Nootropics
reddisert | 3 years ago
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We need bulk uridine, a membrane phosphatide? precursor that accelerates neuronal remodeling at the level of the bilayer... this stuff should be a pretty big deal pretty soon
Harvard and MIT are going ape nuts.
How often do you read about "restorative" effects in conditions like this via nutrition alone?
It has also been shown to increase cognition in healthy adult gerbils.
Neurosci Res. 2008 Aug 3. [Epub ahead of print]Click here to read Links
Restorative effects of uridine plus docosahexaenoic acid in a rat model of Parkinson's disease.
Cansev M, Ulus IH, Wang L, Maher TJ, Wurtman RJ.
Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, Cambridge, MA 02139, USA; Uludag University School of Medicine, Department of Pharmacology and Clinical Pharmacology, Bursa 16059, Turkey.
Administering uridine-5'-monophosphate (UMP) and docosahexaenoic acid (DHA) increases synaptic membranes (as characterized by pre- and post-synaptic proteins) and dendritic spines in rodents. We examined their effects on rotational behavior and dopaminergic markers in rats with partial unilateral 6-hydroxydopamine (6-OHDA)-induced striatal lesions. Rats receiving UMP, DHA, both, or neither, daily, and intrastriatal 6-OHDA 3 days after treatment onset, were tested for d-amphetamine-induced rotational behavior and dopaminergic markers after 24 and 28 days, respectively. UMP/DHA treatment reduced ipsilateral rotations by 57% and significantly elevated striatal dopamine, tyrosine hydroxylase (TH) activity, TH protein and synapsin-1 on the lesioned side. Hence, giving uridine and DHA may partially restore dopaminergic neurotransmission in this model of Parkinson's disease.
Harvard and MIT are going ape nuts.
How often do you read about "restorative" effects in conditions like this via nutrition alone?
It has also been shown to increase cognition in healthy adult gerbils.
Neurosci Res. 2008 Aug 3. [Epub ahead of print]Click here to read Links
Restorative effects of uridine plus docosahexaenoic acid in a rat model of Parkinson's disease.
Cansev M, Ulus IH, Wang L, Maher TJ, Wurtman RJ.
Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, Cambridge, MA 02139, USA; Uludag University School of Medicine, Department of Pharmacology and Clinical Pharmacology, Bursa 16059, Turkey.
Administering uridine-5'-monophosphate (UMP) and docosahexaenoic acid (DHA) increases synaptic membranes (as characterized by pre- and post-synaptic proteins) and dendritic spines in rodents. We examined their effects on rotational behavior and dopaminergic markers in rats with partial unilateral 6-hydroxydopamine (6-OHDA)-induced striatal lesions. Rats receiving UMP, DHA, both, or neither, daily, and intrastriatal 6-OHDA 3 days after treatment onset, were tested for d-amphetamine-induced rotational behavior and dopaminergic markers after 24 and 28 days, respectively. UMP/DHA treatment reduced ipsilateral rotations by 57% and significantly elevated striatal dopamine, tyrosine hydroxylase (TH) activity, TH protein and synapsin-1 on the lesioned side. Hence, giving uridine and DHA may partially restore dopaminergic neurotransmission in this model of Parkinson's disease.
medicalstudent | 3 years ago
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? | 3 years ago
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From the intro:
We previously observed that chronic oral administration of two circulating phosphatide precursors, uridine (as UMP) and the omega-3 fatty acid DHA, along with dietary choline, can increase neuronal levels of the phosphatides and of specific proteins that characterize synaptic membranes (Wurtman et al., 2006), as well as the numbers of dendritic spines, in rodent brain (Sakamoto et al., 2007).
We previously observed that chronic oral administration of two circulating phosphatide precursors, uridine (as UMP) and the omega-3 fatty acid DHA, along with dietary choline, can increase neuronal levels of the phosphatides and of specific proteins that characterize synaptic membranes (Wurtman et al., 2006), as well as the numbers of dendritic spines, in rodent brain (Sakamoto et al., 2007).
cognitivefun | 3 years ago
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keep in mind the dosages used in this study were probably astronomical... another paper talked of 300mg/kg dha per day... insane.
the dose of uridine in some papers was .5% of the diet. I am guessing this means by weight so assuming a 3000cal diet and the average weight of food is 6cal/g (~protein+fat+carbs/3) this amounts to 500g.
