I've noticed,
in the past of course since I no longer drink, that piracetam potentiates the affects of alcohol. Take your b-complex early in the day and a methyl-b12 lozenge along with your piracetam throughout the day and drink at night. You will get neuroprotection and won't have to drink an enormous amount of alcohol to get twisted.
Alternately, you could just stop drinking. Piracetam actually has the affect on people in taking away their desire to drink. I was an alcoholic and since taking all my nootropics and supplements, I no longer have the drive whatsoever to even take a sip of alcohol. It is amazing!
Here are some studies:
http://www.ncbi.nlm....Pubmed_RVDocSum1: Lijec Vjesn. 1990 Mar-Apr;112(3-4):111-4.Links
[Cognitive function in alcoholics in a double-blind study of piracetam]
[Article in Croatian]
Buranji I, Skocilić Z, Kozarić-Kovacić D.
Klinicki psiholog, Klinicka psihijatrijska bolnica Vrapce, Zagreb, Bolnicka.
The effects of piracetam on cognitive functions have been studied in alcoholic patients. The investigation was carried out on 27 alcoholics who were admitted to hospital with acute withdrawal syndrome. The trial was performed under double-blind condition. Thirteen patients were treated with piracetam and 14 with placebo. The performance of patients treated with piracetam (experimental group) was significantly better at the Block-Design retest, as compared with the control subjects. This was associated with comparatively good perceptual organization, visual motor coordination and abstract reasoning in these patients. Similar kind of performance of these patients has been achieved in the tests used to measure psychomotor speed and attention capacity. Our findings agree well with some observations of the clinicians and may stimulate further research in this field.
PMID: 2204773 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....Pubmed_RVDocSum1: Biomed Biochim Acta. 1983;42(4):391-8.Links
[Effect of central effective substances on alcohol preference]
[Article in German]
Andreas K, Fischer HD, Schmidt J.
The alcohol preference has been used as a model of drug habituation in animal experiments in order to examine the influence of altered synaptic efficiency of central transmission systems following acute receptor reactions with agonists or antagonists as well as by alterations of receptor sensitivity in mice. Ethanol in 10 per cent solution as the only beverage over 4 weeks produces an ethanol preference quotient 1 in the free choice of ethanol solution and water. Control animals without ethanol exposure before the preference test are only drinking water and refuse ethanol. A single injection of haloperidol increases the preference, apomorphine as well as a long term haloperidol administration producing a dopaminergic supersensitivity diminishes the preference. Moreover the preference is enhanced by atropine, isoprenaline and pholedrine and is decreased by arecoline, propranolol and phenoxybenzamine. Cyproheptadine and picrotoxine do not influence the preference. The results point to a preference promoting influence of the alpha- and beta-adrenergic transmission and to an inhibition by dopaminergic and cholinergic activity. An influence by the 5-HT and GABA system could not be observed. Additionally the paper describes the decrease of the ethanol preference by the nootropics piracetam, meclofenoxane, methylglucamine orotate and nicergoline.
PMID: 6138034 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....Pubmed_RVDocSum1: Biomed Biochim Acta. 1985;44(5):767-71.Links
Influence of nootropic drugs on drinking behaviour in ethanol-preferring mice and ethanol-induced increase of seizure susceptibility.
Dienel A, Andreas K, Schmidt J.
The influence of several nootropic drugs (piracetam, pyritinol, meclofenoxat, methylglucamine orotate (MGO) and dihydroergotoxine (DHET) on both the ethanol preference and the enhanced seizure susceptibility after a single dose of ethanol was studied. Piracetam, MGO and DHET reduce the ethanol drinking in ethanol-preferring mice. The enhanced seizure susceptibility after a single dose of ethanol was abolished by piracetam and MGO.
PMID: 4062922 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....Pubmed_RVDocSum1: Eksp Klin Farmakol. 2006 Jul-Aug;69(4):23-7.Links
[Cardioprotective effect of GABA derivatives in acute alcohol intoxication]
[Article in Russian]
Perfilova VN, Tiurenkov IN, Berestovitskaia VM, Vasil'eva OS.
Cardioprotective properties of GABA analogs under conditions of acute alcoholic intoxication have been studied using the following functional tests: volume loads, tests for adrenoreactivity, and maximum isometric load. The experiments showed that a 32% aqueous ethanol solution intraperitoneally injected in a dose of 8 g/kg produces a cardiotoxic action, which is manifested by a decrease in the inotropic reserve in load tests. Citrocard (50 mg/kg), phenibut (50 mg/kg), and piracetam (200 mg/kg) prevent the alcohol-induced myocardium injury, as shown by the heart contractility retained on a higher level in the test group than in the control group.
