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  1. #1
    Senior Member noos's Avatar
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    which is the half life and solubility of DMAE? I searrched (google, rxlist, pubmed, etc) and could not find it



    only a PDF:

    DMAE acid malate (Cerebrol) (94158-52-8) was readily absorbed by healthy adults. Peak

    plasma concentrations were attained after 30 minutes. Thirty-nine percent of the dose was

    eliminated in the urine within 48 hours (half-life = 3.5 hour; mean transit time = 5.75 hours).-I donīt get this: 3.5hs but 39% in48hs?...oh I see, total dose


    “The peak plasma level and area under the plasma concentration-time curve of [DMAE] were

    greater than those of” DMAE aceglumate (3342-61-8) (Bismut et al., 1986) [French]



    ScottL posted some quite good URLs for drug info but I canīt find them now ,care to repost or PM please?



    Thanks

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    Noos,



    FYI:



    many people especially on this board do not like DMAE at all.



    Lifemirage on the other board prefers centro...centro...whatever it is called as a better source of DMAE
    <span style="color:#FF0000"><span style="font-family:Arial Black">THEORY=/REAL WORLD</span></span>

  3. #3
    Senior Member noos's Avatar
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    Thanks ScottL.



    I am more interested in DMAE as a stimulant than as a choline source.

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    I've rediscovered it.



    At the moment quite likeing it.



    DMAE may cause problems because it steals methyl groups (so I have read) and as such can promote homocysteine.



    I consume it with TMG. In theory, the two together should have some sort of symbiosis in the production of acetyl choline and in brain function. Also take this with Phosphatidyl Serine.
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    Senior Member noos's Avatar
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    I think nobody knows how DMAE works.

    If you search medline you will find articles that say it is a ACH increaser and the opposite. In general there is doubt that it promotes ACH in the brain.



    What I do not see is an explanation for its stimulant effect if it snot a cholinergic.



    Now that you mention methylation I remembered reading DMAE is a methyl donor:

    http://www.google.com/search?hl=en&q=DMAE+methyl+donor



    However I also remembered someone refering to ACH as a tetramethyl, so dimethylaminoethanol would need to add a methyl and not donor it to convert to ACH.



    I looked up in the wikipedia:



    DMAE

    (CH3)2NCH2CH2OH

    2-(dimethylamino)ethanol



    ACH

    CH3COOCH2CH2N+(CH3)3

    2-(acetyloxy)-N,N,N-trimethylethanaminium



    Also, I read different opinions on how to take DAME. Some vendors recommend to take it in the morning due to its stimulant effect and other at night (maybe the reason was that it is slow to process or that ACH helps with sleep I am not sure).



    I would like to know if someone uses DMAE at night.



    Thanks

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    [quote name='noos' date='Aug 12 2005, 11:41 AM']which is the half life and solubility of DMAE? I searrched (google, rxlist, pubmed, etc) and could not find it



    only a PDF:

    DMAE acid malate (Cerebrol) (94158-52-8) was readily absorbed by healthy adults. Peak

    plasma concentrations were attained after 30 minutes. Thirty-nine percent of the dose was

    eliminated in the urine within 48 hours (half-life = 3.5 hour; mean transit time = 5.75 hours).-I donīt get this: 3.5hs but 39% in48hs?...oh I see, total dose


    “The peak plasma level and area under the plasma concentration-time curve of [DMAE] were

    greater than those of” DMAE aceglumate (3342-61-8) (Bismut et al., 1986) [French]



    ScottL posted some quite good URLs for drug info but I canīt find them now ,care to repost or PM please?



    Thanks

    [snapback]263682[/snapback]

    [/quote]



    DMAE is usually found as the bitartrate salt, which is pretty water soluble. Twinlabs DMAE liquid is 50mg/ml. Pure DMAE is a caustic and slightly water soluble liquid that readily forms salts with many acids.

