but it would seem to bit premature.



Its been confirmed by numerous anecdotal reports that NMDA antagonist work against amphetamine tolerance, however there's a flaw in your regime, D-cycloserine is a NMDA agonist and has for example been shown to speed up tolerance to ethanol.

(PMID: 8545482) D-cycloserine enhances rapid tolerance to ethanol motor incoordination
The enhancement of ethanol tolerance by D-cycloserine and the antagonism of this effect by ketamine cannot be attributed to changes in pharmacokinetics of ethanol. Taken together, these results confirm the participation of the NMDA receptor system in the development of tolerance to ethanol, and reinforce earlier findings about the involvement of learning in tolerance.

Consedering NMDA antagonism has been found succesfull by many for amphetamine tolerance, it wont be suprising if this one ends up accelerating tolerance to your amphetamine.


Yes, but the anxiolytic and multifarious cognitive enhancing associated with enhanced NMDA receptor activity, or in my case, modulation, greatly exceed concerns with tolerance---which is influenced by several other variables besides a amphetamine mediated altereration in NMDA receptor expression. There are some real concerns with even selective antagonism of NMDA receptors, since subjectively speaking, I believe there to be a dysregulation between NMDA, AMPA, and KA receptor expression---which can be corrected through the use of a co-agonist at the NMDA site. Indeed, I think I've arrived at the conclusion that the NMDA receptor antagonism is a poor pharmacological target for almost every condition save ALS and Huntington's, and that very low doses of agents like valproic acid may be better suited for addressing the ubiquitous problem of glutamate receptor hyperactivity in certain parts of the brain---which in my case, I speculate to be in the prefrontal cortex. As for my regimen, some interesting changes have been made, and a summary of will be forthcoming when I can secure the time. For now, tomorrow's responsibilities will force me to chemically induce a deep sleep.

Edited by Rol82, 11 September 2010 - 03:02 PM.


#16 Rational Madman

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Posted 11 September 2010 - 06:30 AM

Cerebral Health's Memeron: 2 capsules per day: Probably the best memory enhancer in the supplemental marketplace, and far superior to the garbage product that Life Enhancement produces.


Thanks for the heads up, I've been looking into Galantamine recently. What aspects make Cerebral Health's Galantamine product Memeron that great and superior to Galantamind? Is it possible to divide the dose into two by cutting the pill or dissolving it in liquid?


My opinion on this matter is driven largely by personal experience, and not comparative assays or inquiries about sourcing and manufacturing standards. Life Enhancement products are poorly formulated, terribly over priced, and in isolated cases, have failed to deliver products that live up to their descriptions. For instance, they once sold a formulation that contained Huperzine A as an active ingredient, but was shockingly discovered in an assay to contain an amount of Huperzine A that was significantly less than advertised! Take a close look at their products, doses, prices, and results reported by users. Your findings will likely extinguish any interest that you might have. Instead, try Cerebral Health or Relentless Improvement, which I've had good luck with.

Edited by Rol82, 11 September 2010 - 06:41 AM.


#17 medievil

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Posted 11 September 2010 - 01:00 PM

Although amphetamine tolerance is often a problem with users, I believe that Minocycline and possibly Strattera--at least in theory---should help in that regard. If not, there are other adjuncts to consider. The only other risk is Strattera tolerance, and I'm still considering some options to mitigate that possibility, but it would seem to bit premature.



Its been confirmed by numerous anecdotal reports that NMDA antagonist work against amphetamine tolerance, however there's a flaw in your regime, D-cycloserine is a NMDA agonist and has for example been shown to speed up tolerance to ethanol.

(PMID: 8545482) D-cycloserine enhances rapid tolerance to ethanol motor incoordination
The enhancement of ethanol tolerance by D-cycloserine and the antagonism of this effect by ketamine cannot be attributed to changes in pharmacokinetics of ethanol. Taken together, these results confirm the participation of the NMDA receptor system in the development of tolerance to ethanol, and reinforce earlier findings about the involvement of learning in tolerance.

Consedering NMDA antagonism has been found succesfull by many for amphetamine tolerance, it wont be suprising if this one ends up accelerating tolerance to your amphetamine.


