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Thread: Uridine

  1. #21
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    Quote Originally Posted by rwac View Post
    It makes me sleepy, not entirely sure why.
    You likely have issues within the methylation cycle. When I first started taking methylation supps they made me extremely tired, I'd have to lay down for a power nap. Although the material below maybe slightly different in regard to qualitative experience it still points to a dysregulated methylation cycle. Quoted material from Rich van K: Choline sensitivity & Methylation

    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.

    All the king's horses and all the king's men...

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    Just received this stuff, i do megadose fish oil tough but no of the normal choline sources, do take galantamine and megadoses of alcar (wich kinda acts like a choline source too).

    I would be suprised id even get more benefits out of my regime but we shall see
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    Time for some reports:
    I cannot vouch for uridine or GPC, however I can vouch for citicoline.

    Somehow the combination of tyrosine, malic acid, and citicoline has such a momumental effect on my brain. I literealy have to say it feels like I have gained a 30 point boost in IQ. I have a lot of psychological/cognitive problems, and I have always felt shackled within my own mind so to speak. Endless desire to learn, novel ideas - no energy or cognitive endurance whatsoever to do so. Suddenly... I CAN with this stuff.

    The bad side - It really wears on your endocrine system. It has some effects on Cortisol releasing factor within the brain, and that is contraindicated with people who have adrenal fatigue, diabetes, or anxiety disorders, heart conditions, the like etc, etc.

    I also feel like the day after I have used citicoline, that I am coming down from doing a full blown street drug... And I have a near migraine level headache.

    I believe it goes well with the 30 + GRAMS of fish oil I take.

    I have often wondered if my body just runs out of choline, and that perhaps that has to do with the issues of the citicoline. Alas, given the overwhelming beneficial properties of this substance to increase function in the logical frontal cortex part of my brain - that I must reverse engineer this stuff.

    I have taken other cognitive enhancing supplements. herbs, but they all were much more left brained -borderline manic/acid trip sorts of experiences.
    I am so loving the right brainededness of the citicoline. Is that a scientific term lol?
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    More anecdotal reports:
    I recently started a new regimen. To start my day I take 500mg ALCAR on an empty stomach upon waking with my multivitamin drink (containing 1g of Vit C, Vitamin B3 (Niacinamide), Vitamin B6 (Pyridoxine), Vitamin B12 (Hydroxycobalamin) among others. I've also been taking 50mg Triacetyluridine (TAU; fat soluble) with Fish Oil (providing 400mg DHA) both with breakfast. At that time I also take 4,000 IU Vitamin D3 & 50mcg Vitamin K2, and a different multivitamin drink containing Vitamin A & E, Calcium, Magnesium among others. Mid-afternoon I take another 500mg ALCAR w/ 1.5g piracetam.

    I think I've discovered something most remarkable during my new regimen. I started noticing improved mood after the second day taking uridine/DHA and the rest. Now a week in and I am shocked to report that I am experiencing a very noticeable reduction in my OCD tendencies. For those that don't know, Obsessive-Compulsive Disorder, OCD, is an anxiety disorder and is characterized by recurrent, unwanted thoughts (obsessions) and/or repetitive behaviors (compulsions). My version of OCD is not an extreme case by any means. But I did suffer from feeling the need to check things repeatedly. And obsess over a certain concept and sometimes feel that is the only thing I wanted to talk about (potentially annoying to others let me assure you). I am an avid researcher and can get overly consumed by it at times. So anyway long story short I noticed I am not overcome with the urge to go back and re-visit websites or think about matters to the point it distracts me from work etc. And I'm curious as to just what in my new regimen could be playing a role, if any! I haven't read too much into uridine specifically being used for OCD but on a basic level it has been assumed that serotonin levels may play a role. The B-vitamins I have been taking (read: high quality vitamers ensuring high bioavailability i.e. hydroxocobalamin for B12) could certainly be playing a role: Vitamin B-3, or niacin, increases tryptophan, an amino acid, which is a precursor in producing serotonin, the Linus Pauling Institute notes. Vitamin B-6, or pyridoxine, also aids in serotonin and norepinephrine production. These chemicals are significant in calming mood and obsessive thoughts. Also uridine seems to help ease depression and from that article worth noting:

    "If you think of the times when you've been sad or not feeling well, your brain doesn't feel like it has a lot of energy," Renshaw said. "There's a tremendous focus on creatine as an athletic supplement, but it turns out it's not only skeletal muscle that uses creatine to create energy, but also the brain."
    Kondo said for some patients with bipolar illness, "We're actually treating people with uridine on its own."
    "We're reducing depressive symptoms by at least 50 percent within a couple of weeks," Renshaw said. "The two things that are remarkable, is one: it's a very large effect; and two: it's happening very quickly."

    Since it was mentioned in the article, creatine has been of interest to me as well (study). PQQ too. But, getting back on track, my current regimen is working very very well. I am experiencing less mood shifts. Example, the other day I was getting groceries and I did a terrible job of organizing the ingredients in what was a long list. So it became frustrating to have to look over the list again and again (I didn't have a pen) and the weather was terrible and it was taking much too long and I was going to be late getting back home to get to bed etc. and normally I would get SO flustered over something like this but for some reason I was still able to brush it off! Not a desirable situation at all but it didn't bug me in the usual ways. Also before going to bed I am notorious for thinking about things obsessively before sleep but I was able to just let them go for the most part. I feel that I am happier overall since starting this. Keep in mind I have not been clinically depressed at any point prior to this new regimen but I just feel ... great! Clear head. I feel less narrowly focused and am smiling more! It's hard to put into words even. It's not a manic euphoria or anything like that lol.. it's almost like a feeling of optimism? Haha hard to describe.

    Piracetam and ALCAR seem to combine in a different way than when I was taking Choline citrate and then later Alpha GPC (which I only took for GH support for exercise). I added ALCAR at the same time I started uridine combo. Although rare, piracetam had the tendency to make me feel a bit hypomanic at times. Overly talkative, euphoric, go! go! go! yet all of a sudden do a 180 make me feel relaxed to the point of slumber if I let it. To put it another way: sleep was never an issue haha. Additionally, piracetam unfortunately would make my OCD worse. I was invigorated by it but nevertheless a lot of that brainpower would go to waste, essentially. ALCAR and I suspect uridine and "co-factors", due to the positive indications in bipolar disorder, has evened it out. Verbal fluency is still enjoyed from piracetam but it just feels "cleaner" .. eh hard to describe again. But it's not a bad thing. It's a smooth combination. No headaches, no sleepiness yet no issues falling asleep, and also waking up feeling well rested (even if I happen to only catch 6 or 7 hours instead of my solid 8). Another quick thing I'll mention is that I am now able to read and listen to music at the same time. Don't laugh at me hear me out! I never understood how people could listen to music while reading or attending to other things. I would get so distracted by this. But just tonight I was listening to music and decided, while listening, to research an issue real quick but it ended up requiring more reading that initially thought. But I never had to turn off the music and I was able to do both at once. For the first time ever. I know it's odd. But at least you should see that I notice the little things too. Kind of like how when I took piracetam for a bit I'd notice that my typing abilities were much improved. I would backspace much less and type with much more efficiency. You can roll your eyes all you want but you'll just have to believe me lol...

    I want to thank Mr Happy for shamelessly plugging uridine as the solution to all that ails us ( ) and bringing it to my attention because, well ... I think this is actually working . And the reduced OCD tendencies have made me more productive. I am less distracted and feel my well-being is enhanced. Granted, this could all be placebo. But I have always been able to pay close attention to my body and there is something different. Something positive from this. Hopefully others can share more of their experiences as we go.