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    Noos if you haven't read it:



    http://www.bulknutrition.com/?ingredients_id=46



    Not to sound immodest, but relative to most of the so-called DMAE experts, I've actually read all of the stuff out there and not just cherry-picked the research that supports my side. And, I at least have a clue about how scientific methodology works: uncontrolled studies from the 70's can be all but ignored. But, it looks like you've already caught on.



    I don't see why people think DMAE is a stimulant. Even though there is (fairly weak) evidence it helps hyperactive kids, that certainly doesn't mean it's a stimulant. Drowsiness and such have certainly been reported a lot more in the literature than the reverse. Indeed, give a kid a sedative, he'll probably stop acting less hyperactive.
    -David Tolson
    My articles

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    So does it promote ACH or not?



    I was under the impression that this much was known.



    Yes, Choline is tetra methyl glycine. I also read (not a study though) that DMAE causes a rise in homo-cysteine but now I am wondering if this was based on the theory that an extra 2 methyl grups woud be needed to make ACH out of DMAE.



    HOWEVER, this is why I suggest taking TMG (Tri-Methyl Glycine) with it. If DMAE does indeed take methyl donors from the pool, it will ultimately lead to problems i.e. potentially depleting SAMe and other methylation processes. This could explain why in some people it produces opposite effects - the presence of other nutrient availability being dfferent? To me, it does exactly what it says it does - promotes tooth grinding at night, increases concentration, and I find it stimulating.



    Only the tooth grinding aspect was when I first took it. Now I find this has stopped, and it has occured that the TMG might be involved, but of course many factors may be present.



    I was waking up with jaw and face pain so it seems pretty clear it did this originally.



    Could you post any data you know?
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    Effect of dimethylaminoethanol, an inhibitor of betaine production, on the disposition of choline in the rat kidney.



    Lohr J, Acara M.



    Department of Medicine, Veteran's Administration Medical Center, Buffalo, New York.



    The choline metabolite betaine has been shown to be an important organic osmoregulatory solute in the kidney. The isolated perfused rat kidney and kidney slice incubations were used to investigate the effect of 2-dimethylaminoethanol (DMAE), a choline oxidase inhibitor, on the renal excretion and metabolism of choline. In the isolated perfused kidney, [14C]choline, at an initial perfusate concentration of 300 microM, was effectively removed from the perfusate over 25 min, with nearly all the 14C in the perfusate accounted for by betaine during the remainder of the 90-min perfusion. DMAE at concentrations of 3.0 or 5.0 mM significantly decreased the rate of removal of [14C]choline from the perfusate and the rate of addition of [14C]betaine to the perfusate, yet [14C]betaine remained the only metabolite of choline in perfusate and urine. In kidney tissue slice experiments, conversion of [14C]choline to [14C]betaine was found in cortical, outer medullary and inner medullary regions of rat kidney. DMAE at 5.0 mM significantly inhibited [14C]betaine production in each of the three regions studied. These data show that DMAE is an effective inhibitor of betaine production by the kidney and, as such, may be an important agent for the study of osmoregulation by the kidney.



    PMID: 2405150 [PubMed - indexed for MEDLINE]


    2 points:



    2-dimethylaminoethanol, , a choline oxidase inhibitor



    and DMAE is an effective inhibitor of betaine production by the kidney.



    I dont know how this relates to the brain, but what I have read so far is that



    "Dimethylaminoethanol (DMAE), a competitive inhibitor of choline transport, elicited dysmorphology beginning at the mid-blastula stage, with anomalies beginning progressively later as the concentration of DMAE was lowered. Pretreatment, cotreatment, or delayed treatment with acetylcholine or choline prevented the adverse effects of DMAE. Because acetylcholine was protective at a lower threshold, the DMAE-induced defects were most likely mediated by its effects on acetylcholine synthesis"



    although that is on Sea Urchins!



    http://ehp.niehs.nih.gov/members/2003/6429/6429.htm



    The above quote assumes harmful consequences on DMAE in large concentrtion on the growth of sea urchin, through the impact on acetyl choline. It assumes that because adding the acetyl choline reduced this impact, that the effect was caused by the depletion of ACh in some way. But could it have been down to methyl depletion? If as the first of the two quotes says - DMAE inhibits TMG production, then the addition of choline may eliminate that problem (by donating methyl groups rather than boosting ACh). It may be that DMAE triggers the brain to make ACh, and not use ACh already available, pulling methyls away for each, from other critical processes?