Yes, but the anxiolytic and multifarious cognitive enhancing associated with enhanced NMDA receptor activity, or in my case, modulation, greatly exceed concerns with tolerance---which is influenced by several other variables besides a amphetamine mediated altereration in NMDA receptor expression. There are some real concerns with even selective antagonism of NMDA receptors, since subjectively speaking, I believe there to be a dysregulation between NMDA, AMPA, and KA receptor expression---which can be corrected through the use of a co-agonist at this NMDA site. Indeed, I think I've arrived at the conclusion that the NMDA receptor is a poor pharmacological target for almost every condition save ALS and Huntington's, and that very low doses of agents like valproic acid may be better suited for addressing the ubiquitous problem of glutamate receptor hyperactivity in certain parts of the brain---which in my case, I speculate to be in the prefrontal cortex. As for my regimen, some interesting changes have been made, and a summary of will be forthcoming when I can secure the time. For now, tomorrow's responsibilities will force me to chemically induce a deep sleep.

Personally i beleive NMDA antagonism is the key for OCD and also potentially very interesting for social anxiety disorder as glutamate has been implicated in both conditions. Personally my memantine works very well for my OCD wich can be said is very severe, besides that i take several meds that could have rapid tolerance problems such as AMT and amp, on mind and muscle ive explained my reasening behind AMT.

Anyway guys, i beleive in serotonine releasers as the future antidepressants, 2 study's by nichols et al showed that they are superior to sertraline (1) and have a more rapid effect then standard antidepresants (2). SSRI's work by elevating serotonine however the serotonine autoreceptors lower serotonine again untill they downregulate and serotonine is elevated high enough for the patient to notice a antidepressant effect, however many patients are treatment resistant, activity of the 5HT1A autoreceptors has been associated with that atleast according to a study in mice (3).
Serotonine releasers effectively bypass the autoreceptors by forcing serotonine release resulting in a more robust response.

Some selective serotonine releasers are available as research chemicals however they dont have any research behind them in humans and could carry risk, an exception of this is AMT or alpha methyl tryptamine, it has been in clinical use for 20 years in the sovjet union, besides serotonine release its also a dopamine releaser wich further potentiates the antidepressant effects.

It is true that combined serotonine and dopamine release leads to neurotoxiticy, as seen with MDMA, however with MDMA there are 3 major factors contributing, first oxidative stress caused by massive monoamine release, AMT in low daily doses doesnt cause a massive elevation and oxidative stress will be minimal, hyperthermia if hyperthermia is abolished MDMA's neurotoxiticy is gone too, AMT in low doses doesnt cause any hyperthermia and last the toxic metabolites, wheter AMT has those is unclear (or i'm just not aware of that).

In conclusion i beleive that switching to a SSRI would decrease all benefits ive got up till now, and i beleive that the best strategy would be augmenting AMT.
AMT also lacks the impotence and other side effects seen with SSRI's, and it by itself fixes me up a great deal, so its definatly going to be a keeper.


1. The Effect of Selective Serotonin Releasing Agents in the Chronic Mild Stress Model of Depression in Rats.". Stress. PMID 9787258.
2. Effects of 5-HT-releasing agents on the extracellullar hippocampal 5-HT of rats. Implications for the development of novel antidepressants with a short onset of action. Unfortunately as a research chemical it's legality is subject to change. PMID 10428424.
3. RGS inhibition at Gαi2 selectively potentiates 5-HT1A–mediated antidepressant effects PNAS 107/24/11086


I also take nicotine wich normally causes a rapid tolerance in me and so far memantine seems to be working excellent for that, but thats only up till now (short term).

Also since there's allready a drastic change in my behavor but i still have the "i want to get out feeling" in social situations i'm planning to add in AMP soon to fully resolve that.

Those are several things i beleive memantine shows incredible potential regarding tolerance, and so far my experience with it has been very good.

I agree that its possible that amp induced tolerance is mediated by other factors besides just nmda activation by its glutamate efflux, however NMDA antagonists upregulate several dopamine receptors and as confirmed by several anecdotal reports its possible just by its nmda antagonism to overpower the other mechanism involved in tolerance and keep tolerance prevented.

