37 replies to this topic

[Area-1255]

No Ach doesn't lower 'IQ' it induces some depressive symptoms (problems assimilating and conentration) and with chronic raised levels it will tank serotonin (and by extention melatonin - causing insomnia), raise noradrenaline causing anxiety, hypervigulance and lower dopamine causing decreased hedonic tone. Obviously you are unlikely to have a gross increase in Ach across the entire brain in a mental illness and this is why supplements are less likely to cause all of these effects. The decrease in those types of neurons firing will only be in certain pathways that are effected by Ach ex: Mesolimbic and Mesocortical pathways (pleasure, motivation etc) which have very little to do with memory and learning functions per se (although they provide the motivation the excitation to other areas). These symptoms aren't the result of 'low dopamine' - which has very little directly to do with learning.

The only half reasonable way I can think of to lower Ach is TCA therapy.

Yes he is absolutely right, but on average, having acetylcholine on the higher end of the range is a good thing - but you are right, it will do nothing for short-term memory, but it does play a role in releasing neurotrophic factors and potentiating long-term memory and good memory consolidation. However, it seems the link here is individualized receptor based calcium channel modulation, and because the hippocampus which is largely involved with spatial memory, it would be expected that low acetylcholine individuals would have trouble remembering directions and where they put their keys etc...

I also know that low ach levels are associated with more aggressive mindsets, but because of a totally different reason than what high ach would bring . Low AcH tends to create overstimulation just like high levels...but I would mirror high levels to be more like that of glutamate excess (racing mind etc) - whereas too low would be almost purely adrenaline like....the difference you might ask?

 

Say you go for a walk - and someone pisses you off or sais something you don't like - low ach levels would make it so you wouldn't even think of it and you would probably react really quickly, almost in a tourette's like fashion...whereas high levels of ach you would probably be more cunning and pre-meditated.

 

At the same time though, even with being naturally undermotivated, high ach individuals tend to have more long-term goals and as such generally refrain from violence.

 

So if I were to choose from the two, high ach would be better because I could always tone dopamine on necessary points, but most preferably...having a balanced level of the two ....which would be moderate dopamine for common sense and logic, and moderate to high ach for more complex tasks and remembering what is necessary...then you also need glutamate for detail oriented things, and attention to details and philosophical thinking.

[John Schlongfellow]

oxcarbazepine FTW !

 

now does anyone have imput on how that drug fits in this convo , if at all?

 

a longer question would only make me look goofy, I can save time and face LOL.....

 

[StevesPetRat]

I wonder if it's really the high acetylcholine that makes you dumb. I'm more inclined to think it's the rebound effect described in the paper attached that does it. Basically, the gist is that an AChEI or other surge of acetylcholine, e.g. due to stress, ends up leading to long lasting upregulation of AChE and downregulation of ACh synthesis.

The ideal way to manipulate ACh would be at the epigenetic level. If anybody knows of anything that can do that, please, do tell
(Only candidate I have yet found is fisetin, which inhibits the cFos pathway that lead to the downregulation, but it's not clear that inhibiting this pathway after the fact would have much effect).

Attached Files

•  393373a0.pdf   512KB   8 downloads

[JellyRev]

I have been wondering if different choline sources form acetylcholine at different places in the brain bc they have different methods\steps of metabolism.
Similar to how certain drugs seem to produce their effect in a localized area

[Caravaggio]

 

 

 

I have asked this question many times, but never found a reasonable answer - how do you lower excess acetylcholine (assuming that your baseline ACH is "high")?

Lammas, try DMAE. Taitaa olla laitonta Suomessa. Works wonders for me to reduce ACh. It is a false cholinesource used to induce ACh depletion in research. Dozens of studies on that. Massive clarity and energy.

 

Do you think centrophenoxine will work as well (I have access to that)? Considering it is DMAE+pCPA http://en.wikipedia....i/Meclofenoxate
Could you provide some links about DMAE depleting ACh or explain how is it doing that?

Also, forskolin upregulates AChE expression, so more ACh gets broken down.
http://www.longecity...620#entry596755

 

Lots of studies you can easily find. Do Medline queries with deanol, false, acetylcholine, precursor etc. as search words. One study here. As to what Centro does? Beats me. Likely would lower ACHe while suppressing choline intake to brain due to being metabolized into DMAE. What that does overall...no idea.

http://www.ncbi.nlm....v/pubmed/727735

 

 
Sorry to dig out this old thread but I have to clarify this.
 