    So far the biggest shocker here has not been the antidepressant effects (although welcome) from a mere 50mg TAU taken orally (when clinical trials would use in excess of 6 grams!). It has been the reduction of obsessive thoughts. I was not expecting this in the least. It has been too noticeable to ignore.
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    I'm not noticing the same benefits as you are and I have similar problems. I'm using uridine/tau, citicoline and omega-3, and one cap of oxiracetam. Yesterday it seemed things were getting better but as usual everything bad came back again today. Really sucks, I often feel like I'm wasting my time and money with these matters, and that there are no conceivable answers for me, and I'll be stuck in a pit of depravity for my entire life. But for now I'll keep my head up and keep looking for the answers. hopefully this ends up being beneficial, I just think I'm really figuratively at the end of my rope here.... unfortunately. Glad it's working out for you though.

    I've been using 300mg UMP bid sublingually (total 600mg) + 75mg TAU (split 3 25mg doses) and feel good....focused, improved clarity and feel on top of my game...definite improvement. And waking up at 4am every morning wide awake and good to go while before would drag myself out of bed at 5:30am.
    Damn almost been up 24 hours trying to finish this paper due in less than 24 hours. I've been drinking relentless energy drink, had 350mg modalert, at least 200 mg TAU, b comples, 750 mg CDP Choline, 2000mg DHA, a few liters of water. Mealwise in these 24 hours? 1 burger :/
    Somethings killing my apetitite. But i can't believe im still productive. I only had 4 hours of sleep. This can't be good for my health.
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    Depression:
    Depression, bipolar disorder treated by natural substances - WDAM TV - Channel 7 - Hattiesburg and Mississippi News
    http://cds.ismrm.org/ismrm-2004/Files/001482.pdf
    Mary Ann Liebert, Inc. - Journal of Child and Adolescent Psychopharmacology - 21(2):171
    Just wanted to add my experience to this thread. I'm bipolar II, mostly depressed although ahve been feeling pretty good the last two months due to increased exercise and DHEA, but still having some trouble with mood, insomnia, and some obsessive-compulsive tendencies (and a lot of mental "chatter", which also correllates to hypomanias or mixed states).

    Maybe this is just placebo effect but i'm on second day of 25mg triacetyluridine 3x a day, along with 1250mg of DHA (and 2000mg EPA), along with my regular meds and supplements, but I feel a noticable reduction in obsessiveness and reduction in level of mental chatter. I have been having insomnia issues but slept a little bit better last night...most noticable thing was the reduction in chatter and obsessive/compulsive thinking behavior. Again may be placebo but wanted to add my experience. I will update as things go along. Also mood feels stable and "normal". Was just prescribed a SSRI a few days ago but haven't gotten it filled yet...in just two days i'm reevaluating the need for it after addition of Triacetyluridine

    How are the other people trying TAU doing? Can you post updates?
    One
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  7. #27
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    My update is that TAU @ 100mg w/ food ONCE per day in the AM works all day and keeps moods stable and "normal" as you said. It's so hard to describe because when someone says they feel "good" the inclination is to think "euphoria" and it's not like that. But I just feel good is all I can say. After some experimenting and self-evaluation I came to find that after running off of a lower amount of sleep and working overnight shift and then coming home in the morning and staying up until noon or past that will enduce a hypomanic state. I will think of some of the funniest things and I swear my creative abilities go through the roof. But I recognize that its not healthy. My father is bipolar. I was diagnosed as bipolar but I've been diagnosed with a lot of things in my teens. The bipolar was because of my unstable emotions after going on a benzo binge and adderall that the doctor didn't know about etc. It was impossible for him to give me an accurate diagnosis. I have never ever been truly manic or severely depressed. But I feel that racetams can induce hypomania on occasion and lack of sleep can induce it like clockwork. This returned a few days ago after I ran out of TAU for a few days while waiting for my order to arrive. I started back in yesterday and after my 100mg dose I feel right as rain again. I feel that I could fall under the label of Cyclothymia "similar to bipolar II disorder in that it presents itself in signature hypomanic episodes. Because hypomania is often associated with exceptionally creative, outgoing, and high-functioning behavior, both conditions are often undiagnosed." I never have the deep depression but there are other symptoms of the down cycle. Maybe this is why I respond so well to uridine? I dunno. But I am going to continue to take it because I think its amazing and I don't feel like I'm "on" something either. It's a beautiful thing. And like I said before it also seems to help with sleep in some way and reduced my OCD tendencies. It allows me to settle down and focus on things better. All I can say is wow. I cannot believe a cheap supplement has this much power!
    Choline + Uridine: Build New Neurons and Protect Against Alzheimer's! |*Smart Publications