My biggest issue's are social anxiety, ocd and ADD, anhedonia too, but the social aspect of those stimulants i take is something that tends to build up tolerance fast too, making memantine a essential component in my regime.

Perhaps i should make my own thread about my regime and the rationals behind it, srry for the brief manifesto in your topic :laugh: .

#18 Rational Madman

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Posted 13 September 2010 - 07:07 AM

Although amphetamine tolerance is often a problem with users, I believe that Minocycline and possibly Strattera--at least in theory---should help in that regard. If not, there are other adjuncts to consider. The only other risk is Strattera tolerance, and I'm still considering some options to mitigate that possibility, but it would seem to bit premature.



Its been confirmed by numerous anecdotal reports that NMDA antagonist work against amphetamine tolerance, however there's a flaw in your regime, D-cycloserine is a NMDA agonist and has for example been shown to speed up tolerance to ethanol.

(PMID: 8545482) D-cycloserine enhances rapid tolerance to ethanol motor incoordination
The enhancement of ethanol tolerance by D-cycloserine and the antagonism of this effect by ketamine cannot be attributed to changes in pharmacokinetics of ethanol. Taken together, these results confirm the participation of the NMDA receptor system in the development of tolerance to ethanol, and reinforce earlier findings about the involvement of learning in tolerance.

Consedering NMDA antagonism has been found succesfull by many for amphetamine tolerance, it wont be suprising if this one ends up accelerating tolerance to your amphetamine.


Yes, but the anxiolytic and multifarious cognitive enhancing associated with enhanced NMDA receptor activity, or in my case, modulation, greatly exceed concerns with tolerance---which is influenced by several other variables besides a amphetamine mediated altereration in NMDA receptor expression. There are some real concerns with even selective antagonism of NMDA receptors, since subjectively speaking, I believe there to be a dysregulation between NMDA, AMPA, and KA receptor expression---which can be corrected through the use of a co-agonist at this NMDA site. Indeed, I think I've arrived at the conclusion that the NMDA receptor is a poor pharmacological target for almost every condition save ALS and Huntington's, and that very low doses of agents like valproic acid may be better suited for addressing the ubiquitous problem of glutamate receptor hyperactivity in certain parts of the brain---which in my case, I speculate to be in the prefrontal cortex. As for my regimen, some interesting changes have been made, and a summary of will be forthcoming when I can secure the time. For now, tomorrow's responsibilities will force me to chemically induce a deep sleep.

Personally i beleive NMDA antagonism is the key for OCD and also potentially very interesting for social anxiety disorder as glutamate has been implicated in both conditions. Personally my memantine works very well for my OCD wich can be said is very severe, besides that i take several meds that could have rapid tolerance problems such as AMT and amp, on mind and muscle ive explained my reasening behind AMT.

Anyway guys, i beleive in serotonine releasers as the future antidepressants, 2 study's by nichols et al showed that they are superior to sertraline (1) and have a more rapid effect then standard antidepresants (2). SSRI's work by elevating serotonine however the serotonine autoreceptors lower serotonine again untill they downregulate and serotonine is elevated high enough for the patient to notice a antidepressant effect, however many patients are treatment resistant, activity of the 5HT1A autoreceptors has been associated with that atleast according to a study in mice (3).
Serotonine releasers effectively bypass the autoreceptors by forcing serotonine release resulting in a more robust response.

Some selective serotonine releasers are available as research chemicals however they dont have any research behind them in humans and could carry risk, an exception of this is AMT or alpha methyl tryptamine, it has been in clinical use for 20 years in the sovjet union, besides serotonine release its also a dopamine releaser wich further potentiates the antidepressant effects.

It is true that combined serotonine and dopamine release leads to neurotoxiticy, as seen with MDMA, however with MDMA there are 3 major factors contributing, first oxidative stress caused by massive monoamine release, AMT in low daily doses doesnt cause a massive elevation and oxidative stress will be minimal, hyperthermia if hyperthermia is abolished MDMA's neurotoxiticy is gone too, AMT in low doses doesnt cause any hyperthermia and last the toxic metabolites, wheter AMT has those is unclear (or i'm just not aware of that).