is it even economically feasible to consume 2.5g of uridine every day?
humans might get by with a lower dose, however
phosphatides... hmmmm...
the dose of uridine in some papers was .5% of the diet. I am guessing this means by weight so assuming a 3000cal diet and the average weight of food is 6cal/g (~protein+fat+carbs/3) this amounts to 500g.
is it even economically feasible to consume 2.5g of uridine every day?
humans might get by with a lower dose, however
phosphatides... hmmmm...
medicalstudent | 3 years ago
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? | 3 years ago
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cdp-choline might mediate its effects on phosphatides through uridine, but it seems like doses over 2000mg are overkill.
maybe if you spread it out during the day you could get a better dose response?
cdp-choline can be bought online but doses this high are exorbitant
it also seems to have neuroprotective and stimulant effects on dopaminergic neurons... a friendly finding
membrane modifiability is central to synaptic plasticity, phosphatides are a worthwhile candidate for therapeutic modulation... increased synaptogenesis could be clinically useful
Int J Neurosci. 2007 Jul;117(7):985-98.Click here to read Links
CDP-choline reduces dopaminergic cell loss induced by MPP(+) and glutamate in primary mesencephalic cell culture.
Radad K, Gille G, Xiaojing J, Durany N, Rausch WD.
Department of Pathology Faculty of Veterinary Medicine, Assiut University, Assiut, Egypt.
Cytidine-5'-diphosphocholine (citicoline or CDP-choline) is an essential endogenous intermediate in the biosynthesis of phosphatidylcholine. In the present study, primary dopaminergic cultures from mouse mesencephala were treated with citicoline to investigate its neuroprotective potential on the survival of dopaminergic neurons exposed to MPP(+) and glutamate. Treatment with citicoline alone significantly increased the survival of dopaminergic neurons compared to controls. MPP(+) or glutamate decreased the total number of dopaminergic neurons whereas citicoline afforded significant protection against either toxicity. Moreover, citicoline significantly decreased propidium iodide uptake by cultured cells. The study concludes that citicoline exerts stimulant and neuroprotective actions on cultured dopaminergic neurons.
Biochem Pharmacol. 2000 Oct 1;60(7):989-92.
> Effect of oral CDP-choline on plasma choline and uridine levels in humans.
>
> Wurtman RJ, Regan M, Ulus I, Yu L.
>
> Department of Brain 500, 2000, and 4000 mg) or a placebo orally at 8:00 a.m. on four different treatment days. Eleven plasma samples from each subject, obtained just prior to treatment (8:00 a.m.) and 1-12 hr thereafter, were assayed for choline, cytidine, and uridine. Fasting terminated at noon with consumption of a light lunch that contained about 100 mg choline. Plasma choline exhibited dose-related increases in peak values and areas under the curves (AUCs), remaining significantly elevated, after each of the three doses, for 5, 8, and 10 hr, respectively. Plasma uridine was elevated significantly for 5-6 hr after all three doses, increasing by as much as 70-90% after the 500 mg dose, and by 100-120% after the 2000 mg dose. No further increase was noted when the dose was raised from 2000 to 4000 mg. Plasma cytidine was not reliably detectable, since it was less than twice blank, or less than 100 nM, at all of the doses. Uridine is known to enter the brain and to be converted to UTP; moreover, we found that uridine was converted directly to CTP in neuron-derived PC-12 cells. Hence, it seems likely that the circulating substrates through which oral citicoline increases membrane phosphatide synthesis in the brains of humans involve uridine and choline, and not cytidine and choline as in rats.
maybe if you spread it out during the day you could get a better dose response?
cdp-choline can be bought online but doses this high are exorbitant
it also seems to have neuroprotective and stimulant effects on dopaminergic neurons... a friendly finding
membrane modifiability is central to synaptic plasticity, phosphatides are a worthwhile candidate for therapeutic modulation... increased synaptogenesis could be clinically useful
Int J Neurosci. 2007 Jul;117(7):985-98.Click here to read Links
CDP-choline reduces dopaminergic cell loss induced by MPP(+) and glutamate in primary mesencephalic cell culture.
Radad K, Gille G, Xiaojing J, Durany N, Rausch WD.
Department of Pathology Faculty of Veterinary Medicine, Assiut University, Assiut, Egypt.
