12 replies to this topic

[the_apollo]

I've been reading and searching about everything in between A and Z about nootropics and Rx-drugs to put together a nootropics/drug-list to treat my ADHD (inattention),
social problems (lack of social capability) and OCD symtoms.
The list i come up with so far is to mainly increase dopamine-receptors (for social and motivation),
overall intelligence/capacity to think and function, and for memory and ability to concentrate my thinking.

So anyway, i would like some opinions on my list, see if it can be optimized or can cause a problem (hopefully not).

The List:

DA and Noradrenaline
Pramipexole (Dopamine D2-receptorgroup agonist)
Concerta
Hordenine
BCAA

HISTAMINE
Betahistidine (Increase wakefulness)

CHOLINE
DMAE 100mg
Memeron 500mg (alpha-GPC and Galantamine) (Gonna take it every other day)
Alpha-GPC 500mg
Centrophenoxine 100mg

Serotonin
Kanna 50mg (Herbal SRI)
Bacopa Monnieri 500mg
Inositol 2000mg

Glutamate
Serine (NMDA agonist and gliotransmitter)
Oxiracetam (Said to increase memory retention)
Piracetam 500-1000mg (Neuroprotective, and general cognitive enhancer)

And also
SAMe (Used in processes involving metabolism of amino acids and such)
Noopept 20mg (increase NGF + BDNF)
Lion's mane mushroom ( May increase NGF, and myelination)
Creatine 1000mg (involved with ATP production, which also Q-10 and ALCAR is)
Q-10 100mg
Alcar 100mg
Rhodiola Rosea 400mg (adaptogen)

(Not included, but i will/is already taking a full range of vitamins and minerals, and will supplement with low-doses of amino acids)
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To explain short, dopamine enhancing is for the ADHD and social problem, serotonin för the OCD problem and glutamate for memory and cognitive stuff,
choline for memory and related, and histamine for wakefulness.
I plan on taking it easy, start slow and go with low dosages of the chemical drugs, and generally try to keep every part as low as functionally possible, so to say.
To make it better, but not over-dosing.
I do know that methylphenidate and glutamate can be neurotoxic, and that due to the serotonin-enhancing drugs combined with the SRI-effects of Kanna can cause serotonin syndrome,
but as i said, i plan to be safe and take it easy, and that it may take a couple of weeks for some drugs to reach full potential. (I've covered the basics, just saying)
I haven't listed doses for all the drugs, but those without a dosage is the drugs i'm gonna "try and feel", so to say, advance on the dosage until its perfect or maybe not working at all,
and to make sure that i dont over-dose on anything, especially when it comes to dopamine and glutamate.


Hope that diden't sound too cocky,, anyway,
i appreciate any advice and thoughts/opinions i can get about my list/Regimen, is there something i need to change? What should i be aware of?, and such on.
All help i can get i greatly appreciate,, Thank you.

(Also, there is no need to remind me of my lack of writing capabilities and such, as i can't change it. ADHD's a bitch, also, english is my second language)

[summertimex]

i find that increasing various different neurotransmitter systems doesnt work out as its planned, and for some reason the brain-mind rejects some of the will towards it when finding out how energies shift and what is does to consciousess when competing streams culminate blindly in various chain reactions.

for example an SRI lowers vigilance, and causes brain fogginess. dopaminergism goes down and that attentive state resides. then when it is counter-balanced with dopamine, the empathetic depth resides and it becomes boring.

also the difference between acetylcholine and serotonergism is vastly different.

it might be beneficial for your brain to try to push it to recalibrate, but these things usually have different ends. it might turn out to basically block each other out, or have too much of a fuzzy stream of neurotransmitter consciousness to really settle in to any place.


well i find that acetylcholine and serotonin get along more than other combinations.

might as well try to re-create yourself with psychedelic theraphy or something of that sort.

i didnt find my trial to be appealing or effective in structural changes, but it doesnt mean that there wont be enhancement.

it really depends on what you are missing and targeting those areas.


the problem with higher level neurotransmitter release is that its not directly on the build-chain, but it does increase the build chain. this is the kind of topographical thinking of western medicine, sometimes its better to try to be modulatory instead.

Edited by gen6k, 22 August 2012 - 06:26 PM.

[the_apollo]

Since i posted this thread i have (of course, with my luck) found out that pramipexole have higher affinity for the inhibitory dopamine receptor D2sh, which cause a lower effect at the inhibitory receptors (D2L, D3, D4),
but i've read about the antipsycotic drug called 'Amisulpride', which in low dose have preferred binding to the D2sh receptor with effect as an inhibitor,
is it possible to use Amisulpride as a "activity increase" drug for pramipexole?
The thing is with Amisulpride, that so far i havn't found anything relating to it's serotonin antagonist properties at low dosages,,
it would be a shame if the drug combination increase dopamine levels and all that good stuff but in the process decrease levels of serotonin..

I know that this DA-combo probably never been tried before, but its eighter this (for social capability, memory, motivation) or amphetamine,
and amph isn't something that i would like to go onto using, not even as a ADHD-drug.