In conclusion i beleive that switching to a SSRI would decrease all benefits ive got up till now, and i beleive that the best strategy would be augmenting AMT.
AMT also lacks the impotence and other side effects seen with SSRI's, and it by itself fixes me up a great deal, so its definatly going to be a keeper.


1. The Effect of Selective Serotonin Releasing Agents in the Chronic Mild Stress Model of Depression in Rats.". Stress. PMID 9787258.
2. Effects of 5-HT-releasing agents on the extracellullar hippocampal 5-HT of rats. Implications for the development of novel antidepressants with a short onset of action. Unfortunately as a research chemical it's legality is subject to change. PMID 10428424.
3. RGS inhibition at Gαi2 selectively potentiates 5-HT1A–mediated antidepressant effects PNAS 107/24/11086


I also take nicotine wich normally causes a rapid tolerance in me and so far memantine seems to be working excellent for that, but thats only up till now (short term).

Also since there's allready a drastic change in my behavor but i still have the "i want to get out feeling" in social situations i'm planning to add in AMP soon to fully resolve that.

Those are several things i beleive memantine shows incredible potential regarding tolerance, and so far my experience with it has been very good.

I agree that its possible that amp induced tolerance is mediated by other factors besides just nmda activation by its glutamate efflux, however NMDA antagonists upregulate several dopamine receptors and as confirmed by several anecdotal reports its possible just by its nmda antagonism to overpower the other mechanism involved in tolerance and keep tolerance prevented.

My biggest issue's are social anxiety, ocd and ADD, anhedonia too, but the social aspect of those stimulants i take is something that tends to build up tolerance fast too, making memantine a essential component in my regime.

Perhaps i should make my own thread about my regime and the rationals behind it, srry for the brief manifesto in your topic :laugh: .


I'm not doubting that NMDA antagonism can provide symptomatic relief for a number of disorders, and your success with Memantine seems evident to everyone. However, Memantine would be contraindicated for subjects possessing schizoid traits----which in my case, are extremely subtle and unremarkable upon superficial examination, and thankfully, not pervasive enough to be debilitating----and has the highly undesirable effect of impairing the induction of memories----which has been observed repeatedly in studies. Since obsessive compulsive disorder, and several other disorders of a similar etiology do not manifest with NMDA dysfunction in every region of the brain, recipients of the drug will be sacrificing long term memory formation for neuroprotection, and symptomatic relief. Because of this effect, and my pathology, this drug is not for me, and certainly not for everyone. Rather than NMDA receptor blockade, I believe a better strategy would involve the promotion of the reelin protein, probably by utilizing an agent that selectively reduces the secretion of ACTH----but there aren't any perfect candidates, and the other known reelin promoters have drawbacks that render them unpalatable.

#19 kismet

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Posted 17 September 2010 - 05:57 PM

I strongly disapprove. You forgot the disclaimer but I will do it for you: Kids, don't try this at home!
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#20 Rational Madman

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Posted 18 September 2010 - 12:50 AM

I strongly disapprove. You forgot the disclaimer but I will do it for you: Kids, don't try this at home!


You're absolutely right, and from henceforth, discussion will be confined to agents that can be procured through normal channels. However, private inquiries about the additional constituents of my cocktail will be responded to in some circumstances provided that they not be posted or discussed in any imminst threads. I want to echo Kismet's comments, and urge users to not proceed carelessly with the use of prescription drugs.

Edited by Rol82, 18 September 2010 - 12:54 AM.


#21 Rational Madman

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Posted 20 September 2010 - 02:40 AM


Here's a list of targets, and remedies that I've been considering. Again, I want to be emphatic about not self-medicating, and encourage interested parties to do their utmost to convince their physicians to prescribe the treatments listed below. Although the list below would be in contravention with my previous posting, I think it would appropriate to discuss prescription drugs on the condition that a disclaimer is attached, and provided that self-medication is actively discouraged. As I've recently concluded, relying on supplements alone is likely to deliver suboptimal results, so I think we need to move beyond our supplement fixation, and become a bit bolder if we have a serious and earnest desire for radical life extension. But, to the considerable dismay of many, there has yet to be a panacea pill that substitutes for healthy eating, exercise, and lifestyle choices---which remain paramount, and possess the greatest empirical support. However, the best approach should incorporate all approaches: a sound diet, a healthy lifestyle, medication, and supplementation. So, please be adults, and don't try to carelessly emulate me. Furthermore, please spare me of the sort sanctimonious lectures that I've become all too familiar with, since I'm cognizant about the inherent risks, and moral/ethical dilemmas that I must contend with. Although I'm willing to engage critics, it's unlikely that the likely criticisms---that I've exhaustively considered myself---will resonate with me.


