co na koncentracje?

Om i jak dawkowac to cudo??

moze i racja bo ona na mnie tez mowi miśku
3ba cos zmienic huehuheuh

a przyczyna jest taka ze nie mam ochoty na nauke

Deanol
deanol
nootropicum, psychostimulans
N06BX
Działanie: Trzeciorzędowa amina pochodna kwasu benzoesowego będąca prekursorem acetylocholiny. Zwiększa syntezę acetylocholiny w OUN i poprawia przekaźnictwo neuronalne. Wykazuje działanie stymulujące na OUN, poprawia zdolność koncentracji i sprawność psychofizyczną oraz zmniejsza zapotrzebowanie na sen.

Wskazania: Przewlekłe zaburzenia emocjonalne, zespoły psychoorganiczne, związane z procesami atroficznymi OUN, encefalopatia miażdżycowa, przewlekłe zmęczenie, moczenie nocne (wg niektórych doniesień działanie porównywalne z placebo), nietrzymanie stolca u dorosłych i dzieci, zaburzenia koncentracji i uczenia się u dzieci.

Przeciwwskazania: Padaczka. Stany pobudzenia i niepokoju.

Interakcje: Nasilenie działań toksycznych alkoholu (reakcja typu disulfiramowego).

Działanie niepożądane: Nadpobudliwość, zaburzenia snu (w tym bezsenność), bóle głowy i mięśni, wzrost napięcia mięśni, zaparcie, świąd, rumień, obniżenie ciśnienia tętniczego.

Ciąża i laktacja: Ze względu na brak odpowiednich badań nie zaleca się stosowania u kobiet w ciąży lub podczas karmienia piersią.

Dawkowanie: Dorośli początkowo 25-50 mg/d w 2 dawkach podzielonych, dawkę można stopniowo zwiększyć do 150 mg/d lub więcej. Po kilku tygodniach dawkę zmniejszyć do podtrzymującej 25-50 mg/d. Dzieci 7.-15. rż.: w zaburzeniach koncentracji 300 mg/d rano, po ok. 3 tyg. i uzyskaniu poprawy zmniejszyć do 100 mg/d; w moczeniu nocnym 75-100 mg/d w 3-4 dawkach podzielonych przez 3-4 tyg. Niekiedy podaje się w wątpliwość skuteczność małych dawek.

Preparaty
deanol

czyli lecisz na 2 fronty ?

Ej jakie byście mi Omega 3 polecili jakiej firmy?

Synonyms: 2-dimethylaminoethanol, dimethylethanolamine, deanol

This supplement has been proposed for the following purposes or treating the following conditions. Also given is the current scientific support for use (on a scale of 0-10). Note that a low rating does not necessarily indicate that a supplement does not work, just that research is either unavailable or has not demonstrated a benefit.


ADD/ADHD - 7
Learning/memory - 3
Alzheimer's - 1
Tardive dyskinesia - 1


Side effects


Reported side effects associated with DMAE use include gastrointestinal disturbances, bad body odor, drowsiness, sedation, retardation, confusion, increased blood pressure, depression, and hypomania.

DMAE may cause a decrease in the levels of some choline metabolites. Choline supplementation may help to correct this.

DMAE should be avoided under all circumstances by pregnant women.


DMAE is a naturally occuring analogue of choline. It is mareketed primarily as a memory enhancing agent and anti-aging nutrient. This article will review the presently available research on DMAE and whether or not it supports these claims.

Centrophenoxine (CPH), an established nootropic and anti-aging nutrient, is DMAE bonded to p-chlorophenoxyacetic acid (PCPA). CPH is a potent OH radical scavenger and also prevents the buildup of the age-related pigment lipofuscin. According to some research, the properties of CPH can be primarily attributed to DMAE moiety, while the PCPA just allows for better penetration of the blood brain barrier [1-2]. If this were the case, DMAE would be pharmacologically very similar to CPH, but with a higher amount needed for the same effect. However, other research contradicts this idea. For example, an in vitro study found that DMAE did not reduce age pigment accumulation, but the combination of DMAE and PCPA did [3]. Another found that PCPA had superoxide radical scavenging properties, whereas DMAE did not, although high concentrations of the substances were used [4]. Other researchers also indicate that PCPA is responsible for some of the important actions of CPH [5].