Cytidine-5'-diphosphocholine (citicoline or CDP-choline) is an essential endogenous intermediate in the biosynthesis of phosphatidylcholine. In the present study, primary dopaminergic cultures from mouse mesencephala were treated with citicoline to investigate its neuroprotective potential on the survival of dopaminergic neurons exposed to MPP(+) and glutamate. Treatment with citicoline alone significantly increased the survival of dopaminergic neurons compared to controls. MPP(+) or glutamate decreased the total number of dopaminergic neurons whereas citicoline afforded significant protection against either toxicity. Moreover, citicoline significantly decreased propidium iodide uptake by cultured cells. The study concludes that citicoline exerts stimulant and neuroprotective actions on cultured dopaminergic neurons.
Biochem Pharmacol. 2000 Oct 1;60(7):989-92.
> Effect of oral CDP-choline on plasma choline and uridine levels in humans.
>
> Wurtman RJ, Regan M, Ulus I, Yu L.
>
> Department of Brain 500, 2000, and 4000 mg) or a placebo orally at 8:00 a.m. on four different treatment days. Eleven plasma samples from each subject, obtained just prior to treatment (8:00 a.m.) and 1-12 hr thereafter, were assayed for choline, cytidine, and uridine. Fasting terminated at noon with consumption of a light lunch that contained about 100 mg choline. Plasma choline exhibited dose-related increases in peak values and areas under the curves (AUCs), remaining significantly elevated, after each of the three doses, for 5, 8, and 10 hr, respectively. Plasma uridine was elevated significantly for 5-6 hr after all three doses, increasing by as much as 70-90% after the 500 mg dose, and by 100-120% after the 2000 mg dose. No further increase was noted when the dose was raised from 2000 to 4000 mg. Plasma cytidine was not reliably detectable, since it was less than twice blank, or less than 100 nM, at all of the doses. Uridine is known to enter the brain and to be converted to UTP; moreover, we found that uridine was converted directly to CTP in neuron-derived PC-12 cells. Hence, it seems likely that the circulating substrates through which oral citicoline increases membrane phosphatide synthesis in the brains of humans involve uridine and choline, and not cytidine and choline as in rats.
medicalstudent | 3 years ago
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medicalstudent | 3 years ago
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NMR Biomed. 2008 Sep 24. [Epub ahead of print]Click here to read Links
Citicoline enhances frontal lobe bioenergetics as measured by phosphorus magnetic resonance spectroscopy.
Silveri MM, Dikan J, Ross AJ, Jensen JE, Kamiya T, Kawada Y, Renshaw PF, Yurgelun-Todd DA.
Cognitive Neuroimaging Laboratory, McLean Hospital, Belmont, MA, USA.
Citicoline 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 ((31)P) 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(R) Citicoline (Kyowa Hakko Kogyo Co., Ltd, Ibaraki, Japan) for 6 weeks. Individual (31)P metabolites were quantified in the frontal lobe (anterior cingulate cortex) and a comparison region (parieto-occipital cortex). Significant increases in phosphocreatine (+7%), beta-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. Copyright (c) 2008 John Wiley & Sons, Ltd.
Straight out of Harvard last month...
500mg will be my dose
Citicoline enhances frontal lobe bioenergetics as measured by phosphorus magnetic resonance spectroscopy.
Silveri MM, Dikan J, Ross AJ, Jensen JE, Kamiya T, Kawada Y, Renshaw PF, Yurgelun-Todd DA.
Cognitive Neuroimaging Laboratory, McLean Hospital, Belmont, MA, USA.
Citicoline 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 ((31)P) 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(R) Citicoline (Kyowa Hakko Kogyo Co., Ltd, Ibaraki, Japan) for 6 weeks. Individual (31)P metabolites were quantified in the frontal lobe (anterior cingulate cortex) and a comparison region (parieto-occipital cortex). Significant increases in phosphocreatine (+7%), beta-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. Copyright (c) 2008 John Wiley & Sons, Ltd.
Straight out of Harvard last month...
500mg will be my dose
medicalstudent | 3 years ago
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been on for about 40 days ~ 6 weeks
citicoline is being designated an LTK; i come across LTK's (usually) about once a year.
LTK = long-term keeper
citicoline is being designated an LTK; i come across LTK's (usually) about once a year.