Reelin Promotion: Low dose Valproic Acid, Tianeptine, and or low dose Amisulpride.
Acetylcholinesterase Inhibition: Donepezil, but the ideal dosage remains shrouded.
Maintenance of Tyrosine Hydoxylase, Glial Cell Line Derived Neurotrophic Factor, and the promotion of SOD: Rasagiline, at doses of 1-4 mg/day.
Glutathione Promotion: Cabergoline, twice weekly.
Activation of Nuclear Receptors: Pioglitazone, or Acitretin.
mTOR and calciuneurin inhibition: Once or twice weekly use of Rapamycin.
Sirtuin 1 activation, and Phosphodiesterase 4 Inhibition: Luteolin, which I've concluded to be superior to Resveratrol.
Protein Biosynthesis Enhancer: Cerebrolysin, or Pioglitazone.
Neutralizing the Effects of Alcohol: Valdoxan, or something melatonergic.
Concentration: Amphetamine in conjunction with xanthines like green tea or freeze dried organic coffee (which is exceptionally rich in pyroglutamic acid).
Learning Enhancer: The racetams in conjunction with intramuscular choline alfoscerate, nicotine, Acitretin, or Pioglitazone.
Mitochondrial Energy: Rasagiline, Pioglitazone, Methylene Blue (pharmaceutical grade), or Dimebon, once the price inevitably falls.
Inflammation: Rapamycin, Pioglitazone, Acitretin, fish oil, flavonoids, Rasagiline, and xanthines.
Preventing the breakdown of Cyclic adenosine and cyclic guanosine monosphosphate: Perhaps Cialis, which has considerable appeal, and when used adjunctively with cranial electrotherapy, should induce oxytocin release without resulting in cognitive impairment. Anecdotally, I find Cialis to be an exceptionally pro-social drug.
Neuroplasticity: Tianeptine, Valdoxan, SSRIs, and one of the racetams.
Nicotinic receptors: Donepezil, Varenicline, Tropisetron, and nicotine (I haven't decided on the best delivery mechanism, but to my girlfriend's chagrin, my favorite has become pipe smoking).
Visual Processing: Probably Tolcapone or Entacapone.
Prepulse Inhibition and Prefrontal Efficiency: Either Tolcapone or Entacaopone, but most likely the latter because of serious safety concerns.
Executive Function: Agents that are dopaminergic and noradrenergic.
Reward: Running, at home acupuncture, or perhaps upregulation of opioid receptors with Naltrexone.
V2 receptor upregulation: Critical, but I have no ideas. Desmopressin or testosterone may work, but I'm dubious.
Telomerase Activation: Cycloastragenol, but there has to be something better out there.
Tumor Necrosis Factor Inhibition: Rapamycin.
Protein Kinase Expression: Copious amounts of phosolipids.
Promotion of Neurotrophic Factors: Valproic Acid and Rasagiline.
Mood Enhancement: Valdoxan, Tianeptine, SSRI, and light therapy.
Stress: Valdoxan, Tianeptine, meditation, sensory deprivation, massage, acupuncture, and cranial electrotherapy,
Environmental Richness: Exercise, socializing, and light and sound devices.
Diet: Flavonoid dense that closely resembles a Mediterranean or East Asian diet.
Sleep: Valdoxan, or single malt scotch whiskey (seriously, give it a try).
Reactive Oxygen Species: Luteolin, Pioglitazone, Acitretin, and Rasagiline.
Glucose Metabolism: Pioglitazone, and Acitretin.
Energy: Modafinil, and low dose hydrocortisone.
Blood Pressure: Guanfacine, and fish oil.
Vague, and Undefined Infections: Minocycline, and/or Valtrex.
Chelation: Valtrex (unsubstantiated pet theory of mine).
Liver: Intramuscular choline.
Stomach Ailments: Ondansetron, or Tropisetron.
Anxiety: Amisulpride, Tianeptine, amphetamines, SSRI, Cialis, Sceletium Tortuosum, and/ or alcohol.
Obsessiveness: Salvinorin A, Sigma 1 agonist, and/or intramuscular oxytocin.


