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Anyone else taking Citicoline?

Discussion in 'General Treatment' started by Athene, Feb 4, 2012.

  1. Athene

    Athene Never give up

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    I've just recently started taking Citicoline. It's supposed to improve brain function and also help you sleep better. I'm sleeping better already. I don't know if I am becoming more intelligent yet, it's too early to say.

    Just wondering if anyone else uses it, and what has it done for you?


    Here's the bumf:

    Citicoline [stabilized CDP Choline (cytidine 5diphosphocholine)] is a naturally occurring intermediate involved in the synthesis of phosphatidylcholine, a major constituent of the grey matter of brain tissue (30%).* Citicoline consumption promotes brain metabolism by enhancing the synthesis of acetyl-choline, restoring phospholipid content in the brain and affecting neuronal membrane excitability and osmolarity.*

    Studies suggest that CDP-choline supplements increase dopamine receptor densities,[1] and suggest that CDP-choline supplementation can ameliorate memory impairment caused by environmental conditions.[2] Preliminary research has found that citicoline supplements help improve focus and mental energy and may possibly be useful in the treatment of attention deficit disorder.[3][4] Citicoline has also been shown to elevate ACTH independent of CRH levels and to amplify the release of other HPA axis hormones such as LH, FSH, GH and TSH in response to hypothalamic releasing factors.[5] These effects on HPA hormone levels may be beneficial for some individuals but, may have undesirable effects in those with medical conditions featuring ACTH or cortisol hypersecretion including, but not limited to, PCOS, type II diabetes and major depressive disorder.
  2. beaverfury

    beaverfury beaverfury

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    Hi Athene,

    I've only just read about citicoline. It sounds good. http://www.mindandmuscle.net/forum/4073-cpd-choline-alpha-gpc

    How is it going for you ?
    AFCFS likes this.
  3. Sushi

    Sushi Moderator and Senior Member Albuquerque

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    Athene

    I used to take it, substituting it for phos choline complex in methylation treatment. I was excited after reading about it but actually did not notice any effect.

    There was some discussion with Rich about it a few years ago:

    Citicoline substituted for phosphatidylserine complex – posted November 19, 08

    Lotus97 likes this.
  4. AFCFS

    AFCFS Senior Member

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    Sounds interesting. I would like to see some more long-term use studies on it, for safety and effectiveness, or more anecdotal feedback for use and use over time. I wonder if citicoline's presence in 5-hour ENERGY® tells us anything (e.g. duration of effect)?
  5. beaverfury

    beaverfury beaverfury

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    I went into a decent remission for about two weeks around christmas time, after taking citicoline . I had no pain and no payback after exersize. I was swimming, running, doing weights. Unfortunately it made me massively depressed, which is a problem i havent had since getting cfs.

    I went off it and the pain and PEM came back slowly. This morning i was in so much pain i took more citicoline and the pain subsided within half an hour, so it seems to have a big effect on me.

    My question is... how can i take this stuff and avoid getting taken into a black hole?? Because for me at least it seems to have real benefits of pain relief and energy boosting.

    Should i take less/more, stack it with something that offsets the gloom?Just wondering if the pain relieving effect can be extracted from the depressive effect?

    I have noticed before that during periods of remission from cfs, depression has come back...and in the middle of cfs it actually seems impossible for me to get depressed. ?? Weird. Anyone had this pattern?
    I dont attribute it to anything psychological.

    I think Adreno has tried citicoline and Lansbergen seems to know a bit about acetylcholine. I will try and rope them into the thread.

    I know a theory of a malfunctioning acetylcholine system has been suggested in Gulf War Syndrome.
    And as Sushi said, Rich has discussed its role in methylation
  6. Marco

    Marco Old blackguard

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    Interesting post Athene.

    I've been working on a 'glutamine' hypothesis of ME/CFS which is being 'serialised' on Cort's new site.

    Citicoline also appears to reduce excess glutamate by increasing re-uptake

    beaverfury - your experiences ring a bell with me. My first ME symptoms were relatively mild physically but I had severe depression (new onset). When my physical symptoms got much worse many years ago the depression disappeared pretty much completely and hasn't returned. I have a lot of anxiety instead but not the 'black hole' of depression.