LTK = long-term keeper
medicalstudent | 3 years ago
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cevapcici | 3 years ago
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subjective: less mental fatigue, trend towards improved verbal memory (remembering verbal factoids)
objective: abundance of neuroprotective literature, trophic effects on the dopaminergic system, low/nonexistent toxicity, not expensive
This drug seems more like a brain-precursor supplement; it gives the brain resources to optimize its' functioning, rather than "forcing" a pharmacological effect. It seems to do something very fundamental... and i like that.
However, I have not "measured" these effects... and even if I did, a sample size of one with a host of other variables would undoubtedly invalidate my results.
LTK status is, primarily, reflected by a favorable risk/reward ratio.
Methods Find Exp Clin Pharmacol. 2006 Sep;28 Suppl B:1-56.Click here to read Links
Citicoline: pharmacological and clinical review, 2006 update.
Secades JJ, Lorenzo JL.
Medical Department, Grupo Ferrer S.A., Barcelona, Spain.
"Thus, citicoline has been experimentally shown to increase norepinephrine and dopamine levels in the CNS. Owing to these pharmacological mechanisms, citicoline has a neuroprotective effect in hypoxic and ischemic conditions, decreasing the volume of ischemic lesion, and also improves learning and memory performance in animal models of brain aging. In addition, citicoline has been shown to restore the activity of mitochondrial ATPase and membrane Na+/K+ATPase, to inhibit activation of certain phospholipases, and to accelerate reabsorption of cerebral edema in various experimental models. Citicoline has also been shown to be able to inhibit mechanisms of apoptosis associated to cerebral ischemia and in certain neurodegeneration models, and to potentiate neuroplasticity mechanisms. Citicoline is a safe drug, as shown by the toxicological tests conducted, that has no significant systemic cholinergic effects and is a well tolerated product."
objective: abundance of neuroprotective literature, trophic effects on the dopaminergic system, low/nonexistent toxicity, not expensive
This drug seems more like a brain-precursor supplement; it gives the brain resources to optimize its' functioning, rather than "forcing" a pharmacological effect. It seems to do something very fundamental... and i like that.
However, I have not "measured" these effects... and even if I did, a sample size of one with a host of other variables would undoubtedly invalidate my results.
LTK status is, primarily, reflected by a favorable risk/reward ratio.
Methods Find Exp Clin Pharmacol. 2006 Sep;28 Suppl B:1-56.Click here to read Links
Citicoline: pharmacological and clinical review, 2006 update.
Secades JJ, Lorenzo JL.
Medical Department, Grupo Ferrer S.A., Barcelona, Spain.
"Thus, citicoline has been experimentally shown to increase norepinephrine and dopamine levels in the CNS. Owing to these pharmacological mechanisms, citicoline has a neuroprotective effect in hypoxic and ischemic conditions, decreasing the volume of ischemic lesion, and also improves learning and memory performance in animal models of brain aging. In addition, citicoline has been shown to restore the activity of mitochondrial ATPase and membrane Na+/K+ATPase, to inhibit activation of certain phospholipases, and to accelerate reabsorption of cerebral edema in various experimental models. Citicoline has also been shown to be able to inhibit mechanisms of apoptosis associated to cerebral ischemia and in certain neurodegeneration models, and to potentiate neuroplasticity mechanisms. Citicoline is a safe drug, as shown by the toxicological tests conducted, that has no significant systemic cholinergic effects and is a well tolerated product."
medicalstudent | 3 years ago
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Metabolism. 2008 Oct;57 Suppl 2:S6-10.Click here to read Links
Synapse formation and cognitive brain development: effect of docosahexaenoic acid and other dietary constituents.
Wurtman RJ.
Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. dick@mit.edu
The brain is unusual among organs in that the rates of many of its characteristic enzymatic reactions are controlled by the local concentrations of their substrates, which also happen to be nutrients that cross the blood-brain barrier. Thus, for example, brain levels of tryptophan, tyrosine, or choline can control the rates at which neurons synthesize serotonin, dopamine, or acetylcholine, respectively. The rates at which brain cells produce membrane phospholipids such as phosphatidylcholine (PC) are also under such control, both in adult animals and, especially, during early development. If pregnant rats are fed the 3 dietary constituents needed for PC synthesis- docosahexaenoic acid, uridine, and choline-starting 10 days before parturition and continuing for 20 days during nursing, brain levels of PC, and of the other membrane phosphatides (per cell or per mg protein), are increased by 50% or more. In adult animals, this treatment is also known to increase synaptic proteins (eg, synapsin-l, syntaxin-3, GluR-l, PSD-95) but not ubiquitous proteins like beta-tubulin and to increase (by 30% or more) the number of dendritic spines on hippocampal neurons. Docosahexaenoic acid currently is widely used, in human infants, to diminish the negative effects of prematurity on cognitive development. Moreover, docosahexaenoic acid, uridine (as uridine monophosphate), and choline are all found in mother's milk, and included in most infant formulas. It is proposed that these substances are part of a regulatory mechanism through which plasma composition influences brain development.