On a separate note, my enthusiasm for Minocycline and Cycloreine has diminished because of the theoretical conflict between the inhibition of protein synthesis, and long term induction. Additionally, although my experience was positive, I am no longer endorsing the use of ergoloid mesylate, because its modulatory effects are not universally ideal, and because much about its mechanism and effects remain murky. The use of SSRIs has also become somewhat questionable, but some within this class like fluoxetine and the sigma agonists remain to be highly efficacious. In my case, though, I think the inhibition of monoamine degradation, and creating a ratio that favors catechloamines---especially in in frontal cortical regions---will be more fruit bearing. Anyway, here is an update on my current regimen:

1. AOR's Orthocore: 6 capsules Daily.
2. Cerebral Health's Synaptine Excel Powder: 1 teapsoon daily in two divided doses.
3. AOR's Methylcobalamin: 30 mg.
4. Lutimax's Luteolin: Experimenting with doses of 4 to 8 lozenges daily.
5. Nordic Natrual's Pro-Omega D Liquid: 2 teaspoons daily.
6. Rev Genetic's Master Gene P-16: One to two capsules daily in one week cycles.
7. Rev Genetic's Astral Fruit C: Three capsules daily in one week cycles.
8. DoMatcha Green Tea Powder: One teaspoon daily.
9. Mount Hagen's Organic Freeze Dried Instant Coffee: 1 tablespoon daily.
10. Sunfood Nutrition's Cocoa Powder: 1 to 3 tablespoons daily.
11. North American Herb and Spice Company's Oreganol P73: 16 to 32 drops daily.
12. Life Extension's Melatonin: 3 mg.
13. AOR's Peak K2: 15 mg.
14. Life Extension's Mitochondrial Energy Optimizer: 4 to 6 capsules daily.
15. Relentless Improvement's Idebenone: 300 mg.
16. Red Tea Roiboos' Sceletium Tortuosum: When needed.
17. Alcohol and Tobacco: Aged Laphroaig, Maison Louis Jadot Burgundy, and Ashton pipe tobacco.
18. Vyvanse: 30 mg.
19. Strattera: 80 mg.
20. Remeron: 30 mg.
21. Stablon: 37.5 mg/ three divided doses.
22. Solian: 100 mg.
23. Rasagiline: Slowly titrating to a target dose of between 1 and 2 mg.
24. Cabergoline: 0.25 mg/twice weekly.
25. Ondansetron: When needed.

En Route: Valproic Acid, Intramuscular Gliatilin, and Acitretin.

Actively considering after necessary adjustments are made: low doses of Donepezil or Razadyne, infrequent use of low dose Rapamycin, low dose of Pioglitazone, Valdoxan in place of melatonin, Varenicline, acupuncture that's either self administered/or professionally applied, testosterone, Cerebrolysin, and Ritalin or Modafinil in conjunction with a lower Vyvanse dosage.

As for lifestyle changes, I've begun taking cold showers daily to increase beta endorphin levels and synaptic noradrenaline. Historically, it appears that Thomas Jefferson and Theodore Roosevelt endorsed cold water therapy, but the scientific community remains tepidly interested.

I know, I've already entered Kurzweil territory, but where would we be without the extremists? And, since I'm at no risk of becoming destitute, the most important impediment is removed from my pathway.

Edited by Rol82, 22 September 2010 - 05:49 AM.


#22 John Barleycorn

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Posted 20 September 2010 - 04:26 AM

Perhaps Cialis, which has considerable appeal, and when used adjunctively with cranial electrotherapy, should induce oxytocin release without resulting in cognitive impairment. Anecdotally, I find Cialis to be an exceptionally pro-social drug.


LOL, just as I'm wading through the professorial exposition, you slip in that nugget to disarm me! Are we talking about oxytocin release as a consequence of the PDE-5 inhibition alone, or as a consequence of what it makes us go out and do? :-D

Obsessiveness: Salvinorin A, Sigma agonist, and/or intramuscular oxytocin.