    I can sympathize with your dilemma. Personally I'd try less. Perhaps less gain but also less pain?
  7. beaverfury

    beaverfury beaverfury

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    Hi Marco,

    I enjoyed your Neuroinflammatory article over at Healthrising. Keep them coming!

    The remission or lessening of cfs symptoms/depression switch over is weird. It has happened to me a few times and is very distinct.

    I wouldnt tell a psychologist because they might interperet it as some form of somatic transference or fear of transitioning back into normal life.

    Taking citicoline elicited this response in me a couple of months ago. This morning it took pain away very quickly, and by this afternoon i was starting to feel depressed, so i'm stopping it.

    One could ask 'which is worse'?.. and i would say, the depression from it is very acute and i cant stand it. My suffering from cfs is tied up with its chronic-ness and i manage it somehow.

    I may try a lower dose, or cycling it. I havent heard of anyone getting past an initial period of start up symptoms like you might an antidepressant. I think if i kept taking it for eight weeks it would just be eight weeks of pain free depression. But i dont know.

    Going into some sort of remission is not to be sneezed at, (though i didnt get to be elated), so i want try to find what mechanism of citicoline worked. (I did eliminate other factors and am convinced it was citicoline making the difference). Uridine also brings on depression for me.

    The good news is- if i stay in my pain ridden, energy deficient, brain numb state- i dont get depressed:thumbsup:
  8. lansbergen

    lansbergen Senior Member

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    I remember an UK researcher found choline excess in the brain. One needs 10 times more choline than acetylkcholine to get the same result.

    Levamisole stimulates the nicotine receptors. It has only a small indirect effect on muscarine receptors.

    Levamisole is known as an immune modulator. That it eased the pain within 10 minutes was a suprise. Nobody could explain it.

    I was glad it did so I kept taking it.

    I do not have depression that I know of so I can not comment on that.

    If I were you I would try to figure out the lowest dosis needed for pain relief.
  9. beaverfury

    beaverfury beaverfury

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    Thanks Lansbergen

    I read on wiki that Levamisole also may have an antidepressant effect. I will read a few more of your posts.
    I wonder how you come across levamisole and whether it helps with other me/cfs symptoms?

    Regarding the excess choline in the brain, i dont know what the current research conclusion is. This is an interesting article i keep going back to by Rich Vank , and i guess it explains why i might get depressed on citicoline. http://www.mindandmuscle.net/forum/neuroscience-nootropics/40965-uridine-2.html

    As you probably know, choline comes partly from the diet, and part of it is made in the body. The connection with the methylation cycle is that it is thought that the second largest use of methylation in the body (after the synthesis of creatine, thought to be number one) is the conversion of phosphatidylethanolamine to phosphatidylcholine. Phosphatidylcholine is an important phospholipid, making up the cellular membranes. It is also an important component of bile.

    Some of the phosphatidylcholine is broken down, and the choline used for other purposes. A major one is the synthesis of acetylcholine. Acetylcholine serves as a neurotransmitter in parts of the brain, it serves as the neurotransmitter between the nerves and the muscle cells, and it serves as the neurotransmitter for the parasympathetic nervous system in general.

    In chronic fatigue syndrome, it is my current hypothesis that choline, phosphatidylcholine, and acetylcholine are depleted. I realize that some of the magnetic resonance spectroscopy studies have concluded that choline is elevated in the brain, but I think this conclusion was based on a faulty assumption. In these studies, the ratio of choline to creatine was found to be higher than normal. It was assumed that creatine was unchanged between normal, healthy people and PWCs, so the conclusion was that choline was elevated. However, because of the partial methylation cycle block, I think we should expect that creatine is depleted in CFS, and if it is depleted more than choline is depleted, the ratio would be higher than normal, even though both these substances were depleted.

    I expect that there will be an MRS study coming out soon that will report on absolute measurement of these metabolites, rather than simply ratios, and I expect that it will show that choline and creatine are both below normal in CFS.

