155 replies to this topic

[medievil]

I beleive NMDA hyperactivity rather then hypoactivity is more of a problem in my case, i tolerate memantine VERY well, and the only thing i notice are benefits, no downsides even at 60mg a day! I notice extra clarity, great reduction in OCD and extra feeling of wellbeing. EDIT: Oh yeah and unusual motivation on 60mg!

I'm wondering if some of your D2 and D3 receptors are hyperactive

Why? It seems that dopaminergics are the most efficient for my condition, also i found some relief using low dose amisulpiride in doses selective for the presynaptic receptors, wich raise dopamine, all togheter i'm pretty sure my dopamine system is hypoactive and not hyperactive.

I have taken seroquel in the past and it made me feel ALOT worse, i havent really tried other antipsychotics and not really planning to as i'm against them.

Or where you talking about D2/D3 autoreceptor hyperactivity? Yeah that could be an issue, amisulpiride can help this, and it worked for me in the past, however i gained a permanent tolerance to it, and low dose sulpiride didnt create the same results.

Edited by medievil, 24 October 2010 - 11:42 AM.

[Knine]

so today morning will be the last day of my initial semax experience, i honestly am almost done my 0.1 and have a little more of the 1%. I sort of used half of each bottle on wednesday (4 days ago), then when i came home again i started with 1% 1 drop, and started getting profound effects, especially with phentrolpil and triplelecithin (soy derived- choline).

wednesday- 1ml injection into left shoulder, 1ml into right buttocks, 0.5 ml in left and right ear lobes (crb)
half a bottle of 0.1 and 1 semax each
popped 4 phenotropils
after all of this i took the subway to neighboring city where i have school and stay for a few days, i smoke marijuana when im away from home, the marijuana made me sort of like the drugs i was now taking, but because of placebo effect of CRB is the highest, it was what i was most thinking about

saturday (yesterday) - mom snatched all my injection needles with alcohol swabs clean water and other stuff, i was going to use clean water to flush the CRB out of the effected areas, as it was still sore there yesterday, but now i could not. anyways i finished off some more semax 1 and 0.1, (has sort of a burning sensation on the nose with a sort of swimming pool/mediciny smell) popped some more phenotropil and lecithin and wow i was completely bonkers, felt awareness but i felt like over the year i have developed a musical tick in my right temporal hemisphere, music had way more profound effects on my brain, and it was telling me which songs to go for and which to just skip. (by a clicking sensation in my skull, schizophrenia is quite common in parts of my family)

the ear lobe thing, i think its purely subcutaneous and that after you inject your ears go really red, and then the liquid simply gets distributed from your ears to the back side of the neck, which is kind of weird, and which is why i distinctly heard a voice in my head say: cerebrolysin is toxic throw that shit down the drain. before bed yesterday night, sleeping was sort of gay yesterday and the last few days, if i sleep i sleep, but if i wake up its hard to go back to sleep unless i move around or go into fetal position, and i also remember having dreams of being asleep (closed eyed) but thinking to myself that i am awake, when will i get back to sleep.

i dont think i will be trying CRB again for quite some time, as it has cost me trouble with my mom and other issues, until i feel more comfortable or speak to someone around here that knows more about it personally. it is still in the fridge tho.

Sunday (today) - first i would like to say before i finish off my bottles, i think semax definitely has a nootrpoic effect with very little drawbacks, but honestly the lack of marketing with the product simply makes me paranoid. anyways i am going to try it again with phenotropil and lecithin. yesterday i was really jittery grinding my teeth skipping songs (good ones) obtrusively, probably because of the 3 red bulls and cigarettes i was also having added to this effect.

the part of semax i liked, was if i closed my eyes to nap for 5 minutes, (some reason i felt tired and awake at the same time (overstimulate)) in a tired state but still awake to do things as i am a student.
i felt like i had a sense of where everything was in the room even thought my eyes were closed, and the sharpness of this feeling was sort of periodically shifting sometimes sharper sometimes not (getting distracted by visual images (hallucination/thinking/add) etc) this effect i sort of remember from childhood as when ever i slept and woke up, i felt like the "view" of my room never left site. But i did not have this feeling for longer than maybe 1-2 or 3 years.

i think the effectiveness of semax nasally is very effective, i was thinking about injected yesterday, but my supplies got stolen, and i have things to do so, good bye semax (for now)

[Animal]

What dose of AMT do you take daily? Is it a single dose in the morning, or is re-dosing involved? What issues do you believe it resolves? Remember that it is not simply a tryptamine, it also has phenylethylamine characteristics, and given the toxicity of it's close analogue AET it is likely to have similar neurotoxicity. Especially considering their mechanisms of action are virtually identical, it even has the potential to cause agranulocytosis just like AET given it's known effects in reducing the granulocyte population in humans.