It is indeed difficult to be too obsessive under the influence of salvinorin. Or are you referring to the aftereffects? :cool:

Edited by John Barleycorn, 20 September 2010 - 04:31 AM.


#23 Logan

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Posted 20 September 2010 - 04:38 AM

Are you going to do straight up valproic acid or sodium valproate?

Why no lithium?

Edited by morganator, 20 September 2010 - 04:38 AM.


#24 Rational Madman

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Posted 20 September 2010 - 06:11 AM

Perhaps Cialis, which has considerable appeal, and when used adjunctively with cranial electrotherapy, should induce oxytocin release without resulting in cognitive impairment. Anecdotally, I find Cialis to be an exceptionally pro-social drug.


LOL, just as I'm wading through the professorial exposition, you slip in that nugget to disarm me! Are we talking about oxytocin release as a consequence of the PDE-5 inhibition alone, or as a consequence of what it makes us go out and do? :-D

Obsessiveness: Salvinorin A, Sigma agonist, and/or intramuscular oxytocin.


It is indeed difficult to be too obsessive under the influence of salvinorin. Or are you referring to the aftereffects? :cool:


The oxytocin release is indeed influenced by the inhibition of phosphodiesterase 5, but is not sufficient in the absence cranial electrical stimulation. So, the combination of Cialis and a cranial electrotherapy device---like Alpha Stim, perhaps---should probably lead to a release of oxytocin in humans, but this has yet to be confirmed. An alternative, empirically confirmed method would be through the activation of 5ht1a receptors, but activating this target leads to reduced NMDA receptor activity, which is undesirable in most pathologies.

As for Salvinorin, by activating 5ht2a receptors, and consequentially reducing orbitofrontal cortex activity, it may be a promising therapy---in addition to the tryptamines---for some subsets of OCD sufferers. Acquiring it, though, is another thing.

Edited by Rol82, 20 September 2010 - 07:50 AM.


#25 Rational Madman

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Posted 20 September 2010 - 06:37 AM

Are you going to do straight up valproic acid or sodium valproate?

Why no lithium?


Lithium has unwanted effects on inositol metabolism, and reduces neurotrophic factors in certain parts of the brain---like the hippocampus. Further, it has yet to be agreed upon effects on the reelin glycoprotein---possible downregulation for one, which would be at odds with the impetus for use. Since I'm not using valproic acid for the treatment for manic depression, and since I'm starting at a base of 30 mg, its efficacy as a mood stabilizer at this dose is beside the point, since neuroprotection and reelin promotion is what I'm looking for. However, since I'm starting at a low base, and because the efficacy of low dose therapy remains uncertain, I'm a bit in the dark. and it will take some time to arrive at an effective dose.

Edited by Rol82, 20 September 2010 - 06:38 AM.


#26 Rational Madman

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Posted 20 September 2010 - 12:03 PM

Perhaps Cialis, which has considerable appeal, and when used adjunctively with cranial electrotherapy, should induce oxytocin release without resulting in cognitive impairment. Anecdotally, I find Cialis to be an exceptionally pro-social drug.


LOL, just as I'm wading through the professorial exposition, you slip in that nugget to disarm me! Are we talking about oxytocin release as a consequence of the PDE-5 inhibition alone, or as a consequence of what it makes us go out and do? :-D

Obsessiveness: Salvinorin A, Sigma agonist, and/or intramuscular oxytocin.


It is indeed difficult to be too obsessive under the influence of salvinorin. Or are you referring to the aftereffects? :cool:


The oxytocin release is indeed influenced by the inhibition of phosphodiesterase 5, but is not sufficient in the absence cranial electrical stimulation. So, the combination of Cialis and a cranial electrotherapy device---like Alpha Stim, perhaps---should probably lead to a release of oxytocin in humans, but this has yet to be confirmed. An alternative, empirically confirmed method would be through the activation of 5ht1a receptors, but activating this target leads to reduced NMDA receptor activity, which is undesirable in most pathologies.

