14 replies to this topic

[CWF1986]

Choline is highly recommended on these boards.  There's theoreticals it's beneficial and countless testimonies as well.  This is undeniable.

 

However, I believe there is a population that responds poorly to these.  I am one of these people.  Even relatively low doses of lecithin can cause me high levels of anxiety and depression.  Huperzine A makes me dysfunctional for the day because of the intense anxiety and depression with suicidal ideation going as far to how to plan it out.  If I knew everyday would be as bad as a day after taking huperzine a I very well might carry it out. 

 

Disclaimer:  I am not suicidal and do not have plans to carry out harm to myself or others.    

 

Here's an excellent thread from this very subforum from 2005:

http://www.longecity...ium-hypothesis/

 

I'm going to try to look up some literature review and studies later since I should be trying to sleep right now.  

[Mind_Paralysis]

It's not far-fetched, I'll give you that - the antidepressant effects of Bupropion have for some time now been suspected to be connected to its ANTICHOLINERGIC effects - not the stimulatory, monoaminergic ones.

 

There's also the fact that there's some evidence that the old TCA's are MORE effective than corresponding SNRI's - HOW? They've got a similar central effect... well, not quite... The TCA's actually have ANTICHOLINERGIC effects as well.

 

As such, some people respond very poorly to excessive cholinergic signalling, that's obvious - these are the peeps which will respond better to anticholinergic effects.

 

I'm not one of them though, Buproprion caused intense cognitive issues for me - I seem to have naturally low cholinergic signalling. It also caused the most bizarre mood-swings, strange antisocial behaviour. I have been prescribed multiple antidepressants and stimulants, and NONE of them cause such behaviour in me (you'd think I'd get like that from the stimulatory effects, but this doesn't seem to be the case - if 70 mg Vyvanse doesn't turn me antisocial and aggressive, then it's not very plausible to be stimulatory effects.), as such, I can only conclude that it's the anticholinergic effects which cause this debilitating behaviour.

[jack black]

every couple of months people report here bad reaction to choline products and it's known to trigger depression in susceptible individuals. I believe borderline personality folks are especially sensitive. similarly, anticholinergics trigger mania in some bipolar persons.

here is a thought, maybe piracetam will be helpful for you?

be careful though, it's know to trigger mania in some.

Edited by jack black, 07 December 2017 - 07:03 PM.

[Kinesis]

We have to take a balanced perspective. And avoid the temptation to put black and white hats on substances as if human physiology were a spaghetti western.

Choline is regarded by many authorities as an essential nutrient. Meaning if you don’t get any, you’re putting yourself in harm’s way.

https://www.ncbi.nlm...pubmed/2010061/

Does that mean that more is better? No... Water is obviously essential, but if you try drinking six gallons at a sitting it could be fatal.

Bottom line is there is an optimal intake of choline, and it varies between individuals. You get some in your food. If it turns out that your dietary intake is optimal, then taking more is going to move you in a suboptimal direction. If your optimal level is higher than what you get in your diet, taking more will improve your choline status.

[gamesguru]

Avoiding choline is one way of solving the problem, but this is only the effect of the cause.  Dopamine is the root, it is upstream (via nigro-striatum) of the relevant choline pathways.

Dopamine normally suppresses acetylcholine.  Toying carelessly with this balance often leads to classic symptoms of tardive diskinesia, extra-pyrimidal syndrome, and more.

 

I suggest you rather increase your dopamine levels over a period of weeks (ginkgo, exercise, etc), then you should become gradually more tolerant of acetylcholine.

 

 

see figure 5-11C of the following resource (the rest of it is an interesting read as well though)

http://stahlonline.c...4th_chapter.jsf

[jack black]

see figure 5-11C of the following resource (the rest of it is an interesting read as well though)

http://stahlonline.c...4th_chapter.jsf

 

nice try, but you have to be subscribed to see that content.

[gamesguru]

shit my bad, no you don't.. i just used the truncated URL by mistake.

this one should redirect you properly, figure 5-11 part C is the most relevant but the others are interesting too

 

http://stahlonline.c...5&title=Summary

[CWF1986]

Avoiding choline is one way of solving the problem, but this is only the effect of the cause.  Dopamine is the root, it is upstream (via nigro-striatum) of the relevant choline pathways.