I like the first sentence, and the penultimate one...
Mama knows best, right?
Synapse formation and cognitive brain development: effect of docosahexaenoic acid and other dietary constituents.
Wurtman RJ.
Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. dick@mit.edu
The brain is unusual among organs in that the rates of many of its characteristic enzymatic reactions are controlled by the local concentrations of their substrates, which also happen to be nutrients that cross the blood-brain barrier. Thus, for example, brain levels of tryptophan, tyrosine, or choline can control the rates at which neurons synthesize serotonin, dopamine, or acetylcholine, respectively. The rates at which brain cells produce membrane phospholipids such as phosphatidylcholine (PC) are also under such control, both in adult animals and, especially, during early development. If pregnant rats are fed the 3 dietary constituents needed for PC synthesis- docosahexaenoic acid, uridine, and choline-starting 10 days before parturition and continuing for 20 days during nursing, brain levels of PC, and of the other membrane phosphatides (per cell or per mg protein), are increased by 50% or more. In adult animals, this treatment is also known to increase synaptic proteins (eg, synapsin-l, syntaxin-3, GluR-l, PSD-95) but not ubiquitous proteins like beta-tubulin and to increase (by 30% or more) the number of dendritic spines on hippocampal neurons. Docosahexaenoic acid currently is widely used, in human infants, to diminish the negative effects of prematurity on cognitive development. Moreover, docosahexaenoic acid, uridine (as uridine monophosphate), and choline are all found in mother's milk, and included in most infant formulas. It is proposed that these substances are part of a regulatory mechanism through which plasma composition influences brain development.
I like the first sentence, and the penultimate one...
Mama knows best, right?
medicalstudent | 3 years ago
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cevapcici | 3 years ago
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How marvelous that is to hear! I already happen to be taking uridine, citicoline, DHA, and a-gpc mentioned elsewhere in the thread. I had no idea it was that beneficial.
This is a great supplement complex (supposing it contains what they claim and supposing it's pure):
http://www.lef.org/Vitamins-Supplements/Item00922/Cognitex-with-Pregnenolone-NeuroProtection-Complex.html
It has all of the following (by the manufacturer's purports of course):
1. A-GPC
2. Phosphatidylserine
3. Pregnenolone (interesting to me because newer models of the remedial effects of SSRIs suggest that the pathway by which they abate depression is the stimulation of the release of neurosteroids which suppress glucocorticoids which either directly damage the hippocampus or damage it indirectly by suppressing nerve growth factors which preserve and maintain it.)
4. Vinpocetine
5. Vitis Vinifera
6. Blueberry extract
7. A patented form of Ashwagandha that supposedly doesn't have the anticholinergic effects seen in other Ashwagandha formulations.
8. Uridine-5'-monophosphate
9. Rosemary
10. Ginger
11. Humulus Lupulus
Each of them is by itself wonderful, save perhaps the last three into which I have done little research.
As, I've said before though, what I am really interested in are the following:
Ghrelin
Nerve Growth Factor
Brain Derived Nerve Growth Factor
The various neurotrophins
Ampakines
Proglumide
Dimebon
Cypin
Creb
In particular Cypin. It seems that a fair bit of extremely promising research was conducted on Cypin (in 2004) and then... nothing. If you do a google search for it you find only a few thousand results. It's very strange to me that a chemical which have been shown to have the potential to dramatically increase human intelligence and memory should have so precious little written about it and that so few should seem to take interest in it.