That's interesting what you mention about the Memantine being dopaminergic, it is something I have considered trying, but currently the potential negative effects on cognition put me off.

[medievil]

What dose of AMT do you take daily? Is it a single dose in the morning, or is re-dosing involved? What issues do you believe it resolves? Remember that it is not simply a tryptamine, it also has phenylethylamine characteristics, and given the toxicity of it's close analogue AET it is likely to have similar neurotoxicity. Especially considering their mechanisms of action are virtually identical, it even has the potential to cause agranulocytosis just like AET given it's known effects in reducing the granulocyte population in humans.

That's interesting what you mention about the Memantine being dopaminergic, it is something I have considered trying, but currently the potential negative effects on cognition put me off.

I take 7,5mg AMT in the morning, it never wears off for me, atleast it works untill i go to sleep even if i wake up 6 o clock for work and go sleep 3 o clock at night, i never redose during the day and i make sure to allways take a break of a few days once and awhile.

Yes i'm absolutely convinced it has the same neurotoxiticy as AET however i think this would be minimal in therapeutic doses, since monoamine release would be low (atleast far lower then recreational doses) and hyperthermia (essential for MDMA induced neurotoxiticy) is minimal.

Still keeping potential toxiticy in mind is allways a good idea for me the benefits definatly outweigh the risk. (or what i assume are the risk, getting all research papers will give us more answers).

As far as agranulocytosis you can be correct that its an issue, however indopan seemed to have been in clinical use for 20 years, and a moderator on bluelight (i know this isnt really evidence but its someone i would trust, even tough he uses recreational drugs, he's aware of the potential risks, and also was one of the main guys against the toxic mephedrone.)
Has checked out the russion toxicology database to check for any issues and said nothing was documented.

He also looked into the papers im trying to get atm, here's a list of the most interesting one's:

Title: [APROPOS OF THE USE OF INDOPAN IN CLINICAL PSYCHIATRY.]
Author: LEVIT, V G
Add.Author / Editor: MOROZOVA, T N
POPOVA, A N
Citation: Zh Nevropatol Psikhiatr Im S S Korsakova
Volume: 64, Date: 1964 , Pages: 768-70
http://www.labmeetin...ical-psychiatry


Title: [Pharmacological properties of indopane (alpha-methyltryptamine HCl).]
Author: MASHKOVSKII, M D
Add.Author / Editor: TRUBITSYNA, T K
http://www.labmeetin...yptamine-hcl%29

Title: [On the mechanism of action of indopan]
Author: Popova, E N
Citation: Zh Nevropatol Psikhiatr Im S S Korsakova
Volume: 67, Issue: 1, Date: 1967 , Pages: 125-31
http://www.labmeetin...tion-of-indopan


Title: [Effect of indopan on cerebral circulation]
Author: Mashkovskiĭ, M D
Add.Author / Editor: Lanskiĭ, V P
Citation: Farmakol Toksikol
Volume: 31, Issue: 5, Pages: 587-90
http://www.labmeetin...ral-circulation


Title: [EFFECT OF INDOPAN ON THE BIO-ELECTRIC ACTIVITY OF THE BRAIN.]
Author: ROSHCHINA, L F
Add.Author / Editor: MASHKOVSKII, M D
Citation: Zh Nevropatol Psikhiatr Im S S Korsakova
Volume: 63, Date: 1963 , Pages: 1679-87
http://www.labmeetin...ty-of-the-brain


Title: [Morphophysiologic studies of the effect of indopan on the process of higher nervous activity]
Author: Krivitskaia, G N
Add.Author / Editor: Mering, T A
Citation: Zh Vyssh Nerv Deiat Im I P Pavlova
Volume: 16, Issue: 4, Pages: 648-54
http://www.labmeetin...ervous-activity


Title: [Group toxicity of indopan and its reaction to various neurotropic drugs]
Author: Trubitsyna, T K
Add.Author / Editor: Mashkovskiĭ, M D
Citation: Farmakol Toksikol
Volume: 28, Issue: 1, Pages: 23-7
http://www.labmeetin...urotropic-drugs


Title: Activation of brain 5-HT neurons by two alpha-methylated tryptamine derivatives.
Author: Arai, Y
Add.Author / Editor: Tadano, T
Yonezawa, A
Fujita, T
Kinemuchi, H
Kisara, K
http://www.labmeetin...ine-derivatives

Pubget doesnt hold the PDF's on any of them, however ppl have suggested me to go to university's and ask there.

I'm also trying to get this paper:

Agranulocytosis following Monase therapy.
BUTIN JW.
J Kans Med Soc. 1962 Aug;63:338-40. No abstract available.
PMID: 13875179 [PubMed - indexed for MEDLINE]
Related citations


To see how big the risk of agranulocytosis was with AET.