Dopamine normally suppresses acetylcholine.  Toying carelessly with this balance often leads to classic symptoms of tardive diskinesia, extra-pyrimidal syndrome, and more.

 

I suggest you rather increase your dopamine levels over a period of weeks (ginkgo, exercise, etc), then you should become gradually more tolerant of acetylcholine.

 

 

see figure 5-11C of the following resource (the rest of it is an interesting read as well though)

http://stahlonline.c...4th_chapter.jsf

 

Please correct me if I'm wrong about this, but I believe I'm already taking some much heavier hitters already.

 

I take the TCA nortriptyline at an antidepressant dose and my blood levels are within the therapeutic window and that's directly an anticholinergic.  I also take the dopaminergic stimulant adderall.  I take lexapro as well.  I remember reading some things about how SSRIs indirectly lower acetylcholine levels.  Hopefully, I can find that again.

 

Is there a particular part of the brain or specific D-receptors that you're talking about?  Or am I already doing a very heavy handed approach already?

[gamesguru]

I also take the dopaminergic stimulant adderall.  I take lexapro as well. Hopefully, I can find that again.

 

Is there a particular part of the brain or specific D-receptors that you're talking about?  Or am I already doing a very heavy handed approach already?

 

you have all the right ideas but all the wrong reasons.  things are rarely as simple as presented, and the approach will backfire in the long-term.  by watering a cornstalk once, you give it live and vitality.. but if you repeat this process too frequently you wash away the very soil on which it depends, and that's receptor dynamics in a nutshell

 

yes, all of them.  now excuse me while i reduce a brick wall to ashes using only my forehead out of pure frustration

Edited by gamesguru, 14 December 2017 - 12:10 AM.

[Kinesis]

It's not far-fetched, I'll give you that - the antidepressant effects of Bupropion have for some time now been suspected to be connected to its ANTICHOLINERGIC effects - not the stimulatory, monoaminergic ones.

There's also the fact that there's some evidence that the old TCA's are MORE effective than corresponding SNRI's - HOW? They've got a similar central effect... well, not quite... The TCA's actually have ANTICHOLINERGIC effects as well.

As such, some people respond very poorly to excessive cholinergic signalling, that's obvious - these are the peeps which will respond better to anticholinergic effects.

I'm not one of them though, Buproprion caused intense cognitive issues for me - I seem to have naturally low cholinergic signalling. It also caused the most bizarre mood-swings, strange antisocial behaviour. I have been prescribed multiple antidepressants and stimulants, and NONE of them cause such behaviour in me (you'd think I'd get like that from the stimulatory effects, but this doesn't seem to be the case - if 70 mg Vyvanse doesn't turn me antisocial and aggressive, then it's not very plausible to be stimulatory effects.), as such, I can only conclude that it's the anticholinergic effects which cause this debilitating behaviour.

Just goes to show the importance of accounting for individual differences. Bupropion was the most powerful nootropic I ever took. And this was when it was added to a notorious anticholinergic, the tricyclic amitriptyline. As a musician, I did some of the best and most complex arrangements I’ve ever done taking bupropion.

You also have to distinguish between muscarinic anticholinergic activity and antinicotinic activity; they’re very different. For most people, bupropion is not classically anticholinergic, or mildy so at best. It’s frequently prescribed as an alternative to classically anticholinergic drugs.

...

Edited by Kinesis, 14 December 2017 - 12:41 AM.

[Mind_Paralysis]

 

It's not far-fetched, I'll give you that - the antidepressant effects of Bupropion have for some time now been suspected to be connected to its ANTICHOLINERGIC effects - not the stimulatory, monoaminergic ones.

There's also the fact that there's some evidence that the old TCA's are MORE effective than corresponding SNRI's - HOW? They've got a similar central effect... well, not quite... The TCA's actually have ANTICHOLINERGIC effects as well.

As such, some people respond very poorly to excessive cholinergic signalling, that's obvious - these are the peeps which will respond better to anticholinergic effects.

I'm not one of them though, Buproprion caused intense cognitive issues for me - I seem to have naturally low cholinergic signalling. It also caused the most bizarre mood-swings, strange antisocial behaviour. I have been prescribed multiple antidepressants and stimulants, and NONE of them cause such behaviour in me (you'd think I'd get like that from the stimulatory effects, but this doesn't seem to be the case - if 70 mg Vyvanse doesn't turn me antisocial and aggressive, then it's not very plausible to be stimulatory effects.), as such, I can only conclude that it's the anticholinergic effects which cause this debilitating behaviour.