Edited by the_apollo, 24 August 2012 - 08:35 AM.

[summertimex]

APs usually make people less sociable, serotonin antagonism and dopamine antagonism.

this is what i would recommend.

ocd: alpha-gpc, oxiracetam, aniracetam, pramiracetam

it kind of opens up the thinking channels more space


for social capability you have to get the serotonin to the right places as well as more executive confidence.

for adhd its better to find ways that actually gets closer to the bottom of it instead of straight stimulants cause the exitotoxicity can over time lower vigilance and corrupt the hippocampus.

obviously if you do take nicotine or stims your dopamine binding would increase, but i dont think that is the missing peice of adhd.

make sure you take enough antioxidants to protect the dopamine activity.

im sure you can eventually improve all of it, ocd by 70%, adhd by 60%, sociability 30-40%

the sociability is about recreating your inner self more often, like rising above it and finding reasons to.

ocd isnt that hard serotonin, nmda, plasticity type thing

adhd, theres usually endogenous deficiets or like dopamine toxicity, or hippocampal low up-keep. things of that sort.

find more orthomolecular peices for it.

[summertimex]

plus if you wanna cure anything you have to see what it is for yourself, not from a dsm standard or common pathway only. if you think about the people that have social withdrawel it could be for any reason, some people feel too much and their feelings get hurt, others are obsessed with a project in their mind, some have high anxiety, others dont register cues, etc.

[the_apollo]

APs usually make people less sociable, serotonin antagonism and dopamine antagonism.

this is what i would recommend.

ocd: alpha-gpc, oxiracetam, aniracetam, pramiracetam

it kind of opens up the thinking channels more space


for social capability you have to get the serotonin to the right places as well as more executive confidence.

for adhd its better to find ways that actually gets closer to the bottom of it instead of straight stimulants cause the exitotoxicity can over time lower vigilance and corrupt the hippocampus.

obviously if you do take nicotine or stims your dopamine binding would increase, but i dont think that is the missing peice of adhd.

make sure you take enough antioxidants to protect the dopamine activity.

im sure you can eventually improve all of it, ocd by 70%, adhd by 60%, sociability 30-40%

the sociability is about recreating your inner self more often, like rising above it and finding reasons to.

ocd isnt that hard serotonin, nmda, plasticity type thing

adhd, theres usually endogenous deficiets or like dopamine toxicity, or hippocampal low up-keep. things of that sort.

find more orthomolecular peices for it.

Well, i dont think Alpha-GPC and racetams would do me any good for OCD, the only thing that works to decrease OCD is serotonin-related supplements, (5-HTP, L-Tryptophan, inositol, and such),
there is also a well-based theory that OCD is serotonin related.
For me, Alpha-GPC is very subtle, i dont really notice anything until i stop taking it, then i notice my abilities to do math and abstrakt thinking is "dumbed down" for a little while.
And racetams do different things, for example; Aniracetam made me feel wierd when i took 700mg one day (morning, w food), and piracetam dident do much, but also very subtle,
i noticed when i used piracetam that my math-skills and language/finding words and saying it perfect got much better than before.
So i dont think that Alpha-GPC and racetams would do me anything in relation with OCD or Social.

And for social, there is a lot of theories and facts about that Dopamine D2 receptor activation /and/or Density relates to social status.
Got a link to an article about it; http://www.scienceda...00203084254.htm
It's kinda logical if you think of it, Dopamine has the function of being a "reward-signal" -transmitter,
but low signaling/low D2 activity would relate to less social behavior due to that you dont have (as much) reward-response from social behavior that D2 cause/are involved in.
And ADHD is partially theorized to be a problem with D2/D3 receptors and low activity or activation.
The Amisulpride drug does cause serotonin and Dopamine antagonism yes, but what i read so far is that the drug have a D2Sh-preferred antagonism at low dose, (<200mg),
which i image would be good due to that pramipexoles side effects is said to be caused by it having a higher preference for the inhibitory dopamine receptor D2Sh.


I appreciate your input,
but i dont think i can get to the big problem by using choline and racetams, i added cholines and oxiracetam + piracetam to my stack mainly because choline does good things on the mathmatical thinking, and oxiracetam because it's involvement with AMPA, and also piracetam due to its multiple actions, enhancing blood flow to brain, enhancing brain metabolism, increasing activity at corpus callosum.
But what do you think about the pramipexole and Amisulpride? Say if i would start of with a dose of 0,125mg pramipexole and 5mg Amisulpride (which for Amisulpride would be a super-low dose),
would it be any danger in trying? Just using those two drugs and maybe concerta, nothing else from the stack, just trying for say a month and see if it would work and such.

[summertimex]

hey. if you feel it intuitively with your system then go for it, but make sure that your brain is well-protected from the bdnf lowering effects of amulsipride.

http://www.ncbi.nlm....pubmed/22826038

it might also be possible to get neurotransmission in to the prefrontal cortex using various things.