Regarding memantine, well id say its definatly worth a try, you can allways see for yourself wheter its effect on cognition will be an issue, subjectively i notice more clarity and dont notice any cognitive impairment after the initial adaptation phase.

Edited by medievil, 24 October 2010 - 06:23 PM.

[scandic]

I have SA as well, and ADD issues.

Vitamin D is involved in the production of dopamine. Perhaps this could be a natural way to max brain-dopamin levels. I need at least 1000 i.u. per day. At the moment I take 4000 i.u. and I can def feel a positive effect.
I mean, I can FEEL the vitamin D doing something beneficial. I know it might not help everybody though.

I haven't red through the entire thread, so maybe it has been covered.
If I go to a social gathering or something I have a combination that is pretty good.
Propranolol (beta-blocker), Xanax, and if necessary a beer. I just seems Xanax makes beer taste like God's nectar -so be careful.

[medievil]

Ive taken vitamin D for a long time, it has no effect on my social anxiety, as for benzo's, ive pretty much tried them all, atleast a great deal of them and none has a positive effect on my social anxiety, the same goes for GHB, opiates and even alcohol, they can make me not care, but i dont care what ppl think of me in the first place.

I attribute my social anxiety to dopaminergic problems, as dopaminergics are the only meds that can help. It also makes sense since dopamine (especially D2 and D3) is highly implicated in social behavor.

Exposure and gaining social skills and confidence is also of major importance, but after years of chronic exposure i cant say it helped me, i may look into CBT tough, but i know little about it.

[scandic]

Vitamin D has not helped my SA either, but it has helped some on my fatigue and perhaps a bit on my ADD.

Only thing that works on my SA is that combo I described. I would like to try CBT, but psychs costs 150$/session here.

[Animal]

Ive taken vitamin D for a long time, it has no effect on my social anxiety, as for benzo's, ive pretty much tried them all, atleast a great deal of them and none has a positive effect on my social anxiety, the same goes for GHB, opiates and even alcohol, they can make me not care, but i dont care what ppl think of me in the first place.

I attribute my social anxiety to dopaminergic problems, as dopaminergics are the only meds that can help. It also makes sense since dopamine (especially D2 and D3) is highly implicated in social behavor.

Exposure and gaining social skills and confidence is also of major importance, but after years of chronic exposure i cant say it helped me, i may look into CBT tough, but i know little about it.

I think excess dopamine disguises your SA, but I don't think lack of dopaminergic tone is your root problem. I say this because if your dopamine levels are low I would expect: depression, lethargy, apathy, anhedonia (I know you suffered from this), low libido, that you easily gain weight, low blood pressure and a lack of sociability among other similar symptoms. But I would certainly not expect anxiety of any kind, the opposite in fact assuming all other neurotransmitter dynamics are normal. The only other explanation is that you have a lack of sensitivity at particular dopamine receptor subtypes. If you could isolate which, you could tailor treatment appropriately.

I believe I suffer from low dopamine levels, and I have virtually all the symptoms listed about when not medicated. But I have never suffered from anxiety, social or otherwise, if anything I have a resistance to the development of anxiety, even when copious anxiety generating drugs are consumed. This is in large due to my personality, but some of it must be physiological.

When you say you have no social psychological issues I find that hard to believe, since anxiety specifically relating to social contact would definitely have a root psychiatric cause. Constitutive anxiety on the other hand can be due to neurochemical imbalances.

Hmmm, you know if AMT didn't have any of the issues I mentioned earlier in the thread it probably is a substance that many people on this forum could benefit from. You don't have a comedown from it? No hangover?

[medievil]

My ADHD is very severe and my biggest issue, and depleted levels of dopamine have been implicated:

J Clin Psychopharmacol. 2008 Jun;28(3 Suppl 2):S39-45.
Catecholamine dysfunction in attention-deficit/hyperactivity disorder: an update.
Prince J.

Department of Child Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. jprince@partners.org
Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous disease that affects children, adolescents, and adults. Genetic research has confirmed that there is a large hereditary component to this condition and has helped identify some of the genes associated with it. Among these are several genes associated with the catecholaminergic system including the dopamine receptor genes (DRD4 and DRD5), the dopamine transporter gene, and the gene for dopamine beta-hydroxylase, which catalyzes conversion of dopamine to norepinephrine. Attention-deficit/hyperactivity disorder is believed to be a result of abnormalities in the frontal regions of the brain, particularly the prefrontal cortex and associated subcortical structures and circuits. Underpinning these abnormalities are disturbances of catecholamine neurotransmission. Studies have demonstrated that patients with ADHD have depleted levels of dopamine and norepinephrine thought to be largely the result of dysfunction of their respective transporter systems. The efficacy of stimulant agents confirms that the neurotransmitter abnormalities seen in ADHD are primarily catecholaminergic in origin. This article focuses on the catecholaminergic networks of higher cognitive functions such as attention and focus and of motor functions that may be associated with such networks, reviewing both the physiology of such functions and the pathophysiology of ADHD. Researchers are currently investigating whether other neurotransmitter systems may be partially involved and are investigating whether agents that affect these other systems will prove complementary to currently used treatments.