    Combined uridine and choline administration improves cognitive deficits in spontaneously hypertensive rats
    N.M.W.J De Bruin , 1, , A.J Kiliaan2, M.C De Wilde, L.M Broersen


    Purchase
    Numico Research B.V., Department of Condition and Disease Specific Research (CDSR)/Neuroendocrinology section, Bosrandweg 20, 6704 PH Wageningen, PO Box 7005, 6700 CA Wageningen, The Netherlands
    Available online 11 April 2003.

    Abstract
    Rationale. Hypertension is considered a risk factor for the development of cognitive disorders, because of its negative effects on cerebral vasculature and blood flow. Genetically induced hypertension in rats has been associated with a range of cognitive impairments. Therefore, spontaneously hypertensive rats (SHR) can potentially be used as a model for cognitive deficits in human subjects. Consecutively, it can be determined whether certain food components can improve cognition in these rats. Objective. The present study aimed to determine whether SHR display specific deficits in attention, learning, and memory function. Additionally, effects of chronic uridine and choline administration were studied. Methods. 5–7 months old SHR were compared with normotensive Wistar–Kyoto (WKY) and Sprague–Dawley (SD) rats. (a) The operant delayed non-matching-to-position (DNMTP) test was used to study short-term memory function. (b) The five-choice serial reaction time (5-CSRT) task was used to assess selective visual attention processes. (c) Finally, the Morris water maze (MWM) acquisition was used as a measure for spatial learning and mnemonic capabilities. Results. (1) SHR exhibited significantly impaired performance in the 5-CSRT test in comparison with the two other rat strains. Both the SHR and WKY showed deficits in spatial learning when compared with the SD rats. (2) Uridine and choline supplementation normalized performance of SHR in the 5-CSRT test. (3) In addition, uridine and choline treatment improved MWM acquisition in both WKY and SHR rats. Conclusion. The present results show that the SHR have a deficiency in visual selective attention and spatial learning. Therefore, the SHR may provide an interesting model in the screening of substances with therapeutic potential for treatment of cognitive disorders. A combination of uridine and choline administration improved selective attention and spatial learning in SHR.

    Keywords: 5-Choice serial reaction time (5-CSRT); Choline; Delayed non-matching to position (DNMTP); Morris water maze; Open-field; Rats; Selective attention; Spatial learning; Spontaneously hypertensive rats (SHR); Uridine; Uridine-5-monophosphate-2Na (UMP); Memory
    Citicoline enhances frontal lobe bioenergetics as measured by phosphorus magnetic resonance spectroscopy M. M. Silveri 1 2 3 *, J. Dikan 1, A. J. Ross 1 2 3, J. E. Jensen 2 3, T. Kamiya 4, Y. Kawada 4, P. F. Renshaw 2 3, D. A. Yurgelun-Todd 1 2 31Cognitive Neuroimaging Laboratory, McLean Hospital, Belmont, MA, USA
    2Brain Imaging Center, McLean Hospital, Belmont, MA, USA
    3Department of Psychiatry, Harvard Medical School, Boston, MA, USA
    4Healthcare Products Development Center, Kyowa Hakko Kogyo Co., Ltd, Tsukuba, Ibaraki, Japan