    The developmental problems which the second quoted source also says have been documented in mammals given DMAe, would be anticipated by this - they were neural tube defects!



    Those are normally prevented by another methyl donor - folic acid. I recall that methyl donors are important in other aspects of development, but I assume that this is less to do with ACh production than effects on other processes such as DNA methylation because Folic Acid is far too small in dose to appreciably effect ACh anyway.
    ------



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    [quote name='noos' date='Sep 13 2005, 08:10 AM']I think nobody knows how DMAE works.

    If you search medline you will find articles that say it is a ACH increaser and the opposite. In general there is doubt that it promotes ACH in the brain.



    What I do not see is an explanation for its stimulant effect if it snot a cholinergic.



    Now that you mention methylation I remembered reading DMAE is a methyl donor:

    http://www.google.com/search?hl=en&q=DMAE+methyl+donor



    However I also remembered someone refering to ACH as a tetramethyl, so dimethylaminoethanol would need to add a methyl and not donor it to convert to ACH.



    I looked up in the wikipedia:



    DMAE

    (CH3)2NCH2CH2OH

    2-(dimethylamino)ethanol



    ACH

    CH3COOCH2CH2N+(CH3)3

    2-(acetyloxy)-N,N,N-trimethylethanaminium



    Also, I read different opinions on how to take DAME. Some vendors recommend to take it in the morning due to its stimulant effect and other at night (maybe the reason was that it is slow to process or that ACH helps with sleep I am not sure).



    I would like to know if someone uses DMAE at night.



    Thanks

    [snapback]269709[/snapback]

    [/quote]





    I take it in the morning.



    On the sleep angle, apparently ACh levels need to be low at night - cant remember now where I read that, but the researchers were reported as quite adament about that.



    So perhaps it is more of a regulator if it helps with sleep, rather than an ACh maker.



    It seems rather muddy these waters.
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    If, and its a big if, DMAE functions the way I summise, and I still know little of it, then the fact that it appears to:



    a - Induce Nueral tube defects in mammals



    b - deplete TMG levels,



    Indicates that it is leaving cellulaar systems undermethylated, potentially leading to reduction in DNA methylation - perhaps the method by which the neural tube defects are induced, and which involves low SAMe (it appears to but the jury remains out that this is how folic acid works to block neural tube defects), then it would follow that DMAE without methyl donors would also induce cancer risks:



    Epidemiologic studies have shown that diminished folate status is associated with colorectal, lung, esophageal, brain, cervical and breast cancers. Data supporting the effect of folate status on carcinogenesis are most compelling for colorectal cancer. The mechanism of the possible anticarcinogenic activity of folate is not well understood. Folate deficiency may induce DNA hypomethylation and gene "unsilencing." Folate is critical for the synthesis of the transmethylating agent S-adenosylmethione (SAMe). SAMe methylates certain bases in DNA leading to gene silencing. Gene "unsilencing" alters gene expression and can disrupt the integrity of the genome. DNA hypomethylation appears to be an early, and consistent event in carcinogenesis, including that of colorectal cancer. Folate deficiency may lead to increased uracil incorporation in DNA. Folate is critical for the formation of thymidylic acid from deoxyuridylic acid. Increased uracil incorporation in DNA can lead to disruption of the integrity of DNA. Folate deficiency may also result in diminished DNA repair, impaired natural killer cell surveillance, secondary choline deficiency, decreased stimulation of T lymphocytes by phytohemagglutinin and activation of tumorigenic viruses. A recent report demonstrated that folate deficiency produced progressive DNA strand breaks in the highly conserved region of the p53 tumor-suppressor gene in rat colon.


