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Omega 3: DHA / EPA / Acetylcholine - between a cure and increased anxiety

acetylcholine dha epa anxiety

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#1 MattMcFly1986

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Posted 21 November 2016 - 05:57 PM


During the summer I added an Omega 3/6 supplement (EPA: 330 mg, DHA: 220 mg) because I can't eat fish and have been experiencing the following "low Dopamine" symptoms for over a year now:

 

  • brain fog
  • lethargy
  • procrastination
  • easily stressed and irritable
  • limited vocabulary, slow thinking and bad memory

 

I took the supplement thinking it would restore my mental capacity, but it gave me horrible side effects (agitation, worsening brain fog) and by day nine I had my first ever full on panic attack. Turns out Omega 3 boosts acetylcholine and can result in people with already high levels to have panic attacks / develop mental problems. Two days after I stopped it I was back to normal again.
 

Unfortunately, I feel like I do need either DHA or EPA, but which of these doesn't raise acetylcholine? I don't want to go through a second panic attack, but I'd rather supplement with one of these acids (ideally in a vegetarian form - algea). It seems to switch whichever article you read. Some say DHA helps mental functions, some EPA.

 

I tried Wellbutrin 150 mg XR for two months early this fall, helped for exactly one week in the middle (made me super fast and productive), but then it pooped out and only the side effects remained (increased social anxiety, sweating and rage outbursts). I recently switched to Aurorix / Moclobemide (a reversible MAOI / RIMA), but so far it is making me more tired and lethargic. I'd rather not take ADs if the answer is a simple brain supplement, but I don't want to repeat past mistakes.

 



#2 FunkOdyssey

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Posted 21 November 2016 - 09:52 PM

I would suggest that you try pure DHA and pure EPA separately to isolate their effects.  Generally, studies have found EPA at a dose of 1 g daily is optimal for depression while DHA is neutral or harmful.  However, there is some preliminary data suggesting your level of inflammation determines the effect of EPA and DHA on depression, where EPA is more helpful and DHA more harmful if you have more inflammation: https://www.ncbi.nlm...les/PMC4581883/

 

I had the same reaction to wellbutrin except the robotic productivity lasted longer (a couple months).  It really wasn't enjoyable but I got alot done.


Edited by FunkOdyssey, 21 November 2016 - 09:52 PM.

  • Informative x 2

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#3 jack black

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Posted 22 November 2016 - 04:25 AM

not sure of the "low Dopamine" symptoms.

some of those things could conceivably be caused by high dopamine. that would explain the poor response to bupropion.


  • unsure x 1

#4 MattMcFly1986

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Posted 22 November 2016 - 03:36 PM

I would suggest that you try pure DHA and pure EPA separately to isolate their effects.  Generally, studies have found EPA at a dose of 1 g daily is optimal for depression while DHA is neutral or harmful.  However, there is some preliminary data suggesting your level of inflammation determines the effect of EPA and DHA on depression, where EPA is more helpful and DHA more harmful if you have more inflammation: https://www.ncbi.nlm...les/PMC4581883/

 

I had the same reaction to wellbutrin except the robotic productivity lasted longer (a couple months).  It really wasn't enjoyable but I got alot done.

 

And how did you progress since? Have you found something that works for you?

Maybe I should add, though I'm not sure if this is relevant to the brain chemistry debate that I was born 3 1/2 weeks early and wasn't able to drink mother's milk for the first 3 days. Does any of that have an influence on DHA / EPA / Dopamine and other mental developments?

So DHA is the one to be more cautious about? I thought since the brain is mostly built from it that it would be the lesser side effects prone of the two acids.



#5 MattMcFly1986

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Posted 28 November 2016 - 07:40 PM

Bump

Does anybody know? I'm currently stuck in a vicious cycle, on ADs, but the only thing that gives me a quick boost is masturbating to internet porn, which I don't want because it is giving me PIED, which is hurting my relationship. I feel like a minor course correction could put me out of this destructive loop. Not feeling whole, so I'm prone to be self-destructive.


Edited by MattMcFly1986, 28 November 2016 - 07:43 PM.


#6 MattMcFly1986

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Posted 04 December 2016 - 10:33 PM

I'm considering bringing up Acetylcholine at my next doctor's appointment this week. Not sure which would be the best angle to tap the subject. How do I lower it without any other side effects?