The substance used in this study is not even plain DMAE it's the p-acetamidobenzoate salt of DMAE.
 
A withdrawn drug for depressed kids.
 

 
"Back in the 1960’s and 1970’s, Riker Laboratories marketed DMAE as a prescription drug named Deaner. Riker Laboratories had obtained authorization from the FDA to market Deaner and promote it as “possibly effective” for the following indications:
 
Learning problems associated with underachieving and shortened attention span
 
Behavior problems associated with hyperactivity
 
Combined hyperkinetic behavior and learning disorders with underachieving, reading and speech difficulties, impaired motor coordination, and impulsive/compulsive behavior, often described as asocial, antisocial, or delinquent
 
In 1983 Riker discontinued Deaner because the FDA demanded additional efficacy studies, which would have been more expensive than the product’s sales would support. However, DMAE has continued to be available as a nutritional supplement."

https://www.fortitec...noethanol-dmae/
 
Maybe it just fried the brain of anti-social kids so they would obey anything.
 
Heres the molecular formula of DMAE:C4H11NO
 
https://pubchem.ncbi...v/compound/7902
 
Here's the molecular formula of Deaner: C13H20N2O4
 
https://pubchem.ncbi.../compound/19265
 
 impaired.gif   124.4KB   0 downloads
 
http://www.bonkersin...w/impaired.html

 

Edit:

 

OK, maybe I exaggerated with the brain frying, it seems just to be another carrier. Could it still have a total different way of how it works compared to DMA bitartrate?

 

Anybody knows in which form it occurs in fish?

 

Here's an interesting post of a father of an ADD kid:

 

https://groups.googl...cit/2NZo2nly794

 

Could the boy have excess (acetyl)choline in the brain and the DMAE p-acetamidobenzoate lowered it?

 

I found out you can still buy it as a supplement: https://shop.biotech...ts/dnz-2-100-mg

 

Who tried DNZ-2 and how does it compare to DMAE bitartrate?

 

Edited by Caravaggio, 20 December 2017 - 09:07 PM.

[CWF1986]

The interesting thing about this is that the symptoms of "had terrible attention spans, as well as dysfunction in working memory and spatial memory" are also result of low dopamine.

ACh is known to have an inverse relationship with dopamine in certain aspects. Anticholinergics were, at one time, used to treat Parkinson's, but the side effects were very bad.

This raises the question, what if cholinergics are combined with dopaminergics.

Theoretically, the problems of each are counterbalanced, although in reality there are bound to be some side effects. My bet would be that it would be severely anxiogenic, but I wonder how high the dose would have to be before the anxiety outweighed the increase in cognition, and if the anxiety could be reduced by a drug acting by a 2ndary mechanism, thus inhibiting the anxiety without inhibiting the cognitive effects.



This is also very, very interesting for another reason. The cholinergic increase decreases fatigue. Maybe this answers why sulbutiamine is useful in chronic fatigue (because it is cholinergic, and NOT because it sensitizes D1).

 

I have adhd, anxiety, and depression which is suggestive of atypical brain wiring/chemistry so take what I have to say with a grain of salt.  But I am currently am doing this in a sense under psychiatric supervision.

 

I take adderall and nortriptyline.  The combination is net anxiolytic.  Even the nortriptyline by itself improves my focus, attention, and short/working memory but that might have as much or completely to do with the NRI effect.  The adderall will reduce restlessness and impulsiveness and increases consciousness but it also increases my tendency to catastrophize and makes small annoying things into something agitating or will even anger me.  

 

The aforesaid negative effects of the adderall are significantly offset by the lexapro and propranolol I take.  

 

If I take cholinergics like huperzine a or precursors I get extreme anxiety and depression and diarrhea combined with stomach discomfort and sometimes even pain.  I avoid them like the plague.  

Edited by CWF1986, 21 December 2017 - 07:26 AM.

[CWF1986]

Also, lets not forget that there's a strong correlation between anticholinergics and dementia.  

[kurdishfella]

Your brain has more inhibitory  neurotransmitters than excitatory. Acetylcholine is latter. So it'd make you smarter. The key is to activate NMDA for intelligence. 

Edited by kurdishfella, 02 May 2022 - 12:31 AM.