PMID: 16995433 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....Pubmed_RVDocSum1: Alcohol Alcohol. 1997 Jul-Aug;32(4):471-84.Click here to read Links
The GABAergic system of the dentate gyrus after withdrawal from chronic alcohol consumption: effects of intracerebral grafting and putative neuroprotective agents.
Cadete-Leite A, Brandão F, Andrade JP, Ribeiro-da-Silva A, Paula-Barbosa MM.
Department of Anatomy, Porto Medical School, Portugal.
We have demonstrated that, in the rat hippocampal formation, withdrawal from chronic alcohol consumption aggravates the ethanol-induced loss of pyramidal neurons and dentate granule cells. We have also shown that intracerebral grafting and piracetam could have a protective effect in these conditions. In this study we utilized immunocytochemical methods to investigate whether gamma-aminobutyric acid (GABA)ergic dentate gyrus cells, which are known to be inhibitory, were also affected by withdrawal from alcohol and, if so, whether putative neuroprotective agents could ameliorate the alterations found. Rats were alcohol-fed for 6 months and further divided into several groups: (1) alcohol-fed for an extra 6 months; (2) withdrawn from alcohol for 6 months; (3) withdrawn and grafted with newborn rat hippocampal tissue; (4) withdrawn and orally treated with piracetam for 6 months; (5) withdrawn and treated systemically with monosialoganglioside GM1 for 6 months; (6) withdrawn and treated with the vehicle used to dissolve the GM1. Control animals were pair-fed. All animals were killed 12 months after the beginning of the experiment and processed for GABA immunocytochemistry. GABA-immunoreactive (IR) neurons in the dentate gyrus were quantified and we found that alcohol-fed animals had a significant reduction in the numerical profile density of GABA-IR neurons in the dentate gyrus as a whole and in the hilus and in the granular layer of the suprapyramidal limb. Withdrawal from alcohol aggravated the GABAergic neuronal loss. Of the treatments used, only piracetam had a striking beneficial effect. Data gathered from the present work and from our previous studies indicate that the neuronal loss following chronic alcohol consumption and withdrawal affects both excitatory and inhibitory neurons in the dentate gyrus and that piracetam may have a useful protective role in this condition.
PMID: 9269855 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....Pubmed_RVDocSum1: Alcohol Clin Exp Res. 1991 Oct;15(5):834-8.Click here to read Links
The effects of piracetam on lipofuscin of the rat cerebellar and hippocampal neurons after long-term alcohol treatment and withdrawal: a quantitative study.
Paula-Barbosa MM, Brandão F, Pinho MC, Andrade JP, Madeira MD, Cadete-Leite A.
Department of Anatomy, Porto Medical School, Portugal.
There is a growing body of evidence indicating that chronic alcohol consumption induces morphological changes in the central nervous system (CNS) similar to those observed during brain senescence, including an increased formation of lipofuscin. In addition, it was also found that alcohol withdrawal does not reverse these changes. On the contrary, most of the alterations observed during alcohol consumption worsen as happens with the increased lipofuscin formation. Thus, using our model of alcohol feeding and withdrawal, we decided to examine the effects of different drugs said to offer neuronal protection during CNS degenerative processes. The action of piracetam, a cyclic derivate of GABA and commonly used as a nootropic agent, was tested by studying the lipofuscin accumulation on the cerebellar Purkinje and hippocampal CA3 pyramidal cells in alcohol-treated and withdrawn rats. Piracetam was found to markedly decrease the formation of neuronal lipofuscin. Whatever the functional implications of this pigment, its reduction in piracetam-treated animals might be related either to a protective effect on the intraneuronal membranous system or to an antioxidant property of this molecule.
PMID: 1755517 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....Pubmed_RVDocSum1: Biull Eksp Biol Med. 1988 Jul;106(7):52-6.Links
[Neurophysiological analysis of the correction by nootropic substances of disorders in the bioelectric activity of the brain in animals during chronic administration of ethanol]
[Article in Russian]
Krapivin SV, Bogdanov NN, Voronin KE.
The influence of some drugs (piracetam and 3-oxypyridine derivative) having a nootropic effect on ethanol-induced changes of bioelectrical activity was studied in experiments on freely moving rats. Discontinuation of ethanol administration (1, 2 g/kg, i.p. for 40 days) has been found to provoke destructuring of Fourier's spectral power of sensorimotor cortex and dorsal hippocamp on the EEG. Long-term administration of piracetam or 3-oxypyridine derivative (300 and 50 mg/kg, respectively, i.p. for 40 days) with ethanol has a protective effect and normalizes EEG at the cortical level. The authors discuss possible neurophysiological mechanisms of nootropic drug action in ethanol-induced pathology.
PMID: 3401579 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....Pubmed_RVDocSum1: Alcohol. 1995 May-Jun;12(3):279-88.Click here to read Links
Piracetam impedes hippocampal neuronal loss during withdrawal after chronic alcohol intake.
Brandão F, Paula-Barbosa MM, Cadete-Leite A.