#7 jack black

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Posted 05 December 2016 - 02:23 AM

did you see this: http://mindrenewal.us/page13.html

a typical MD practitioner is a decade or longer behind cutting edge info. so, i don't expect any knowledge on this topic.



#8 MattMcFly1986

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Posted 05 December 2016 - 07:49 AM

Wow, save for about four or five, I have all of the 42 listed symptoms. Now if only I knew how to lower Acetylcholine without having to give up a healthy diet and exercise?


Edited by MattMcFly1986, 05 December 2016 - 07:49 AM.


#9 Hyperflux

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Posted 07 December 2016 - 04:54 AM

Wow, save for about four or five, I have all of the 42 listed symptoms. Now if only I knew how to lower Acetylcholine without having to give up a healthy diet and exercise?

 

Consume 'racetams.



#10 MattMcFly1986

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Posted 08 December 2016 - 10:35 AM

Did some research, don't sound safe at all. I did find some posts recommending Nigella Seeds.



#11 KingBrown

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Posted 09 December 2016 - 04:52 AM

Black Cumin (nigella sativa) is an ACHE inhibitor, which is not what you want



#12 MattMcFly1986

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Posted 09 December 2016 - 08:24 AM

It isn't? I thought an ACHE inhibitor lowers Acetylcholine?



#13 KingBrown

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Posted 09 December 2016 - 09:02 AM

It reduces the activity of acetylcholinesterase (AChE), the enzyme that metabolises acetylcholine. So it raises it.

 

Forskolin may help, so have a look in to that.



#14 jack black

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Posted 09 December 2016 - 06:01 PM

 

Forskolin may help, so have a look in to that.

 

why would that help? last time i checked it also reduced the activity of acetylcholinesterase (AChE).

 

besides, by flooding with cAMP, it impairs functioning of PFC and probably will not help the OP: https://www.scienced...70420143324.htm

 

i thought it was only good for weight loss and body building?



#15 KingBrown

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Posted 10 December 2016 - 03:28 AM

limited evidence suggests it accelerates Ach receptor desensitisation - https://www.ncbi.nlm.../pubmed/2425358

 

It may well have an effect on AChE ,which is why it would warrant further investigation as to the net result on ACh activity.

 

 



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#16 KingBrown

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Posted 30 December 2016 - 06:26 AM

Annnnnd here was the actual source of my inspiration for advising that the OP look in to Forskolin...

 

 

Molecular and Cellular Biochemistry
October 2006, Volume 290, Issue 1-2, pp 23-32

Title:
Forskolin, an inducer of cAMP, up-regulates acetylcholinesterase expression and protects against organophosphate exposure in neuro 2A cells

Abstract:
Bioscavenger prophylactic therapy using purified human acetylcholinesterase (AChE) or butylcholinesterase (BChE) is a promising treatment for future protection against chemical warfare nerve agent exposure. Potential immune response due to the complex structure of cholinesterases, mutations, post-translational modifications, and genetic variation is a limiting factor against purified enzyme therapy. We investigated an alternative bioscavenger approach using Forskolin, an inducer of intracellular cyclic AMP (cAMP), which activates AChE promoter and up-regulates its expression. A mouse neuronal cell line, Neuro 2A, was treated with various doses of Forskolin and analysis of the expressed enzyme indicates that the AChE activity was significantly increased in cells exposed to repeated administration of the drug every other day for 7–10 days. Cholinesterase enzyme assays showed that the enzyme activity was increased approximately 2-fold for the extracellular enzyme and 3-fold for the intracellular enzyme. The optimal dose found for extracellular enzyme production was 12–24 μM Forskolin, while the optimal dose for intracellular was 12 μM. In parallel with the rise in the AChE level, the morphology of Forskolin-treated cells showed neurite growth with increasing doses. Forskolin treatment protects Neuro 2A cells from Diisopropylflurophophate (DFP), a surrogate of the organophosphate chemical warfare agents soman and sarin, induced toxicity in Neuro 2A cells. These results indicate that transcriptional inducers, such as Forskolin, can sufficiently up-regulate cellular AChE production and protect cells against organophosphate toxicity.
----------------------------------------------------

 

 

http://www.longecity...5?

 







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