Research has also been conducted to see if DMAE shares the anti-aging properties of CPH. Like CPH, DMAE is a potent and site specific OH radical scavenger. This is due to DMAE's ability to become phosphatidyl-DMAE and replace phosphatidylcholine in nerve membranes, thus offering local protection from free radicals [1]. An in vitro study found that adding DMAE to myocytes protected from cell damage from ischemia and metabolic inhibition [6], while a study in mice found that DMAE did not change survival rate, but did reduce lipofuscin content [7]. However, a study in Japanese quail found that administration of DMAE (18 mg/kg) starting late in life actually reduced life span by twenty weeks [8]. Therefore, it is necessary to emphasize caution when applying the effects of CPH to DMAE. It also brings up a larger issue, that of possible toxicity or side effects from DMAE.

Another reputed effect of DMAE supplementation is a rise in choline and acetylcholine levels and a corresponding increase in memory ability. This is based on the assumption that DMAE is a choline precursor [1] and also crosses the blood brain barrier more effectively than choline itself [9], giving it the ability to reach the brain and then increase brain choline levels. DMAE does consistently increase levels of free choline in the brain and body, but this is not because it is a converted to choline – it is because it competitively inhibits choline kinase and choline oxidase, preventing the metabolism of choline to phosphocholine and betaine [10-12]. As mentioned above, this results in the production of phosphatidyl-DMAE. However, this is not necessarily beneficial, since it replaces phosphatidylcholine, and thus may effectively blunt some of the biological actions of phosphatidylcholine [39].

There is very little evidence that this increase in choline levels leads to a consequent rise in acetylcholine, and given that DMAE competitively inhibits choline transport, there is theoretical basis for an anticholinergic effect [10-11, 13-15]. If anything, this renders DMAE supplementation the equivalent of choline supplementation, since that also increases brain choline levels but generally fails to increase acetylcholine [16]. In an in vitro study, DMAE reduced the synthesis of acetylcholine by inhibiting high affinity choline transport, and the same researchers found no effect of DMAE on acetylcholine levels in vivo in rats [17]. In another study in which a wide range of doses of DMAE was administered to mice, there was no increase in brain acetylcholine levels except an increase in the striatum at the highest dose which appeared to be unrelated to tissue DMAE content [18].

Studies on the effects of DMAE on learning and memory have also been discouraging. In mice, DMAE improved one-week retention in mice on a T-maze active avoidance task [19]. However, trials in the healthy elderly and in people with Alzheimer's and amnestic disorders have found no positive effect on memory or cognition [20-23]. One study did report better mood after treatment, but there was no control group [23].

DMAE has also been researched in the treatment of tardive dyskinesia (a type of movement disorder). Although initial results were promising, they failed to be replicated in double-blind, placebo-controlled trials [24-30]. In two of these studies, choline was effective whereas DMAE was not [24, 29]. In one trial, symptoms were worse in the DMAE-treated group, and it was suggested that DMAE had actually interfered with cholinergic function [25].

A final use proposed for DMAE is in the treatment of childhood hyperactivity. A placebo-controlled trial in 74 children found that DMAE at 500 mg daily was as effective as methylphenidate (Ritalin) [15]. The mechanism of action for this effect is not established.

Numerous side effects from DMAE treatment have been reported in the literature. These include gastrointestinal disturbances, bad body odor, drowsiness, sedation, retardation, confusion, increased blood pressure, depression, and hypomania; some of these are causes of frequent withdrawal [20, 31-33]. Airborne DMAE is associated with a variety of adverse events (some of which have been reported in humans exposed to high concentrations in a label printing plant), primarily visual disturbances (blurry, halo, and blue-grey vision, corneal opacity, and decrements in visual acuity and contrast sensitivity) and skin irritation [34-36]. However, it is doubtful that oral supplementation will lead to these effects. DMAE also has potential teratogenic effects due to the fact that it inhibits choline uptake [10]. In one study, rat pups fed a choline-deficient diet containing DMAE died within 36 hours of birth, supporting the notion that DMAE does not function as an effective choline precursor [37]. In another experimental study, the presence of choline or acetylcholine offset developmental toxicity due to DMAE [38].