    I think that low acetylcholine would explain the results of blood flow studies in the forearm reported by Vance Spence's group at the U. of Dundee a few years ago. I think it can also help to explain why the ratio of sympathetic to parasympathetic nervous system activity in CFS is higher than normal, as shown in heart rate variation studies.

    The assumption of constant creatine has carried over to the use of creatinine ratios in urine testing of various metabolites. The assumption of constant creatine to creatinine conversion rate has justified this practice for compensating for differences in urine dilution by water. Normally this is fine, and the creatinine production correlates with lean muscle mass, but is otherwise a constant. But in CFS, we see drops in 24-hour creatinine excretion in urine, and I think that is consistent with the partial methylation cycle block.

    So that's the situation as I see it in CFS in most cases, and I'm hopeful that it will be borne out by work now underway.

    Now, getting to your case, it sounds as though you have an unusual response to choline supplementation. Elevated acetylcholine in the central nervous system can cause depression. My guess is that your body may overproduce acetylcholine, or it may not be able to break acetylcholine down as rapidly as normal, and one or the other of these may account for the depression on supplementing choline. This sounds like a genetic issue, given the experience of your mother and your son as well. The rate-limiting step in the production of acetylcholine in the neurons of the central nervous system is the transport of choline into the neurons. The breakdown of acetylcholine is accomplished by the cholinesterase enzymes.
    So I suspect that you may have inherited a genetic polymorphism that speeds up the action of the choline transporters, or a genetic polymorphism that slows the action of one of the cholinesterases.

    As to what can be done if the acetylcholine level is too high, you are probably aware of scopolamine, which blocks muscarinic acetylcholine receptors, including in the central nervous system. I don't know if that would help you or not, but it's something to look into.
    Lotus97 likes this.
  10. beaverfury

    beaverfury beaverfury

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    Prohealth had an interesting review article implicating acetylcholine mediated vasodilation in cfs, with some of the Vance Spence research that Rich Van mentioned above http://www.prohealth.com/library/showarticle.cfm?libid=10459

    This article is from 2004 and once again you wonder if me/cfs research is stuck in a perpetual time warp?

    'The research group is therefore confident that the findings of increased sensitivity to acetylcholine in CFS patients are robust and unusual'.
  11. perchance dreamer

    perchance dreamer Senior Member

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    Interesting about citicoline. Amazon and iHerb have lots of positive user reviews for this supplement.

    I'm willing to try it. I had tried Alpha GPC and found it had a really bad effect on my sleep, even taken first thing in the morning.

    After that I tried lecithin, and it also screwed up my sleep even though I took it soon after waking. Unfortunately, a lot of supplements have negative effects on my sleep.
  12. Marco

    Marco Old blackguard

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    Many thanks. I hope you enjoy part 2 which should be up in the next few days.

    The bad news for me is that my hypothesis would have predicted both somatic and 'mood' symptoms would improve if the 'neuroinflammation' was treated. My bad but given my own experiences I should have realised there was a contradiction.

    I honestly don't know which is worse. At least at the stage that I had depressive symptoms I was able to function (full time work, holidays and able to tolerate most light manual work).

    It would be a little trite to suggest 'masked depression'. For me the depressive symptoms were so deep and overwhelming that I doubt that any physical symptoms could 'mask' that feeling.

    I'll stick my neck out and suggest that the depressive symptoms may be a form of 'ME - lite' and that the transition from mainly physical symptoms to 'mood' symptoms may be a sign of a step in the right direction. Pure speculation of course but optimistic speculation.

    Actually I just remembered that the wiki page suggests that it can cause problems in those with prior depressive symptoms. That being the case I'm not convinced its the way to go.

    Worth persevering with? Only you can be the judge of that I'm afraid.
  13. lansbergen

    lansbergen Senior Member

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    Beaverfury are you talking about my case? If so you must confuse me with somebody else.