    AbstractCiticoline supplementation has been used to ameliorate memory disturbances in older people and those with Alzheimer's disease. This study used MRS to characterize the effects of citicoline on high-energy phosphate metabolites and constituents of membrane synthesis in the frontal lobe. Phosphorus (31P) metabolite data were acquired using a three-dimensional chemical-shift imaging protocol at 4 T from 16 healthy men and women (mean ± SD age 47.3 ± 5.4 years) who orally self-administered 500 mg or 2000 mg Cognizin® Citicoline (Kyowa Hakko Kogyo Co., Ltd, Ibaraki, Japan) for 6 weeks. Individual 31P metabolites were quantified in the frontal lobe (anterior cingulate cortex) and a comparison region (parieto-occipital cortex). Significant increases in phosphocreatine (+7%), -nucleoside triphosphates (largely ATP in brain, +14%) and the ratio of phosphocreatine to inorganic phosphate (+32%), as well as significant changes in membrane phospholipids, were observed in the anterior cingulate cortex after 6 weeks of citicoline treatment. These treatment-related alterations in phosphorus metabolites were not only regionally specific, but tended to be of greater magnitude in subjects who received the lower dose. These data show that citicoline improves frontal lobe bioenergetics and alters phospholipid membrane turnover. Citicoline supplementation may therefore help to mitigate cognitive declines associated with aging by increasing energy reserves and utilization, as well as increasing the amount of essential phospholipid membrane components needed to synthesize and maintain cell membranes.
    Antidepressant-like effects of uridine and omega-3 fatty acids are potentiated by combined treatment in rats.
    Carlezon WA Jr, Mague SD, Parow AM, Stoll AL, Cohen BM, Renshaw PF.

    Department of Psychiatry, Harvard Medical School, McLean Hospital, Belmont, Massachusetts, USA. carlezon@mclean.harvard.edu

    BACKGROUND: Brain phospholipid metabolism and membrane fluidity may be involved in the pathophysiology of mood disorders. We showed previously that cytidine, which increases phospholipid synthesis, has antidepressant-like effects in the forced swim test (FST) in rats, a model used in depression research. Because cytidine and uridine both stimulate synthesis of cytidine 5'-diphosphocholine (CDP-choline, a critical substrate for phospholipid synthesis), we examined whether uridine would also produce antidepressant-like effects in rats. We also examined the effects of omega-3 fatty acids (OMG), which increase membrane fluidity and reportedly have antidepressant effects in humans, alone and in combination with uridine. METHODS: We first examined the effects of uridine injections alone and dietary supplementation with OMG alone in the FST. We then combined sub-effective treatment regimens of uridine and OMG to determine whether these agents would be more effective if administered together. RESULTS: Uridine dose-dependently reduced immobility in the FST, an antidepressant-like effect. Dietary supplementation with OMG reduced immobility when given for 30 days, but not for 3 or 10 days. A sub-effective dose of uridine reduced immobility in rats given sub-effective dietary supplementation with OMG. CONCLUSIONS: Uridine and OMG each have antidepressant-like effects in rats. Less of each agent is required for effectiveness when the treatments are administered together.
    Oral supplementation with docosahexaenoic acid and uridine-5'-monophosphate increases dendritic spine density in adult gerbil hippocampus.
    Sakamoto T, Cansev M, Wurtman RJ.

    Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

    Docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid, is an essential component of membrane phosphatides and has been implicated in cognitive functions. Low levels of circulating or brain DHA are associated with various neurocognitive disorders including Alzheimer's disease (AD), while laboratory animals, including animal models of AD, can exhibit improved cognitive ability with a diet enriched in DHA. Various cellular mechanisms have been proposed for DHA's behavioral effects, including increases in cellular membrane fluidity, promotion of neurite extension and inhibition of apoptosis. However, there is little direct evidence that DHA affects synaptic structure in living animals. Here we show that oral supplementation with DHA substantially increases the number of dendritic spines in adult gerbil hippocampus, particularly when animals are co-supplemented with a uridine source, uridine-5'-monophosphate (UMP), which increases brain levels of the rate-limiting phosphatide precursor CTP. The increase in dendritic spines (>30%) is accompanied by parallel increases in membrane phosphatides and in pre- and post-synaptic proteins within the hippocampus. Hence, oral DHA may promote neuronal membrane synthesis to increase the number of synapses, particularly when co-administered with UMP. Our findings provide a possible explanation for the effects of DHA on behavior and also suggest a strategy to treat cognitive disorders resulting from synapse loss.
    Alzheimers Dement. 2008 Jan;4(1 Suppl 1):S153-68. Epub 2007 Dec 21.