Yet we dont see the other problems in those ppl you are mentioning. Dopamine "defiency" can cause a variaty of issues imo, depending on the brainarea's involved, receptors etc.

The only other explanation is that you have a lack of sensitivity at particular dopamine receptor subtypes. If you could isolate which, you could tailor treatment appropriately.

That can make sense.

When you say you have no social psychological issues I find that hard to believe, since anxiety specifically relating to social contact would definitely have a root psychiatric cause. Constitutive anxiety on the other hand can be due to neurochemical imbalances.

I used to, but over the years i have build my confidence, gained my social skills and all the rest.

Hmmm, you know if AMT didn't have any of the issues I mentioned earlier in the thread it probably is a substance that many people on this forum could benefit from. You don't have a comedown from it? No hangover?

Ive never noticed a comedown of hangover from it, unlike amphetamine, but the longest ive been on it is 2 months or so now, i can imagine that with chronic treatment for a very long period there would be some withdrawal, and that with my short breaks i just avoid them.

I think excess dopamine disguises your SA

You see what the interesting thing is, the day AFTER i take a recreational dose of amphetamine or MDMA i am 100% free of my social anxiety, yet i'm not high anymore, say for example i take mdma 10 o clock evening, i stay free of SA untill the next day 6 - 8 in the evening, while the high has weared off LONG before that.

As for dopamine and SA, ive recently made a post about that:

School avoidance and social phobia triggered by haloperidol in patients with Tourette's disorder

EJ Mikkelsen, J Detlor and DJ Cohen

Fifteen patients with Tourette's disorder developed school and work avoidance syndromes when treated with low doses (mean 2.5 mg/day) of haloperidol for short periods of time (mean, 8 weeks). The phobic syndromes disappeared completely with discontinuation or reduction of the haloperidol dose. Haloperidol's effects on dopaminergic functioning support a role for catecholamines in the pathogenesis of phobic syndromes. It is not known whether phobias are precipitated by haloperidol only in patients with Tourette's disorder as a consequence of the specific metabolic alterations in this disorder or are a medication side effect in other psychiatric disorders as well.

Altough this is about patients with tourette this further confirms that dopamine is highly implicated in social behaver, and that dopamine antagonism can significantly worsen symptons of social anxiety.

Study's have confirmed that people with social anxiety are at a much higher risk for developping parkinson (1), indicating that we are suffering from dopaminergic dysfunctioning. Dopamine has also been implicated in social status (2) and as last the D2 gene's have been associated with extrovertism (3).

This data supports that dopaminergics are the best treatment for social anxiety, possible options are either MAOI's (parnate, nardil), dopamine agonists (pramipexole, ropinirole) and stimulants (dexedrine, adderall etc).

Anecdotal reports confirm the effiacy of those treatments in social anxiety disorders.

1. Frequency of social phobia and psychometric properties of the Liebowitz social anxiety scale in Parkinson's disease. PMID: 18661550
2. Dopamine Type 2/3 Receptor Availability in the
Striatum and Social Status in Human Volunteers Full text
3. Variation in DRD2 dopamine gene predicts Extraverted personality. PMID: 19897017

I accidently mixed up a reference regarding parkinson, this one shows that many parkinson patients have social anxiety (wich also indicates that dopaminergic problems can cause social issues) however ive had another reference showing that people with social anxiety are at a 6 times higher risk of developping parkinson, i will dig that one up again.

it probably is a substance that many people on this forum could benefit from.

Well it definatly is, but it still an RC, so ppl need to take the potential risks in mind.

Edited by medievil, 24 October 2010 - 08:39 PM.

[Rational Madman]

My ADHD is very severe and my biggest issue, and depleted levels of dopamine have been implicated:

J Clin Psychopharmacol. 2008 Jun;28(3 Suppl 2):S39-45.
Catecholamine dysfunction in attention-deficit/hyperactivity disorder: an update.
Prince J.