Department of Anatomy, Porto Medical School, Portugal.
In previous studies we have demonstrated that prolonged ethanol consumption induced hippocampal neuronal loss. In addition, we have shown that withdrawal after chronic alcohol intake augmented such degenerative activity leading to increased neuronal death in all subregions of the hippocampal formation but in the CA3 field. In an attempt to reverse this situation, we tested, during the withdrawal period, the effects of piracetam (2-oxo-1-pyrrolidine acetamide), a cyclic derivative of gamma-aminobutyric acid, as there is previous evidence that it might act as a neuronoprotective agent. The total number of dentate granule, hilar, and CA3 and CA1 pyramidal cells of the hippocampal formation were estimated using unbiased stereological methods. We found out that in animals treated with piracetam the numbers of dentate granule, hilar, and CA1 pyramidal cells were significantly higher than in pure withdrawn animals, and did not differ from those of alcohol-treated rats that did not undergo withdrawal. These data suggest that piracetam treatment impedes, during withdrawal, the pursuing of neuronal degeneration.
PMID: 7639963 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....Pubmed_RVDocSum1: Orv Hetil. 2003 May 11;144(19):927-30.Links
[Adjuvant therapy with parenteral piracetam in alcohol withdrawal delirium]
[Article in Hungarian]
Kalmár S.
Semmelweis Kórház, Pszichiátriai Osztály, Kiskunhalas.
The author reports his results of parenteral piracetam treatment in 193 patients admitted to the Psychiatric Department of Semmelweis Hospital with alcohol withdrawal delirium. Alcohol withdrawal delirium is a complex metabolic disorder, the disturbance of the highest cerebral integrative functions, which is caused by the impairment of cerebral oxidative metabolism. Piracetam is effective on most neurotransmitter systems, without a specific receptor agonism or antagonism, increases the effectivity of different biogenic amine systems, has also an effect on membrane permeability, increases the concentration of NMDA (methyl-D-aspartate) receptors in the impaired brain and improves cognitive functions. In the patients suffered from alcohol dependence piracetam produces positive morphologic changes, by decreasing lipofuscin accumulation. In early stage it prevents the development of delirium. Despite of the great number (approximately 150) of medication that were tried in the treatment of delirium, the ideal one still has not been found. Among the accessible therapeutic possibilities the author searched for methods which make the treatment more effective. The administration of parental piracetam, therefore was brought into his therapeutical protocol. Parenteral piracetam--similarly to literature data--proved to be effective in the treatment of alcohol withdrawal delirium. Considering the present--insufficient--hospital financing, it is remarkable that though the costs of the new therapy are higher than the traditional meprobamat therapy, through less side effect it is more economical (overall costs lower) and by decreasing the time of delirium it is more humane to the patients.
PMID: 12809069 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm....Pubmed_RVDocSum1: Eur Neuropsychopharmacol. 2001 Feb;11(1):33-40.Click here to read Links
Can nootropic drugs be effective against the impact of ethanol teratogenicity on cognitive performance?
Vaglenova J, Vesselinov Petkov V.
Laboratory of Experimental Psychopharmacology, Institute of Physiology, Bulgarian Academy of Science, 1113, Sofia Bulgaria. vagleju@auburn.edu
Rats exposed pre- (PA) and postnatally (PNA) to ethanol at a dose of 1 g/kg for 24 h developed fetal alcohol effects (FAE). This was measured using a condition-reflex method for active avoidance with punishment reinforcement (shuttle-box) in which pronounced learning and memory deficits in 3-month-old rats were found after ethanol exposure (Vaglenova and Petkov, 1998. Fetal alcohol effects in rats exposed pre- and postnatally to a low dose of ethanol. Alcohol. Clin. Exp. Res. 22(3), 697--703). In the present study the effects of piracetam (Pyramem) at a dose of 600 mg/kg body weight, aniracetam at 50 mg/kg, and meclophenoxate (Centrophenoxine) at 100 mg/kg were studied. The drugs were administered orally during 10 days to separate groups of naive and pre- and postnatally exposed to ethanol rats. All the investigated nootropic drugs showed a significant possibility to alleviate learning and memory disability of rats with FAE. Aniracetam was administered to 1-month-old rats, demonstrating a prolonged (2 months) therapeutic effect, observed in rats aged 3 months. As previously reported (Vaglenova and Petkov, 1998), between male rats with FAE and controls, 66 and 33% were 'poor learners', respectively. In all nootropic treatment groups the percentage of 'poor learners' dropped to 28%. The positive effects of piracetam, aniracetam and meclophenoxate suggest that these drugs could be used for both treatment and prophylactic of FAE-connected disturbances of cognition.
PMID: 11226810 [PubMed - indexed for MEDLINE]
Edited by luv2increase, 07 October 2008 - 03:19 PM.