In conclusion, the scientific literature does not support many of the claims made regarding DMAE, although older research does support a possible benefit in the treatment of hyperactivity. When taken in the right amounts, there are some possible benefits related to its antioxidant effects and benefits resulting from an anticholinergic effect can even be hypothesized. Also, there is not enough research to determine the effects when DMAE and choline are taken together. It is possible that the two would just blunt one another's effects. However, it is also possible that this would offer the best of both worlds, both the antioxidant effects of DMAE but also sufficient choline metabolites to protect against any potential negative effects. Further research is clearly needed, but until then, it is unwise to use DMAE without a protective choline supplement.

1. Ann N Y Acad Sci. 2002 Apr;959:308-20; discussion 463-5. Pharmacological interventions against aging through the cell plasma membrane: a review of the experimental results obtained in animals and humans. Zs-Nagy I.

2. Arch Gerontol Geriatr. 1989 Nov-Dec; 9(3): 215-29. On the role of intracellular physicochemistry in quantitative gene expression during aging and the effect of centrophenoxine. A review. Zs-Nagy I.

3. Exp Aging Res. 1978 Apr;4(2):133-9. Effects of PCA and DMAE on the namatode Caenorhabditis briggsae. Zuckerman BM, Barrett KA.

4. J Free Radic Biol Med. 1985; 1(5-6): 403-8. Superoxide radical scavenging ability of centrophenoxine and its salt dependence in vitro. Semsei I, Zs-Nagy I.

5. Pol J Pharmacol Pharm. 1976;28(2):137-42. Further study on pharmacology of meclophenoxate and it components in mice. Meszaros J, Gajewska S.

6. Am J Physiol. 1995 Feb; 268(2 Pt 2): H773-80. Phosphatidylethanolamine and sarcolemmal damage during ischemia or metabolic inhibition of heart myocytes. Post JA, Bijvelt JJ, Verkleij AJ.

7. Mech Ageing Dev. 1988 Feb; 42(2): 129-38. Effect of lifetime administration of dimethylaminoethanol on longevity, aging changes, and cryptogenic neoplasms in C3H mice. Stenback F, Weisburger JH, Williams GM.

8. J Gerontol. 1977 Jan;32(1):38-45. Effects of dimethylaminoethanol upon life-span and behavior of aged Japanese quail. Cherkin A, Exkardt MJ.

9. Ann Neurol. 1978 Oct;4(4):302-6. Deanol acetamidobenzoate inhibits the blood-brain barrier transport of choline. Millington WR, McCall AL, Wurtman RJ.

10. FASEB J. 2002 Apr;16(6):619-21. Perturbations in choline metabolism cause neural tube defects in mouse embryos in vitro. Fisher MC, Zeisel SH, Mar MH, Sadler TW.

11. Teratology. 2001 Aug;64(2):114-22. Inhibitors of choline uptake and metabolism cause developmental abnormalities in neurulating mouse embryos. Fisher MC, Zeisel SH, Mar MH, Sadler TW.

12. J Neurochem. 1981 Aug;37(2):476-82. Deanol affects choline metabolism in peripheral tissues of mice. Haubrich DR, Gerber NH, Pflueger AB.

13. J Neurochem. 1990 May; 54(5): 1467-73. Choline uptake by cerebral capillary endothelial cells in culture. Estrada C, Bready J, Berliner J, Cancilla PA.

14. J Nucl Med. 1985 Dec; 26(12): 1424-8. Carbon-11 choline: synthesis, purification, and brain uptake inhibition by 2-dimethylaminoethanol. Rosen MA, Jones RM, Yano Y, Budinger TF.

15. Clin Pharmacol Ther. 1975 May;17(5):534-40. Deanol and methylphenidate in minimal brain dysfunction. Lewis JA, Young R.

16. Mech Ageing Dev. 2001 Nov;122(16):2025-40. Treatment of cognitive dysfunction associated with Alzheimer's disease with cholinergic precursors. Ineffective treatments or inappropriate approaches? Amenta F, Parnetti L, Gallai V, Wallin A.

17. J Pharmacol Exp Ther. 1979 Dec;211(3):472-9. Dimethylaminoethanol (deanol) metabolism in rat brain and its effect on acetylcholine synthesis. Jope RS, Jenden DJ.

18. J Pharmacol Exp Ther. 1977 Mar;200(3):545-59. Is 2-dimethylaminoethanol (deanol) indeed a precursor of brain acetylcholine? A gas chromatographic evaluation. Zahniser NR, Chou D, Hanin I.

19. Neurobiol Aging. 1983 Spring;4(1):37-43. Memory retention: potentiation of cholinergic drug combinations in mice. Flood JF, Smith GE, Cherkin A.