/A real concern for me has been that wealthy and powerful people alone should be able to attain these drugs, widening the gap between the lower classes and further rarefying the possibility of the lower classes overthrowing the corrupt oligarchs who are now in the process of destroying and bankrupting this country. (Sorry for the tangential rant)
This is a great supplement complex (supposing it contains what they claim and supposing it's pure):
http://www.lef.org/Vitamins-Supplements/Item00922/Cognitex-with-Pregnenolone-NeuroProtection-Complex.html
It has all of the following (by the manufacturer's purports of course):
1. A-GPC
2. Phosphatidylserine
3. Pregnenolone (interesting to me because newer models of the remedial effects of SSRIs suggest that the pathway by which they abate depression is the stimulation of the release of neurosteroids which suppress glucocorticoids which either directly damage the hippocampus or damage it indirectly by suppressing nerve growth factors which preserve and maintain it.)
4. Vinpocetine
5. Vitis Vinifera
6. Blueberry extract
7. A patented form of Ashwagandha that supposedly doesn't have the anticholinergic effects seen in other Ashwagandha formulations.
8. Uridine-5'-monophosphate
9. Rosemary
10. Ginger
11. Humulus Lupulus
Each of them is by itself wonderful, save perhaps the last three into which I have done little research.
As, I've said before though, what I am really interested in are the following:
Ghrelin
Nerve Growth Factor
Brain Derived Nerve Growth Factor
The various neurotrophins
Ampakines
Proglumide
Dimebon
Cypin
Creb
In particular Cypin. It seems that a fair bit of extremely promising research was conducted on Cypin (in 2004) and then... nothing. If you do a google search for it you find only a few thousand results. It's very strange to me that a chemical which have been shown to have the potential to dramatically increase human intelligence and memory should have so precious little written about it and that so few should seem to take interest in it.
/A real concern for me has been that wealthy and powerful people alone should be able to attain these drugs, widening the gap between the lower classes and further rarefying the possibility of the lower classes overthrowing the corrupt oligarchs who are now in the process of destroying and bankrupting this country. (Sorry for the tangential rant)
Okinamaro | 3 years ago
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? | 3 years ago
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? | 3 years ago
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"A real concern for me has been that wealthy and powerful people alone should be able to attain these drugs, widening the gap between the lower classes and"
i think about this as well... money does a pretty good job of propagating itself now, but what happens when you can *buy* intelligence? then your kids will have supreme advantages
we have no choice... it is going to happen.. one way (drugs) or another (eugenics)
i think transhumanism is part of our evolution, ethical or not
we have no choice... it is going to happen.. one way (drugs) or another (eugenics)
i think transhumanism is part of our evolution, ethical or not
medicalstudent | 3 years ago
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Yep. Actually, you should check the discussion history. If I recall correctly, three already exist.
I highly recommend Huperzine A, for example.
I highly recommend Huperzine A, for example.
? | 3 years ago
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Thanks to (I assume) cognitivefun for bridging one of the older discussions here. ;-)
Another I recommend is Alpha-GPC. I took it for the first time hours ago and how it affects me is subtle and yet striking. I have a slight headache, but my behaviour is much more patternable than with Huperzine A only. Huperzine A rendered my thinking process more lucidly geometric, and now I suspect Alpha-GPC will add to this (they relate to the same neurochemical elements).
I'll say it again. Do research.
Another I recommend is Alpha-GPC. I took it for the first time hours ago and how it affects me is subtle and yet striking. I have a slight headache, but my behaviour is much more patternable than with Huperzine A only. Huperzine A rendered my thinking process more lucidly geometric, and now I suspect Alpha-GPC will add to this (they relate to the same neurochemical elements).
I'll say it again. Do research.
? | 3 years ago
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Okinamaro | 3 years ago
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Would you mind sharing the dosages you were taking and how you feel about it now in retrospect? Would you take more or less of any of them? I too am going though severe depression and want to create a nootropic regiment to hopefully help ease the symptoms. Thanks!
? | 4 weeks ago
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My experience with nootropics
I was reading through some of the old comments and I noted that someone had asked whether anyone had had experience with any of the nootropics listed in Wikipedia article on nootropics. I have and would like to share mine. I thought it would be best to start a new thread since otherwise this would be apt to be a waste of my time.
I'll start by saying that I began taking nootropics both because I am a dummy and because I have severe depression (depression involves the destruction the brain cells particularly within the hippocampus and many nootropics by fomenting the growth of new neura within the hippocampus can alleviate depression).