Just goes to show the importance of accounting for individual differences. Bupropion was the most powerful nootropic I ever took. And this was when it was added to a notorious anticholinergic, the tricyclic amitriptyline. As a musician, I did some of the best and most complex arrangements I’ve ever done taking bupropion.

You also have to distinguish between muscarinic anticholinergic activity and antinicotinic activity; they’re very different. For most people, bupropion is not classically anticholinergic, or mildy so at best. It’s frequently prescribed as an alternative to classically anticholinergic drugs.

...

 

 

Fair enough - there are multiple, HUGE differences in the signalling-cascades which these receptors control - there are also some similarities however... For instance, it's well-known that some people benefit tremendously cognitively from nicotine - and using nicotine-gum at the same time as Buproprion actually blocked some of the cognitive deficits. (it did not improve eye-sight however, which was absolutely dreadful at 600 mg - a dosage which was an obvious mistake in hindsight)

 

Another big difference between the nicotinic and muscarinic receptors, is the fact that I found an article a few months back which showed an intriguing connection between schizophrenia, cognitive deficits, and the immune-system - seems like the alpha-7-receptor is involved in modulating the immune system. I'm actually going to post about that soon, because a fellow with dysautonomia seems to have a very specific relationship to choline - might be that since dysautonomia is often involved with autoimmune issues, then perhaps alpha-7-modulation could be the answer for him.

[Kinesis]

Duplicate deleted.

Edited by Kinesis, 15 December 2017 - 04:58 AM.

[Kinesis]

Interesting point, Stink ... as it happens, I occasionally used nicotine gum at the time I was taking bupropion and amitriptyline, and it’s possible it amplified the nootropic effect of the bupropion. Look forward to your post about the cognitive-immune connection...

[Mind_Paralysis]

Interesting point, Stink ... as it happens, I occasionally used nicotine gum at the time I was taking bupropion and amitriptyline, and it’s possible it amplified the nootropic effect of the bupropion. Look forward to your post about the cognitive-immune connection...

 

'Ere we go, mate - data regarding the newly discovered effects of acetylcholine on immune-system regulation! = )

 

 

Modulatory effects of α7 nAChRs on the immune system and its relevance for CNS disorders

https://www.ncbi.nlm...les/PMC4894934/

 

Neuroimmune Interactions in Schizophrenia: Focus on Vagus Nerve Stimulation and Activation of the Alpha-7 Nicotinic Acetylcholine Receptor

https://www.ncbi.nlm...les/PMC5449450/

 

Alpha7 Nicotinic Acetylcholine Receptor Is a Target in Pharmacology and Toxicology

https://www.ncbi.nlm...les/PMC3292018/

 

 

Fairly interesting how one particular sub-receptor of a subset of receptors, can have such an important role. Goes to show how much we need to stop thinking about neurotransmitters doing the same thing all the time... they can have contrary effects in multiple occassions.

[Kinesis]

Interesting point, Stink ... as it happens, I occasionally used nicotine gum at the time I was taking bupropion and amitriptyline, and it’s possible it amplified the nootropic effect of the bupropion. Look forward to your post about the cognitive-immune connection...

'Ere we go, mate - data regarding the newly discovered effects of acetylcholine on immune-system regulation! = )


Modulatory effects of α7 nAChRs on the immune system and its relevance for CNS disorders
https://www.ncbi.nlm...les/PMC4894934/

Neuroimmune Interactions in Schizophrenia: Focus on Vagus Nerve Stimulation and Activation of the Alpha-7 Nicotinic Acetylcholine Receptor
https://www.ncbi.nlm...les/PMC5449450/

Alpha7 Nicotinic Acetylcholine Receptor Is a Target in Pharmacology and Toxicology
https://www.ncbi.nlm...les/PMC3292018/


Fairly interesting how one particular sub-receptor of a subset of receptors, can have such an important role. Goes to show how much we need to stop thinking about neurotransmitters doing the same thing all the time... they can have contrary effects in multiple occassions.

Wow ... thanks. And FWIW I strongly agree. We just don’t know enough to simplistically assume that if we feel X, then we need more/less of neurotransmitter Y. These things act in a complex interconnected web of pathways and don’t necessarily even produce the same effects in different parts of the CNS. Well done.