Department of Child Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. jprince@partners.org
Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous disease that affects children, adolescents, and adults. Genetic research has confirmed that there is a large hereditary component to this condition and has helped identify some of the genes associated with it. Among these are several genes associated with the catecholaminergic system including the dopamine receptor genes (DRD4 and DRD5), the dopamine transporter gene, and the gene for dopamine beta-hydroxylase, which catalyzes conversion of dopamine to norepinephrine. Attention-deficit/hyperactivity disorder is believed to be a result of abnormalities in the frontal regions of the brain, particularly the prefrontal cortex and associated subcortical structures and circuits. Underpinning these abnormalities are disturbances of catecholamine neurotransmission. Studies have demonstrated that patients with ADHD have depleted levels of dopamine and norepinephrine thought to be largely the result of dysfunction of their respective transporter systems. The efficacy of stimulant agents confirms that the neurotransmitter abnormalities seen in ADHD are primarily catecholaminergic in origin. This article focuses on the catecholaminergic networks of higher cognitive functions such as attention and focus and of motor functions that may be associated with such networks, reviewing both the physiology of such functions and the pathophysiology of ADHD. Researchers are currently investigating whether other neurotransmitter systems may be partially involved and are investigating whether agents that affect these other systems will prove complementary to currently used treatments.

Yet we dont see the other problems in those ppl you are mentioning. Dopamine "defiency" can cause a variaty of issues imo, depending on the brainarea's involved, receptors etc.

The only other explanation is that you have a lack of sensitivity at particular dopamine receptor subtypes. If you could isolate which, you could tailor treatment appropriately.

That can make sense.

When you say you have no social psychological issues I find that hard to believe, since anxiety specifically relating to social contact would definitely have a root psychiatric cause. Constitutive anxiety on the other hand can be due to neurochemical imbalances.

I used to, but over the years i have build my confidence, gained my social skills and all the rest.

Hmmm, you know if AMT didn't have any of the issues I mentioned earlier in the thread it probably is a substance that many people on this forum could benefit from. You don't have a comedown from it? No hangover?

Ive never noticed a comedown of hangover from it, unlike amphetamine, but the longest ive been on it is 2 months or so now, i can imagine that with chronic treatment for a very long period there would be some withdrawal, and that with my short breaks i just avoid them.

I think excess dopamine disguises your SA

You see what the interesting thing is, the day AFTER i take a recreational dose of amphetamine or MDMA i am 100% free of my social anxiety, yet i'm not high anymore, say for example i take mdma 10 o clock evening, i stay free of SA untill the next day 6 - 8 in the evening, while the high has weared off LONG before that.

As for dopamine and SA, ive recently made a post about that:

School avoidance and social phobia triggered by haloperidol in patients with Tourette's disorder

EJ Mikkelsen, J Detlor and DJ Cohen

Fifteen patients with Tourette's disorder developed school and work avoidance syndromes when treated with low doses (mean 2.5 mg/day) of haloperidol for short periods of time (mean, 8 weeks). The phobic syndromes disappeared completely with discontinuation or reduction of the haloperidol dose. Haloperidol's effects on dopaminergic functioning support a role for catecholamines in the pathogenesis of phobic syndromes. It is not known whether phobias are precipitated by haloperidol only in patients with Tourette's disorder as a consequence of the specific metabolic alterations in this disorder or are a medication side effect in other psychiatric disorders as well.

Altough this is about patients with tourette this further confirms that dopamine is highly implicated in social behaver, and that dopamine antagonism can significantly worsen symptons of social anxiety.

Study's have confirmed that people with social anxiety are at a much higher risk for developping parkinson (1), indicating that we are suffering from dopaminergic dysfunctioning. Dopamine has also been implicated in social status (2) and as last the D2 gene's have been associated with extrovertism (3).

This data supports that dopaminergics are the best treatment for social anxiety, possible options are either MAOI's (parnate, nardil), dopamine agonists (pramipexole, ropinirole) and stimulants (dexedrine, adderall etc).

Anecdotal reports confirm the effiacy of those treatments in social anxiety disorders.

1. Frequency of social phobia and psychometric properties of the Liebowitz social anxiety scale in Parkinson's disease. PMID: 18661550
2. Dopamine Type 2/3 Receptor Availability in the
Striatum and Social Status in Human Volunteers Full text
3. Variation in DRD2 dopamine gene predicts Extraverted personality. PMID: 19897017

I accidently mixed up a reference regarding parkinson, this one shows that many parkinson patients have social anxiety (wich also indicates that dopaminergic problems can cause social issues) however ive had another reference showing that people with social anxiety are at a 6 times higher risk of developping parkinson, i will dig that one up again.

it probably is a substance that many people on this forum could benefit from.

Well it definatly is, but it still an RC, so ppl need to take the potential risks in mind.

Remember, not all antidepressants are created equal, so keep an open mind. You're flying in uncharted territory in spite of a great deal of the world being already mapped.

[medievil]

Remember, not all antidepressants are created equal, so keep an open mind. You're flying in uncharted territory in spite of a great deal of the world being already mapped.