20. Am J Psychiatry. 1981 Jul;138(7):970-2. Double-blind trial of 2-dimethylaminoethanol in Alzheimer's disease. Fisman M, Mersky H, Helmes E.

21. Ateneo Parmense Acta Biomed. 1980;51(4):383-9. [The effect of Deanol on amnesic disorders. A preliminary trial (author's transl)] [Article in Italian] Caffarra P, Cattelani R, Mazzucchi A, Moretti G, Parma M.

22. Psychopharmacology (Berl). 1979;66(1):99-104. The effects of deanol on cognitive performance and electrophysiology in elderly humans. Marsh GR, Linnoila M.

23. J Am Geriatr Soc. 1977 Jun;25(6):241-4. Senile dementia: treatment with deanol. Ferris SH, Sathananthan G, Gershon S, Clark C.

24. Psychopharmacology (Berl). 1979 May 25;63(2):143-6. Dimethylaminoethanol (deanol): effect on apomorphine-induced stereotypy and an animal model of tardive dyskinesia. Davis KL, Hollister LE, Vento AL, Beilstein BA, Rosekind GR.

25. Psychopharmacology (Berl). 1979 Nov;65(3):219-23. Ineffectiveness of deanol in tardive dyskinesia: a placebo controlled study. de Montigny C, Chouinard G, Annable L.

26. Acta Neurol Scand. 1978 Aug;58(2):134-8. Deanol and physostigmine in the treatment of L-dopa-induced dyskinesias. Lindeboom SF, Lakke JP.

27. JAMA. 1978 May 12;239(19):1997-8. Double-blind evaluation of deanol in tardive dyskinesia. Penovich P, Morgan JP, Kerzner B, Karch F, Goldblatt D.

28. Neuropsychobiology. 1978;4(3):140-9. Deanol, lithium and placebo in the treatment of tardive dyskinesia. A double-blind crossover study. Jus A, Villeneuve A, Gautier J, Jus K, Villeneuve C, Pires P, Villeneuve R.

29. Arch Neurol. 1977 Dec;34(12):756-8. Deanol acetamidobenzoate treatment in choreiform movement disorders. Tarsy D, Bralower M.

30. Am J Psychiatry. 1977 Jul;134(7):769-74. Cholinergic influences in tardive dyskinesia. Tamminga CA, Smith RC, Ericksen SE, Chang S, Davis JM.

31. Cochrane Database Syst Rev. 2002;(3):CD000207. Cholinergic medication for neuroleptic-induced tardive dyskinesia. Tammenmaa IA, McGrath JJ, Sailas E, Soares-Weiser K.

32. Schizophr Res. 1999 Aug 23;39(1):1-16; discussion 17-8. The treatment of tardive dyskinesia--a systematic review and meta-analysis. Soares KV, McGrath JJ.

33. Psychopharmacology (Berl). 1979 Apr 11;62(2):187-91. Mood alterations during deanol therapy. Casey DE.

34. Occup Environ Med. 2003 Jan;60(1):69-75. Visual and ocular changes associated with exposure to two tertiary amines. Page EH, Cook CK, Hater MA, Mueller CA, Grote AA, Mortimer VD.

35. Vet Hum Toxicol. 1996 Dec; 38(6): 422-6. Acute toxicity and primary irritancy of alkylalkanolamines. Ballantyne B, Leung HW.

36. J Appl Toxicol. 1996 Nov-Dec; 16(6): 533-8. Developmental toxicity study in Fischer 344 rats by whole-body exposure to N,N-dimethylethanolamine vapor. Leung HW, Tyl RW, Ballantyne B, Klonne DR.

37. Pediatr Res. 1978 Sep;12(9):952-5. Effects of dietary choline and N,N-dimethylaminoethanol on lung phospholipid and surfactant of newborn rats. Katyal SL, Lombardi B.

38. Environ Health Perspect. 2003 Nov;111(14):1730-5. The sea urchin embryo as a model for mammalian developmental neurotoxicity: ontogenesis of the high-affinity choline transporter and its role in cholinergic trophic activity. Qiao D, Nikitina LA, Buznikov GA, Lauder JM, Seidler FJ, Slotkin TA.