As for Salvinorin, by activating 5ht2a receptors, and consequentially reducing orbitofrontal cortex activity, it may be a promising therapy---in addition to the tryptamines---for some subsets of OCD sufferers. Acquiring it, though, is another thing.


Actually, I was embarrassingly mistaking the mechanism of salvinorin A and psilocybin, because salvinorin A doesn't have much of an affinity for 5ht2a. Like I said later, its effect on kappa receptors is key. On a separate note, does anyone know if David Pearce is a member of Imminst? I personally love the guy, and would be thrilled if he decided to join our lovely community, and impart some of his sage wisdom. In fact, I think I'll start a correspondence. At the very least, I would like to hear a status update, and see if I can help with the maintenance of his websites, which are extremely valuable resources.

Edited by Rol82, 21 September 2010 - 09:18 PM.


#27 medievil

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Posted 20 September 2010 - 12:05 PM

What is your reasening behing increasing cAMP and cGMP? I think your best bet would be a non selective PDE inhibitor but i'm not sure what anti aging/neuroprotective benefits this would have, please enlighten me.

You have an extensive regime, personally i'm way to worried about overexpressing certain pathways causing negative effects of destroying the benefits of one particular supplement, i want to see rat study's first where they used an extensive regime of supplements targetting differend pathways (wich should theoretically have a synergetical effect).

#28 Rational Madman

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Posted 20 September 2010 - 12:52 PM

What is your reasening behing increasing cAMP and cGMP? I think your best bet would be a non selective PDE inhibitor but i'm not sure what anti aging/neuroprotective benefits this would have, please enlighten me.

You have an extensive regime, personally i'm way to worried about overexpressing certain pathways causing negative effects of destroying the benefits of one particular supplement, i want to see rat study's first where they used an extensive regime of supplements targetting differend pathways (wich should theoretically have a synergetical effect).


cAMP and cGMP are activators of protein kinase, which in turn activate CREB proteins critical for long term induction. Unchecked, both can interfere with frontal cortical functions, but activation of alpha adrenergic receptors should keep this problem at bay.

Also, I share your concerns, since they occupy my mind from time to time. With a burgeoning regimen of this size and complexity, it becomes increasingly difficult to control for potential interactions and unintended consequences---especially with no precedent as a guide. But, I at least want to make an attempt to satiate my interest in human enhancement/life extension, which has an understandable and captivating allure. In any case, if it becomes evident that my regimen becomes either unworkable, or is yielding progressively worse outcomes as a function of its growing size, then I'll reevaluate, of course, and adopt a more modest approach. What you're witnessing is a trial for the most part, and nothing that can't be altered if I'm confronted with new evidence, or should my personal feelings change.

Edited by Rol82, 20 September 2010 - 01:45 PM.


#29 medievil

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Posted 20 September 2010 - 01:00 PM

Personally i'm avoiding supplements that only target aging at this moment, as i'm still young and i beleive that in the near future we will have more research available, currently my focus goes to avoiding deseases (such as cancer) and supplements that increase my chances of survival in ischemic stroke for example.

At this time i'm sticking to my curcumin and resveratrol combo (wich i beleive look the most promosing for my goals) and will probably add in semax for its protective effects in ischemic stroke. All the rest is to counteract my anxiety, or other purposes. Altough i'm confortable of adding in galantamine into my regime for cognitive enhancement.

By not focussing on aging i can leave out supplements with potentially interfere with my current combo.

Anyway thx for sharing your regime, i find it very interesting and hopefully you will find long term succes and it will adress your goals.

Edited by medievil, 20 September 2010 - 01:01 PM.


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#30 Rational Madman

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Posted 20 September 2010 - 01:14 PM

I'd like to pose a question that has stumped me a bit....

What is the best strategy for upregulating mu and v2 receptors? Both are unrelated, of course, but underappreciated pharmacological targets. There are many well known ligands for the former target, but they carry unpalatable side effects. The latter target is even more frustrating, since Desmopressin appears to be the only attainable substance with a known affinity, but is quickly disqualified because of its multiple side effects. If anyone remembers, the protein RGS-14's binding relationship with the V2 receptor was considered to be especially critical to its cognitive effects, and the neuropsychiatric benefits of mu receptor upregulation should require no explanation.




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