Yes i know rol, but i have a fascination for the therapeutic potential of many psychedelics . Thx for the warning tough, i'm doing my best to get all the research papers and get as much data on it as possible.

[medievil]

Currently im taking:

60 mg memantine
8 mg candesartan
3x 600mg of NAC


Still on a break of everything else, soon will readd:
7,5 mg alpha methyl tryptamine
5mg nebivilol (ran out)
3x 5mg dexedrine
Nicotine
Galantamine
Selank
Piracetam

I have a bad cold and wont restart the amt or amp untill i'm fully recovered, stopped taking them last thursday, will probably make this a weekbreak.

Can any of the mods update my first post? Thx!

Edited by medievil, 26 October 2010 - 12:45 PM.

[aLurker]

Don't forget some ALCAR with the piracetam.
Pretty serious stack there.
Get well soon.

[pycnogenol]

3x 600mg of NAC

Are you taking sustained-release NAC or immediate-release NAC?

Edited by pycnogenol, 26 October 2010 - 03:18 PM.

[medievil]

Immediate-release NAC, would you recommend one above the other?

[medievil]

Don't forget some ALCAR with the piracetam.
Pretty serious stack there.
Get well soon.

Thx mate, just got prescribed antibiotics by my doc, will stay away from most stuff untill i'm back OK.

Yeah alcar is also on my list, and i want to try aniracetam too since its supposed to be anxiolytic, atleast in the rodents.

[Animal]

Ive never noticed a comedown of hangover from it, unlike amphetamine, but the longest ive been on it is 2 months or so now, i can imagine that with chronic treatment for a very long period there would be some withdrawal, and that with my short breaks i just avoid them.

How can there be no negative after effects though, it must deplete monoamine stores if it releases enough to induce euphoria (without Selank). Do you think the Memantine is the reason that you have no hangover?

Can you describe the subjective effects you experience?

I know this sounds hypocritical given my previous posts in this thread, but I'm considering AMT as an enhancing substance for when I go out on a Saturday. On a normal weekday I'm fine, I function well and my mood is good, I've pretty much conquered my major issues, with the only thing being occasional fatigue/daytime sleepiness which I banish with Modafinil. But on a Saturday, where I'll need to function for 18 hours or more, with preferably high energy and mood for the duration of the night out, I end up consuming way too much Modafinil, caffeine and alcohol to sustain my energy levels. This results in a horrific hangover the day after. If AMT is capable of providing sustained energy and mood enhancement for the duration of the night, without a hangover, it sounds ideal, I could drink minimal alcohol in this case.

I don't need much mood enhancement, my normal mood on my current regime is good anyway (thank fuck, took so long to attenuate the dysthymia), but sustained energy would be great, and of course mood enhancement is certainly welcome. I don't want to be high though, and would like to avoid actual euphoria if possible. That would be too much like a recreational thing, and I wouldn't want to become habituated to it.

I still believe it has toxicity issues and abuse concerns when taken daily, but one day every couple of weeks should minimise any harm. I really don't want to risk damaging my brain since my current regime is potently neurotrophic, and I want to maximise the potential my brain has for growth, repair and plasticity. The thought of taking something acutely neurotoxic concerns me, which is why amphetamines are not something I would consider.

So, I would really appreciate you commenting on what a daily experience of AMT is like Medieval, and why you have settled on a dose of 7.5mg/day, which is within the original therapeutic range for depression, so should minimise toxicity. I also want to apologise for my previous overly critical behaviour earlier in this thread. But like I've mentioned to you before Medieval, I see certain characteristics in you that my friends who abuse amphetamines exhibit, and it really sets me off. Ultimately I believe that if a substance truly enhances your quality of life (as opposed to getting you buzzed) then regardless of anything else you should take it, because the most important thing in life is to enjoy it.

[medievil]

Dont worry about it mate, lets be honest i'l allways stay someone thats gonna abuse drugs once and awhile, but with my regime i really want to tackle my issues, rather then getting buzzed, i'm glad you understand this, i also understand your position since there ARE many individuals just taking those chemicals to get buzzed while saying its only for the therapeutic effects.

How can there be no negative after effects though, it must deplete monoamine stores if it releases enough to induce euphoria (without Selank). Do you think the Memantine is the reason that you have no hangover?

No i dont think memantine is what is making the difference, i also think you are wrong that anything that induces euphoria depletes monoamine store's, the therapeutic doses only provide a minimal euphoria, definatly not the same buzz as with amphetamine, altough it can make you quite euphoric, it feels alot more "natural" then the amp buzz. Some ppl get benefits of only 2mg a day, you can start very low and go up untill you get the desired benefits. (if you start this low you can definatly avoid euphoria)

AMT is actually known for its afterglows, altough thats with the recreational doses, ive never seen ppl complaining of a crash or comedown with AMT as they do with amps or MDMA, even tough in recreational doses AMT releases quite a bit of monoamines, its an odd one.