I wished to take a comparatively more scientific approach by taking each supplement one at a time each for at least a couple of months in order to get a fairly decent idea as to which was improving my cognition most, but I just couldn't wait, so I went to the health food store and blew quite a bit of money on various supplements, having done a good deal of research on them beforehand.
They have helped TREMENDOUSLY (certainly it could be the placebo effect, but at any rate both my depression and my memory have improved by leaps and bounds.) I am only 22 years-old but only a few months ago I was in such a degenerated condition of mind, my hippocampus so ravaged by whatever mechanisms act as the aetiology of depression, that I could hardly perform any tasks because by the time I reached the room wherein the task needed to be performed or whence I needed to fetch some implement by which to accomplish the task I had completely forgotten why I had set out for that room in the first place. I encounter this problem only very seldom now; it's a wonderful improvement.
I am currently taking the following:
Vitis Vinifera (grape seed extract)
Bacopa Monnieri / Brahmi / Water Hyssop
Turmeric (curcumin)
Vitamin D
Vitamin E
Vitamin C
Essential Amino Acids
Choline
Inositol
Phosphatidylserine
Ginkgo Biloba
Vinpocetine
Omega 3 fatty acids (seems to occasion the same affective blunting as SSRIs and similarly reduces libido. Great otherwise.)
CoQ10
Melatonin (only on occasion)
Kava Kava
Valerian
Nearly incontrovertibly worthless for most people (I would guess):
Mucuna Pruriens - The majority of the l-dopa that these supplements contain is converted into dopamine peripherally by decarboxylase. You'll get an increased heart rate and not much else. If you want to get any use out of it you'll need a decarboxylase inhibitor impermeable to the blood brain barrier, but these are prescription only and such prescriptions are given only to those who have Parkinson's disease.
Yohimbe - from my experiences and from various anecdotal reports, this isn't a dopaminergic so much as an mu-opioid receptor antagonist, like naloxone or naltrexone. The first time I took yohimbe was when I was on an opiate binge; I became suicidally depressed after taking it. An individual with a profound tolerance to opiates, taking hundreds of milligrams of oxycodone a day, reported that when he took it, within 20 minutes or so he began experiencing all the classic symptoms of withdrawal and had to rush home where he used two to three times his normal dose of oxycodone and still didn't feel quite normal until about 8 hours after.
Now if only I can manage to obtain nerve growth factor, brain-derived neurotrophic factor, neurotrophin 3, neurotrophin 4, cypin, creb, AF267B, and others. Damn FDA...
I'll start by saying that I began taking nootropics both because I am a dummy and because I have severe depression (depression involves the destruction the brain cells particularly within the hippocampus and many nootropics by fomenting the growth of new neura within the hippocampus can alleviate depression).
I wished to take a comparatively more scientific approach by taking each supplement one at a time each for at least a couple of months in order to get a fairly decent idea as to which was improving my cognition most, but I just couldn't wait, so I went to the health food store and blew quite a bit of money on various supplements, having done a good deal of research on them beforehand.
They have helped TREMENDOUSLY (certainly it could be the placebo effect, but at any rate both my depression and my memory have improved by leaps and bounds.) I am only 22 years-old but only a few months ago I was in such a degenerated condition of mind, my hippocampus so ravaged by whatever mechanisms act as the aetiology of depression, that I could hardly perform any tasks because by the time I reached the room wherein the task needed to be performed or whence I needed to fetch some implement by which to accomplish the task I had completely forgotten why I had set out for that room in the first place. I encounter this problem only very seldom now; it's a wonderful improvement.
I am currently taking the following:
Vitis Vinifera (grape seed extract)
Bacopa Monnieri / Brahmi / Water Hyssop
Turmeric (curcumin)
Vitamin D
Vitamin E
Vitamin C
Essential Amino Acids
Choline
Inositol
Phosphatidylserine
Ginkgo Biloba
Vinpocetine
Omega 3 fatty acids (seems to occasion the same affective blunting as SSRIs and similarly reduces libido. Great otherwise.)
CoQ10
Melatonin (only on occasion)
Kava Kava
Valerian
Nearly incontrovertibly worthless for most people (I would guess):
Mucuna Pruriens - The majority of the l-dopa that these supplements contain is converted into dopamine peripherally by decarboxylase. You'll get an increased heart rate and not much else. If you want to get any use out of it you'll need a decarboxylase inhibitor impermeable to the blood brain barrier, but these are prescription only and such prescriptions are given only to those who have Parkinson's disease.