    Oral administration of circulating precursors for membrane phosphatides can promote the synthesis of new brain synapses.
    Cansev M, Wurtman RJ, Sakamoto T, Ulus IH.

    Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.

    Although cognitive performance in humans and experimental animals can be improved by administering omega-3 fatty acid docosahexaenoic acid (DHA), the neurochemical mechanisms underlying this effect remain uncertain. In general, nutrients or drugs that modify brain function or behavior do so by affecting synaptic transmission, usually by changing the quantities of particular neurotransmitters present within synaptic clefts or by acting directly on neurotransmitter receptors or signal-transduction molecules. We find that DHA also affects synaptic transmission in mammalian brain. Brain cells of gerbils or rats receiving this fatty acid manifest increased levels of phosphatides and of specific presynaptic or postsynaptic proteins. They also exhibit increased numbers of dendritic spines on postsynaptic neurons. These actions are markedly enhanced in animals that have also received the other two circulating precursors for phosphatidylcholine, uridine (which gives rise to brain uridine diphosphate and cytidine triphosphate) and choline (which gives rise to phosphocholine). The actions of DHA aere reproduced by eicosapentaenoic acid, another omega-3 compound, but not by omega-6 fatty acid arachidonic acid. Administration of circulating phosphatide precursors can also increase neurotransmitter release (acetylcholine, dopamine) and affect animal behavior. Conceivably, this treatment might have use in patients with the synaptic loss that characterizes Alzheimer's disease or other neurodegenerative diseases or occurs after stroke or brain injury.
    Oral supplementation with docosahexaenoic acid and uridine-5'-monophosphate increases dendritic spine density in adult gerbil hippocampus.
    Sakamoto T, Cansev M, Wurtman RJ.

    Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

    Docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid, is an essential component of membrane phosphatides and has been implicated in cognitive functions. Low levels of circulating or brain DHA are associated with various neurocognitive disorders including Alzheimer's disease (AD), while laboratory animals, including animal models of AD, can exhibit improved cognitive ability with a diet enriched in DHA. Various cellular mechanisms have been proposed for DHA's behavioral effects, including increases in cellular membrane fluidity, promotion of neurite extension and inhibition of apoptosis. However, there is little direct evidence that DHA affects synaptic structure in living animals. Here we show that oral supplementation with DHA substantially increases the number of dendritic spines in adult gerbil hippocampus, particularly when animals are co-supplemented with a uridine source, uridine-5'-monophosphate (UMP), which increases brain levels of the rate-limiting phosphatide precursor CTP. The increase in dendritic spines (>30%) is accompanied by parallel increases in membrane phosphatides and in pre- and post-synaptic proteins within the hippocampus. Hence, oral DHA may promote neuronal membrane synthesis to increase the number of synapses, particularly when co-administered with UMP. Our findings provide a possible explanation for the effects of DHA on behavior and also suggest a strategy to treat cognitive disorders resulting from synapse loss.
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    http://www.patsnap.c...05112635A2.html

    RESULTS [0072] In order to determine whether dopamine release is affected by uridine administration, animals provided UMP in their diets were assessed for dopamine production, both during and following neuron depolarization. Figures lA-E depict the release . profiles of a single uridine-fed rat and a single control rat over repeated stimulations. UMP administration enhanced release of DA (B) and 5-HT (E) both during and after depolarization. DOPAC (A), 5-HIAA ©, and HVA (D) exhibited lower basal levels in the UMP-fed animals, and release was increased, although by a smaller margin than DA and 5-HT, after but not during stimulation. UMP did not affect the total levels of DA and 5-HT in the striatum, while total striatal levels of DOPAC, 5-


    http://web.mit.edu/n...imers-1126.html

    MIT researchers have shown that a cocktail containing three compounds normally in the blood stream promotes growth of new brain connections and improves cognitive function in rodents. The treatment is now being tested in Alzheimer's patients and could hold promise for other brain diseases and injuries.
    The mixture, which includes a type of omega-3 fatty acid, is part of a new approach to attacking Alzheimer's. That approach focuses on correcting the loss of synapses, or connections between neurons, which characterizes the disease.

    http://www.patentgen...nt/4960759.html

    3. Clinical tests

    To evaluate whether the pharmacologic effects of uridine could result in a therapeutical confirmation, the compound was administered to a group of 40 psychotic subjects.