39. Biochim Biophys Acta. 2004 Mar 22;1636(2-3):175-82. Dimethylethanolamine does not prevent liver failure in phosphatidylethanolamine N-methyltransferase-deficient mice fed a choline-deficient diet. Waite KA, Vance DE.

deanol démanol (in F) CR 121 (acetylhydrogenglutamate)
Description
Considered to be a precursor of acetylcholine. Mild psychostimulating, antidepressive and anxiolytic properties reported. Possibly linked with the cerebral effects of meclofenoxate. Investigated in the treatment of tardive dyskinesia, Huntington's chorea, Gilles de 1a Tourette syndrome, behavioral disorders in children and cognitive malfunction in the elderly.
Commercial Info
Acti 5 Pierre Fabre, F: (pyroglutamate) ampoules buvables 100mg/5ml (with two additional drugs)
Acticinco Robapharm, ESP: drink amps. 100mg + additives
Antianorex triple Lesvi, ESP: oral sol. 500mg (aceglutamate)
Astyl Laphal, F: caps. 200mg (bisorcate)
Bimanol Polfa, PL: tabs.25mg, 100mg (acetamidobenzoate)
Cervoxan S. M. B. , B: (p-acetamidobenzoate) tabs. 75mg (deleted)
Clérégil Merck-Clévenot, F: (acetylglutamate = aceglumate) amps. buvables 500mg/5ml (children) and 2g/10ml (adults) (range deleted)
Deaner Riker, USA: (p-acetamidobenzoate) tabs. 25, 100 and 250mg
Deanol Kettelhack Riker, BRD: (p-acetamidobenzoate) tabs. 100mg (deleted)
Débrumyl Pierre Fabre, F: (pyrrolidone carboxylate)
Denubil Pierre Fabre, ESP: (pyrrolidone carboxylate) same comp. as Débrumyl
Doprene Pierre Fabre, Niadas, GR: same composition
Geriatric Pharmaton Bender, A, Pharmaton, BRD: caps.20mg (bitartrate) + add. (deleted in BRD)
Geriavit Pharmaton, CH: caps.26mg+add. - effervescent tabs. 26mg+add.
Geriavit Pharmaton, CH: caps.20mg bitartrate + 40mg
Juniormen Retrain ESP: caps 5mg tartrate + additives
Medacaps N Palmico, ITA, BRD: caps.25mg (bitartrate) (deleted in both countries)
Pharmaton Boehringer Ingelheim, F - Fher, ESP: (bitartrate) caps. 26mg plus about 18 vitamins and trace elements (in NL ''over the counter'' product)
Pharmaton Boehringer Ingelheim, NZ: Ginseng extract + Vitamins + minerals without deanol
Risatarun Ravensberg, BRD: (aceglumate) solution 1g/20ml, 4g/20ml
Rischiaril Piam, ITA: drink amps. 1 1/2 g/15 ml, 3 g/15 ml.
Tonibral adultes GNR-Pharma, F: (hemisuccinate)drink amps. 200mg/10ml
Tonuvital Synthélabo Delalande, F: (bitartrate) sachets 1g with 20mg ribonucleic acid (deleted)
Vigoran Golaz, CH: caps.25mg hydrogenotartrate + 200mg Ginseng extract + 200mg magnseium orotate
Vita Gerin Melisana, CH: caps.22mg orotate + vitamins
Vita Gerin(e) Melisana, CH-Cassella, BRD - Chemomedica, Creutzberg, A: caps.22mg orotate+add.
Vitasana Bendez, A: caps 20mg + additives
References
Whittaker VP: The contribution of drugs and toxins to understanding of cholinergic function. Trends Pharmacol Sci 11: 8-123, 1990
Robinson SE, Martin RM, Davis TR, et al: The effect of acetylcholine depletion on behavior following traumatic brain injury. Brain Research 509: 41-46, 1990
Vita JA, Treasure CB, Nabel EG, et al: Coronary vasomotor response to acetylcholine relates to risk factors for coronary artery disease. Circulation 81: 491-497, 1990.

nie rozumiem, brac 25-50mg dziennie a masz 250mg kapsulki?

zalezy jaki zwiazek deanolu.
inna sprawa ze polskie leki nootropowe sa troche hmm slabe i za drogie...

w stanach np piracetam, deanol, winpocetyna sa bez recepty i smiesznie tanie.

btw robie z siebie cyborga ale to pozniej

jesli chodzi o te ginko to prosze o nazwy jakis konkretnych produktów ?