Yohimbe - from my experiences and from various anecdotal reports, this isn't a dopaminergic so much as an mu-opioid receptor antagonist, like naloxone or naltrexone. The first time I took yohimbe was when I was on an opiate binge; I became suicidally depressed after taking it. An individual with a profound tolerance to opiates, taking hundreds of milligrams of oxycodone a day, reported that when he took it, within 20 minutes or so he began experiencing all the classic symptoms of withdrawal and had to rush home where he used two to three times his normal dose of oxycodone and still didn't feel quite normal until about 8 hours after.
Now if only I can manage to obtain nerve growth factor, brain-derived neurotrophic factor, neurotrophin 3, neurotrophin 4, cypin, creb, AF267B, and others. Damn FDA...
Okinamaro | 3 years ago
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Citicoline is nice -- it increases blood/brain uridine: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T4P-414N6MW-G&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_version=1&_urlVersion=0&_userid=10 citicoline has been found to inhibit activation of exactly this system (caspase-3).
gorelando | 3 years ago
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Odd, my post was cut off. I meant to write that, in the pot thread, the person found occasional use to be very helpful for their Crohn's (not surprising) but was concerned about cognitive issues ... I suggested citicoline as something to check out, as at least one major mechanism of the drug's problematic damaging effect in some areas occurs via activation of certain pro-apoptotic enzymes ... and citicoline has been found to inhibit activation of this very system (caspase-3).
Citicoline also promotes NGF and is dopaminergic, with a significant acute effect on e.g. Parkinsonian symptoms in human trials.
Citicoline also promotes NGF and is dopaminergic, with a significant acute effect on e.g. Parkinsonian symptoms in human trials.
gorelando | 3 years ago
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I'm similar to you. Same situation really. I'd bet money at least half of the anti-depressive effects came from the epa and dha alone, with a some amount of placebo too. Choline might help the brain itself some, but I really doubt whether any of those other things are causing the effect you described, unless you were just very malnourished in a vitamin.
An even greater effect than any of that for restarting neurogenesis in the hippocampus would be lots and lots of cardio exercise.
An even greater effect than any of that for restarting neurogenesis in the hippocampus would be lots and lots of cardio exercise.
? | 3 years ago
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Since these are all orally administered, I have to wonder whether your improvements have been due to a general improvement in health and/or hormonal balance, as opposed to direct effect on the brain. After all, the compounds need to get pass the digestive tract, then the circulatory system, then the blood-brain barrier.
cognitivefun | 3 years ago
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Very possibly, but there are certainly some on the list whose ability to cross the blood brain barrier can hardly be questioned. These are:
Omega 3 fatty acids (docosahexaenoic acid and eicosapentaenoic acid)
CoQ10
Melatonin
Vitamin D
Vitamin E
Vitamin C
Essential Amino Acids
Choline
Valerian (doubtful that this has anything like a direct nootropic effect, but regular sleep is essential mental well-being)
Kava Kava (reduces stress and therefore likely keeps glucocorticoids low which in turn helps to ensure that BDNF levels remain at sufficient levels)
Omega 3 fatty acids (docosahexaenoic acid and eicosapentaenoic acid)
CoQ10
Melatonin
Vitamin D
Vitamin E
Vitamin C
Essential Amino Acids
Choline
Valerian (doubtful that this has anything like a direct nootropic effect, but regular sleep is essential mental well-being)
Kava Kava (reduces stress and therefore likely keeps glucocorticoids low which in turn helps to ensure that BDNF levels remain at sufficient levels)
Okinamaro | 3 years ago
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(Sorry for the vernal reply in aged woods.)
I'd like to note about CoQ10 that it comes in two varieties. The artificial brand is decidedly less soluble than the natural, meaning equivalent to the body's own CoQ10, form; so make sure you purchase one with "natural" somewhere on the label. It makes something of a difference.
This also with the general advice that you must absolutely do your research on these substances before even contemplating putting one in your gut and brain.
I'd like to note about CoQ10 that it comes in two varieties. The artificial brand is decidedly less soluble than the natural, meaning equivalent to the body's own CoQ10, form; so make sure you purchase one with "natural" somewhere on the label. It makes something of a difference.
This also with the general advice that you must absolutely do your research on these substances before even contemplating putting one in your gut and brain.
? | 3 years ago
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