    As it is well known in the medical practice that the neuroleptic drugs very often produce side effects of Parkinsonian type, such as rigidity, tremors and the like, and for this reason it is usual to associate anti Parkinson drugs to the anti psychotic drugs, the experimental pattern was organized so as to be able to evaluate whether uridine, thanks to its pharmacological properties, was able to be substituted in lieu of the anti Parkinson drug normally used.

    Twenty psychotic subjects had been under treatment with neuroleptic drugs for various months and with anti Parkinsonian drugs because Parkinsonian symptoms had appeared among them. In our test, the anti Parkinsonian drug was substituted withuridine. Uridine was administered three times a day as 200 mg pills, along with haloperidol.

    In twenty different psychotic subjects the treatment with anti Parkinsonian drug was interrupted for two weeks (wash out), before starting a treatment based on uridine and haloperidol, at the same dosages as the above indicated group.

    Results

    In the first group of subjects, uridine has shown itself able to efficaciously substitute the anti Parkinsonian drugs. In fact not one of the subjects has shown Parkinsonian symptoms in the two months period of treatment. In the absence of uridine, the tremor and rigidity symptoms usually appear within two to three weeks.

    In the second group the tremor was already evident after the wash out period, before beginning the treatment with uridine.

    With this treatment the Parkinsonian symptoms disappeared within the first ten days of treatment, and the symptoms did not reappear until two months after.

    It can be concluded that uridine is a drug able to block the symptoms of Parkinson's disease when it is administered alone. Uridine is additionally able to inhibit the side effects of neuroleptic drugs, when it is administered together with thelatter in a treatment of psychotic subjects.

    The pharmaceutically active agent according to the present invention can be provided for clinical use in pharmaceutical compositions for oral administration under the form of tablets, pills, granules, capsules, drops, syrups and the like togetherwith pharmaceutically acceptable excipients.

    Moreover, the pharmaceutically active agent can be administered under the form of a pharmaceutical composition for parenteral administration, in the form of injectable solutes along with known pharmaceutically acceptable vehicles.

    A preferred dosage for oral routes is 0.5-5 g/die referred to the pharmaceutically active agent.
    One
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    Senior Member MeDieViL's Avatar
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    Effects:
    It's quite different, in that there is no 'buzz' or stimulant effect whatsoever. The most obvious effect is increased mental clarity, calmness, cognitive ability and recall. A single dose would have little appreciable effect.

    It will also raise your levels of acetylcholine *without* robbing the lipid membranes.

    What it does is gradually repair and enhance your brain on a daily basis, by significantly promoting neurogenesis - you create or repair neurons, dendrites and lipid membranes. This includes receptors as well.

    The overall 'effect' is that you feel like yourself, but unimpeded - existing cognitive or emotional issues disappear over a week or so and you start feeling and being awesome. Your capacity to learn and retain information is noticably better. Particularly when you relax and stop trying to mentally compare your responses to pre-supplementing days, I found.

    My wife was recovering from Zoloft withdrawal, which left her with occasional anxiety attacks and obsessive behaviour. That just got better and then stopped altogether. Essentially she appears to have have made peace with her problems, as they arose, and moved on. Her critical thinking has improved and she is making better decisions overall. Her scores playing online Scrabble have increased to the point where she is just destroying the other players. She was smart to begin with, but now she appears to be 'unshackled', if you like.

    In short, it just makes you a better and more capable person.

    Side effects noticed: none noticed
    Withdrawal effects: none
    Interaction with drugs: none that I've been able to find on pubmed or google, other than mediating side-effects from neuroleptics and antidepressants.