    ------



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    These dudes seem to think the same thing - dont know how accurate their work is though:



    DMAE passes the blood-brain barrier and converts to choline in the brain. Therefore it has cholinergic action & enhances formation of acetylcholine. As a result DMAE is generally very useful in treatment of high dopamine (low histamine, overmethylated) persons, but can seriously harm low dopamine, high histamine, undermethylated persons. We've seen more than 1,500 bipolar patients and confirmed that DMAE is generally effective for the overmethylated phenotype (25% of bipolar cases), but causes great worsening for those who are undermethylated (40% of bipolar cases). DMAE definitely should not be used indiscriminately for persons with serious mental illness.* (Aug 15, 2003)






    From http://www.alternativementalhealth.c...cles/walsh.htm
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  13. #13
    Senior Member noos's Avatar
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    >I don't see why people think DMAE is a stimulant.



    People do not "think" it is a stimulant, they just take it and FEEL stimulation (after a few days), at least in some cases.



    But yes, people can report very different effects (through the years of reading in forums)

    *enhanced dreams

    *enhanced daydreaming

    *less anxiety

    *more anxiety

    *headaches, muscle tension

    *more concentration

    *poorer concentration

    *elevates MAO

    *MAO inhibition

    *more ACH

    *less ACH

    etc.



    :-)

  14. #14
    Senior Member noos's Avatar
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    > apparently ACh levels need to be low at night



    I donīt think that can be true for _all_ sleep phases. During sleep there is memory consolidation and you need ACH for that, but yes I think I read what you mention here n this forum.



    Maybe they mean that ACH removal is needed and everytime high levels are not covenient (like inhibiting ach-esterase is not good)?.



    Honestly I feel like playing with words because this is so difficult.



    edit:

    Two-stage models of memory consolidation rest on observations that the integrity of hippocampal circuitry is necessary for the maintenance of recent memories but is no longer necessary for older, presumably better consolidated memories



    Slow-wave sleep, acetylcholine, and memory consolidation

    Ann E. Power

    http://www.pnas.org/cgi/content/full/101/7/1795

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    From the Bulknutrition link -



    they say that "it is unwise to use DMAE without a protective choline supplement."



    Seems wrong. If they say also that DMAE -





    "competitively inhibits choline kinase and choline oxidase, preventing the metabolism of choline to phosphocholine and betaine [10-12]."



    and thus resulting in the 'illusion' of choline increases, then adding choline will not have the desired effect. Adding betaine should maybe have the effect. TMG also converts to choline in the liver.



    Perhaps it could be that the choline they detect is not all originated from choline that was already there? Perhaps some has been swapped from DMAE sources?



    It strikes me that theres a lot more going on. If you eat fish, you get - choline, TMG, and DMAE in the same package. How about that?



    Strikes me that oily fish never did anything but good, and we see all those agents together, in appreciable doses.



    The effects of DMAE in 'competively inhibiting' various enzymes, might be for other reasons - the body may 'pressume' that other agents are present (such as TMG/Choline) whenever DMAE is present. It normally would be, just as it also expects combinations of amino acids (and they share transport and processing systems/enzymes), so there could be interaction between various enzymes. Perhaps the body assumes that TMG conversion from Choline is not needed, and wishes to spare it?



    Those enzymes might also be used to donate methyl groups, I would hazzard, to other agents, especially in the conversion of choline to TMG. It wouldn't strip its own Choline supply to make TMG, if it can take the methyl directly for something else. Perhaps it assumes that it can get the methyls from an expected TMG consumption along with the DMAE?



    Just some thoughts....
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  16. #16
    Senior Member noos's Avatar
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    ATB I think the cite 10-12 is in regard to what happens in the liver not the brain, but I will have to check



    There is one Brazilian study that showed that DMAE does not raise AVH in the brain which I think is also cited there.

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