Can you describe the subjective effects you experience?

It kinda feels like a day long dose of 5 mg dexedrine, but in a more serotogenic way (cant really explain it in a better way ) its a relaxing energy, not a buzzed up energy like amphetamine gives you.

It takes 2 hours to start working (take it as soon as i wake up).
Cant really give a better description, try it

But on a Saturday, where I'll need to function for 18 hours or more, with preferably high energy and mood for the duration of the night out, I end up consuming way too much Modafinil, caffeine and alcohol to sustain my energy levels. This results in a horrific hangover the day after. If AMT is capable of providing sustained energy and mood enhancement for the duration of the night, without a hangover, it sounds ideal, I could drink minimal alcohol in this case.

I think that AMT will be perfect for that, and it will definatly not cause a hangover.

Here's an account of a friend of me that i recommend AMT:

aMT doesnt do much for my OCD (althouth my OCD is not that bad).
But it does wonders for my ADHD and social anxiety and anhedonia.

Being on aMT is the closest thing to normal that I ve ever been.
I usually combine it with some piracetam and picamilon.

And the greatest thing is that there are no negative aftereffects. Next day you go back to your normal baseline.

He doesnt take AMT every day, only twice a week i think, simular as you want to take it.

and why you have settled on a dose of 7.5mg/day

I feel that thise dose gives me the maximum of therapeutic effects, a higer dose seemed even counterproductive (10mg) as it put me into a weird mindset, not really productive.

I have to admit that because its a psychedelic it blocks me from abusing it (i dont like psychedelics as recreational drugs) and elevating the dose to 10mg doesnt produce any better results. With amp i sometimes let my addictive personality slip, wich only results in bad crashes, so not really intrested in doing that again .

Edited by medievil, 26 October 2010 - 08:02 PM.

[aLurker]

You should become a pharmaceutical rep.

[medievil]

You should become a pharmaceutical rep.

Nope, i will be the person that puts AMT back into clinical trials and gets it approved again!

If only that was possible

[Animal]

I have to admit that because its a psychedelic it blocks me from abusing it (i dont like psychedelics as recreational drugs) and elevating the dose to 10mg doesnt produce any better results. With amp i sometimes let my addictive personality slip, wich only results in bad crashes, so not really intrested in doing that again .

That's interesting, I know that psychedelic effects can become noticeable on as little as 15mg, and I agree with you that these kinds of doses would not be conducive towards normal functionality.

My biggest worry is that I'll enjoy the improved well-being to such an extent that I'll want to take it every day, I mean the price really isn't a limitation. The potential for the development of agranulocytosis worries me too, especially since in some cases removal of the causative agent doesn't result in a recovery of the granulocyte population. You are wise to discontinue taking the AMT until you recover from your current infection, and I suppose speculating on whether or not the AMT is the cause of it is pointless for now.

How are you feeling/functioning at the moment since you're currently taking a break from the AMT and the Dexedrine?

It would be nice to know the true safety profile of AMT, since it seems to have definite therapeutic potential. I think we'll see huge progress in the science of antidepressants within the next decade, especially because new research is being conducted into the potential of tryptamines as therapeutic agents. At some point in the future I believe either everyone will be under the influence of some sort of beneficial psychotropic; or we'll have been more direct and used gene therapy to enhance our neurochemical dynamics. I suppose the concern is that if we medicate away all our psychological flaws, will we be creating a population of bland, indistinct hyperthymics.

[medievil]

and I suppose speculating on whether or not the AMT is the cause of it is pointless for now.

Well, i do beleive the AMT made it easier for my infection to manifest itself, see this study:

[Acute and latent influenzal infection in mice with altered endogenous serotonin metabolism]
http://www.ncbi.nlm....v/pubmed/919502
QUOTE
A steady and long-term increase of the endogenous serotonine concentration in the lungs, spleen, and brain achieved by administration of nontoxic doses of indopan, an inhibitor of monoamineoxidase, caused a significant decrease of resistance of animals to influenza virus in acute infection. After natural route of inoculation with 20 LD50 of the allantoic influenza A3/WSN (HON1) virus strain in the animals treated with indopan the area of lung affection with specific influenza pneumonia increased, the virus concentration in the lungs and spleen rose sharply, the titre of IgM antibody in the blood decreased; the animal mortality in this group also increased. The level of serotonin in the blood and organs of latently infected animals became normal 6 weeks after virus inoculation. In some of these animals, however, indopan caused a greater increase of serotonin level in the lungs than in intact mice of the same weight and age. Without changing the amine levels in the spleen and the brain, indopan caused 4-16-fold increase in the titer of specific antihemagglutinins in the blood, mostly of IgM fraction, as compared with the controls. In latent influenza infection the balance of serotonin metabolism in the lungs in unstable.