[summertimex]

well you have to get serotonin in to the frontal cortex (social thinking)
and dopamine and acetylcholine motoneurons in to the prefrontal cortex (executive function)

[the_apollo]

hey. if you feel it intuitively with your system then go for it, but make sure that your brain is well-protected from the bdnf lowering effects of amulsipride.

http://www.ncbi.nlm....pubmed/22826038

it might also be possible to get neurotransmission in to the prefrontal cortex using various things.

I did a quick search for that BDNF lowering effects of amulsipride, an of what i found it seams to be a problem relating to D3-receptor antagonism,
but thats something that dont occur at that dose i'm thinking of,,
http://www.ncbi.nlm....pubmed/11333982
Or does the BDNF lowering effects occur even at low-dose use? (Not very much information about amulsipride at low doses)

But for the social stuff, i was thinking of upregulating/activity function of Dopamine mainly in the Prefrontal cortex (PFC) and relating frontal cortex due to that Dopamine has a very wide range of actions,
social, memory, reward, thinking (even mathmatical thinking).
and for serotonin, is mainly increased by the reuptake inhibitation, (i dont know if it's even possible for a target-medication changing actions in a specific area of the brain)
so Serotonin levels will just go up, and thats (as said before) mainly because of the OCD.
But for AcH (Choline), i was just thinking of increasing it by using a precursor (Alpha-GPC),
Galantamine because of Reuptake inhibitation, and others like DMAE because it has had good effects on me before.

It would be great if there was drugs who had a specific targeted action on the brain, but the only was (what i have read anyway) by electroshocks or injection of drugs to just that area that the scientists wanted a change in.

[Perek]

I would recommend the Russian anxiolytic Afobazole. It's been a part of my daily regimen for the last 3-4 years and I find it to be nothing short of excellent when it comes to social fobia. 3-6 pills a days for at least 3 weeks could make a big difference !

[Perek]

I am ADD with regular depressions if unmedicated. I had great success with Valdoxan(Agomelatine) for 3 years untill it pooped out some 6 months ago.
Been on even keel with Afobazole, 10 mg Abilify per WEEK, Bacopa and 10-20mg Dexedrine daily. Just ordered Selegeline that I tried with PEA some 10 years ago with good results but will then naturallly need to cut my Dex close to zero.

I would not get anywhere close to SSRI for brain activity/function. Agomelatine and Tianeptine, though not as strong antidepressants as SSRI ans SNRI are worth trying ! Then there are several augmentation strategies that could be helpful depending on your stack.

[Perek]

Since i posted this thread i have (of course, with my luck) found out that pramipexole have higher affinity for the inhibitory dopamine receptor D2sh, which cause a lower effect at the inhibitory receptors (D2L, D3, D4),
but i've read about the antipsycotic drug called 'Amisulpride', which in low dose have preferred binding to the D2sh receptor with effect as an inhibitor,
is it possible to use Amisulpride as a "activity increase" drug for pramipexole?
The thing is with Amisulpride, that so far i havn't found anything relating to it's serotonin antagonist properties at low dosages,,
it would be a shame if the drug combination increase dopamine levels and all that good stuff but in the process decrease levels of serotonin..

I know that this DA-combo probably never been tried before, but its eighter this (for social capability, memory, motivation) or amphetamine,
and amph isn't something that i would like to go onto using, not even as a ADHD-drug.

I've never tried any Dopamine agonist as they tend to be good for a couple of weeks only. But hey, with Amisulpride it could be a winner ! I tried Amisulpride some 10 years ago and it was like an awakener ! I quit it casue it gave my tremendous appetite for food and none for sex. Rather like it to be the other way around...^^

Amisulpride is way under-used. It's a great antidepressant in low dosages being a d2 agonist/dopamine modulator.

I also like to say that it's great to read and understand what drugs may and may not....but after that, trial and error will help you out even better.

[the_apollo]

Since the first post i made on this thread i kinda changed my mind, i didnt really understand the DA-agonist effects of pramipexole, i now know how the drug works and why it may cause addiction to high-stakes-high-reward -behavior.
I'm currently reading up on and studying several drugs and well. things, and recently came across the drug called 'Memantine', a drug that may enhance cognition.
But of what i read about Memantine, it has some concerning choline-antagonist effects, as choline has some positive functions on the brain, lowering choline-levels sounds kinda.. wrong..

But so i'm thinking; What about say an AcHei drug as Donepezil and Galantamine (positive allosteric modulator of nAcH) together with memantine, ? Would that reverse the problems of Memantine?
..Or, it there something about the drug i've missed, say its actually loses choline-antagonist properties after a while or something?
Eccept for the choline-antagonism, it does sound like a pretty good cognitive enhancer with the NAA-increasing effects, and the NMDA-antagonism just being a kind of "normalizer", not crashing normal levels but levels out to norm.

But anyway, as said, i'm interested in knowing more about the choline-antagonist behavior about memantine and if AcH-drugs can reverse the effects without cancelling out the good NAA-side of the drug,
i will continue searching for that information, but i take all the help i can get.