    My working hypothese at the moment is something blocks or inhibits the a7nAchR's. That something is produced by the cellmachenery which is hyjacked by an infectious agent for is own purpose.
  14. Lotus97

    Lotus97 Senior Member

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    I was checking out the customer reviews at iHerb and Citicoline did get a lot of positive reviews, but there were also a couple other people saying that it caused a bad mood. I was reading that Huperzine works similar to SSRIs except that instead of serotonin it works on acetylcholine. This person was saying that if you take Huperzine with supplements that increase acetylcholine it could cause an excess of acetylcholine which might increase brain fog. I suspect this would vary a lot between individuals and some people might need both Huperzine and other supplements to raise acetylcholine. I've seen some companies selling Alpha GPC and Phosphatidyl Serine together. Perhaps some of these supplements work better taken together, but it could also be entirely arbitrary. DMAE is a precursor to choline which is needed for the brain to acetylcholine, but I'm not sure if it's better to just take choline. Phosphatidylserine and choline stimulate the BHMT pathway which might be good, but too much could cause an increase in norepinephrine leading to overstimulation in some people.
  15. beaverfury

    beaverfury beaverfury

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    Yeah, Sorry, I'm all over the place.

    I have read your posts but the science part of my brain is too miniscule to comprehend anything but a basic outline.

    I'm just trying to understand acetylcholines role in muscle pain, simply because citicoline definitely helps me in that regard.
  16. beaverfury

    beaverfury beaverfury

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    That's what i'm telling myself too:)
  17. garcia

    garcia Aristocrat Extraordinaire

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    Just a warning to anyone thinking of trying levamisole. It also stimulates the NMDA receptors, which is exactly the effect we don't want in ME:

    "The rationale for selecting levamisole as an adulterant is unclear, but is likely related to the fact that it shares some physico-chemical properties with cocaine and potentiates the activity of dopaminergic (D2) and NMDA receptors in brain thus enhancing its effects."
    https://ash.confex.com/ash/2010/webprogram/Paper30806.html
  18. lansbergen

    lansbergen Senior Member

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    Levamisole does many things and the core mechanisme is still not known.

    My first question is why do people use cocaine in the first place.

    I do not take supplements and/or use other meds other than sometimes paracetemol and/or tantum creme because of possible interactions.

    Levamisole is not for everybody but I disagree about the NMDA receptors. I want them to be stimulated. I want a good memory and good synaptic plastcity,

    The NMDA receptors need double stimulation. Glutamate binding and d-serine or glycine binding to the allostric site.

    http://en.wikipedia.org/wiki/NMDA_receptor

    The NMDA receptor (NMDAR), a glutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function.[2]
    The NMDAR is a specific type of ionotropic glutamate receptor. NMDA (N-methyl-D-aspartate) is the name of a selective agonist that binds to NMDA receptors but not to other glutamate receptors. Activation of NMDA receptors results in the opening of an ion channel that is nonselective to cations with an equilibrium potential near 0 mV. A property of the NMDA receptor is its voltage-dependent activation, a result of ion channel block by extracellular Mg2+ ions. This allows the flow of Na+ and small amounts of Ca2+ ions into the cell and K+ out of the cell to be voltage-dependent.[3][4][5][6]
    Calcium flux through NMDARs is thought to be critical in synaptic plasticity, a cellular mechanism for learning and memory. The NMDA receptor is distinct in two ways: first, it is both ligand-gated and voltage-dependent; second, it requires co-activation by two ligands: glutamate and either d-serine or glycine.[7]
  19. garcia

    garcia Aristocrat Extraordinaire

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    The problem is that people with ME have already overstimulated NMDA receptors. Stimulating them more is potentially dangerous. We know that decreased mitochondrial function / cellular energy is a core component of ME. When cellular energy goes down in the brain, one of the first things that happens is that the cellular glutamate pumps stop working (since they are energetically very expensive). As a result extracellular glutamate levels rise, and perpetually stimulate NMDA receptors. The classic symptom of this in ME patients is hyper-responsiveness to outside stimuli, which many patients (including myself) get.

    Given that overstimulated NMDA receptors are part of the core pathophysiology of ME, I think it is sensible to avoid taking substances which directly stimulate NMDA receptors further.
  20. Marco

    Marco Old blackguard

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    Garcia. Not that I disagree with these statements but what are you basing them on?

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