Factoring all the potential downsides is important, and i'm not acting ignorant about it.

The potential for the development of agranulocytosis worries me too, especially since in some cases removal of the causative agent doesn't result in a recovery of the granulocyte population.

Can you tell me more about this condition? What are the early signs? How long does it take before it gets dangerous?

How are you feeling/functioning at the moment since you're currently taking a break from the AMT and the Dexedrine?

If i stop taking the AMT i just return to baseline, perhaps with AMT afterglow added but that could be placebo, however if i take dex on top of it, or just take dex on its own for several days and i stop it i definatly notice a withdrawal, generally having alot less energy for a while afterwards.

It would be nice to know the true safety profile of AMT, since it seems to have definite therapeutic potential.

I agree, wich is why i'm doing my best to get the papers on indopan, apperantly there are translated papers in sunderland (somewhere in england) i'l see wheter i can get them otherwise.

especially because new research is being conducted into the potential of tryptamines as therapeutic agents.

Wich is a terrific thing, those chemicals have a impressive therapeutic potential imo, its just a shame the abuse phobia limits research, amineptine being outlawed was a good example, completely ignorant of all ppl taking it and benefitting from it around that time.

Edited by medievil, 26 October 2010 - 10:34 PM.

[pycnogenol]

Immediate-release NAC, would you recommend one above the other?

I much prefer the sustained-release NAC as it brings my blood glucose down along with diet and exercise.

[medievil]

Getting this paper would be great too:

Agranulocytosis following Monase therapy.
BUTIN JW.
J Kans Med Soc. 1962 Aug;63:338-40. No abstract available.
PMID: 13875179 [PubMed - indexed for MEDLINE]

Getting to know how big the risk was with AET is a good thing, then we could know wheter the risk was high or not, for example there's a risk of getting Stevens-Johnson syndrome when taking modafinil, but the chances of that are so small, its worth taking the risk.

Keeping an eye open that this could be a possibility with AMT too is a good idea.

[medievil]

Jeez, my doc had to use this garbage as first line antibiotic .

http://en.wikipedia....ki/Moxifloxacin
http://en.wikipedia....luoroquinolones

I'm gonna stop this crap tomorrow, maybe ask another doc for a better antiobiotic or see wheter there's any improvement and stop using them.

[Thorsten3]

With amt is there anything one could potentially take to minimize neurotoxicity? I'm guessing potent anti-oxidants would only do so much? But hey who knows what these anti-oxidants do - I certainly notice nothing at all from resveratrol

[medievil]

With amt is there anything one could potentially take to minimize neurotoxicity? I'm guessing potent anti-oxidants would only do so much? But hey who knows what these anti-oxidants do - I certainly notice nothing at all from resveratrol

I would say resveratrol or curcumin are a good bet, they have been shown to protect against various toxins such as MPTP so i wouldnt be suprised they can offer some protection here. Its still guesword they can help tough.

Just regular antioxidants wich ppl use to preload on MDMA for example, wont do much except leaving you in the dilusion you are somehow protected against toxiticy, except if you are a rodent that gets a mass dose of vitamine C injected in the brain.

Besides probably not helping, daily high doses of antioxidants can be harmfull, only take supplements wich have been shown to be neuroprotective such as resveratrol, and not high doses of vitamine C, vitamine E etc.

[medievil]

Since i regained my ability to breath thx to this asthma inhaler i'm gonna stop this toxic antiobiotic and just sit it out, before i had this i was coughing non stop, didnt stop when i was out of air wich led to me allmost choking, i had to gasp for air the whole time and sit down for a sec to regain to my positives, even woke up once gasping for air felt like i was choking with my heart racing, took a beta blocker to calm my heart down and then went back to sleep, with this asthma inhaler i feel a ton better atleast.

[Animal]

Can you tell me more about this condition? What are the early signs? How long does it take before it gets dangerous?

Warning signs are soft spongy gums which bleed easily, although this usually only occurs in previously asymptomatic agranulocytosis that has been present for more then two weeks.

The classic symptoms of acute agranulocytosis are a rapid onset fever and sore throat; which can develop into septicaemic infection of multiple organs that progresses to combined renal and hepatic failure within days. Death can occur in as little as a week in severe cases.

The only real way to be safe is to have regular WBC counts, especially when you fall ill for longer then a few days. I know this isn't practical in your case, but there isn't really much else you can do.

[medievil]

I'm thinking that amphetamine may just not be for me, it induces way too much euphoria next to its therapeutic effects and actually keeps me inside because i prefer just listening music here, AMT on its own is far more therapeutic for me, so gonna stop a while with amp, and try other strategy's with AMT.