    My daily morning regime is:
    500mg of alpha-gpc choline
    250mg of uridine-5'-monophosphate
    1 berocca
    Washing down:
    4 capsules of flaxseed oil (I'm vegetarian)
    1 vitamin E capsule
    1 grape-seed extract capsule equiv 12000mg

    My nightly regime is:
    1 lecithin capsule 1200mg
    1 grape-seed extract capsule
    Occasionally a bacopa capsule, 2 hours before sleep. It makes me too sleepy to feel like sex, so not an 'every day' supplement.

    I found 2 American suppliers that sell bulk powder through their websites and also through ebay. Superiornutraceuticals - uridine and nutrabiolabs - alpha-gpc. Quality has been good. Shipping has been very quick.

    The bulk alpha-gpc is annoying to dispense. The uridine jar comes with a 250mg scoop, but since the uridine sticks like crazy, I leave the scoop out of the jar, to prevent wasting it. 1 scoop of uridine in the cup, 2 scoops of alpha-gpc, then add the water and berocca. Stir. Voila.

    Be sure to start adding some extra study matter to your routine - there's no point having extra cognitive ability and not using it to improve your knowledge-base!
    One
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    Senior Member MeDieViL's Avatar
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    And much much much more good shit, let the latest hype get started!
    One
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    So have you noticed any effects from this?

    I am going to try it myself soon but I am pretty petrified (well, wary is a better term) of cholonergics in general because they do induce a miserable mindset and potentiate my depressive disorder. I think I would have actually comitted suicide if I had continued with 300mg of Alpha GPC everyday. Maybe CDP is a different beast especially in combination with the other components mentioned in this thread.

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    Quote Originally Posted by dukes07 View Post
    So have you noticed any effects from this?

    I am going to try it myself soon but I am pretty petrified (well, wary is a better term) of cholonergics in general because they do induce a miserable mindset and potentiate my depressive disorder. I think I would have actually comitted suicide if I had continued with 300mg of Alpha GPC everyday. Maybe CDP is a different beast especially in combination with the other components mentioned in this thread.
    You could use ALCAR instead, I can't tolerate cdp/gpc either.
    Only dead fish follow the stream.

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    Was a source for gram amounts of this stuff ever found?

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    Quote Originally Posted by bdog527 View Post
    Was a source for gram amounts of this stuff ever found?
    ebay.
    Only dead fish follow the stream.

    “The constitution is paper, the bayonet is steel.” - Haitian proverb.

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    Senior Member dukes07's Avatar
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    Does anyone notice depressive side effects from this combo (assuming people are taking this uridine with DPA + cholinergic based substancs..CDP/Alpha/cito).

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    Quote Originally Posted by dukes07 View Post
    So have you noticed any effects from this?

    I am going to try it myself soon but I am pretty petrified (well, wary is a better term) of cholonergics in general because they do induce a miserable mindset and potentiate my depressive disorder. I think I would have actually comitted suicide if I had continued with 300mg of Alpha GPC everyday. Maybe CDP is a different beast especially in combination with the other components mentioned in this thread.
    Please report when you try CDP. I seem to have problems with cholinergics too.

  17. #37
    Senior Member Ex Dubio's Avatar
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    Quote Originally Posted by dukes07 View Post
    Does anyone notice depressive side effects from this combo (assuming people are taking this uridine with DPA + cholinergic based substancs..CDP/Alpha/cito).
    Depressive effects from cholinergic substances are very common.

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    Open-label uridine for treatment of depressed adolescents with bipolar disorder.

    Kondo DG, Sung YH, Hellem TL, Delmastro KK, Jeong EK, Kim N, Shi X, Renshaw PF.
    Source

    The Brain Institute, University of Utah, Salt Lake City, Utah 84108, USA. doug.kondo@hsc.utah.edu

    Abstract


    This report is an open-label case series of seven depressed adolescents with bipolar disorder treated with uridine for 6 weeks. Treatment response was measured with the Children's Depression Rating Scale-Revised and the Clinical Global Impressions scale. Uridine was associated with decreased depressive symptoms, and was well tolerated by study participants. Further systematic studies of uridine are warranted.
    Theoretically it has loads of pote
    ntial for other disorders too; cognitive enhancement and much more.

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    Did you get much from it? I only tried it for a day but wasn't too impressed by it.

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