how do nootropics interact with other commonly used drugs such as weed, alcohol and lsd?
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onge
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ity
Advocacy & Research for Unlimited Lifespans
Posted 01 November 2006 - 12:51 AM
Posted 01 November 2006 - 12:53 AM
topic:
Synergy with Cannabis, which nootropic enhances your high
Posted 01 November 2006 - 01:01 AM
Posted 01 November 2006 - 01:03 AM
Posted 01 November 2006 - 01:17 AM
centurion, have i offened you? why did you try nootropics then?
have i voilated the "image of the immortalist"?
if a thread is out of bounds, let a moderator remove it.
Posted 01 November 2006 - 01:26 AM
Edited by ahoffm, 01 November 2006 - 01:41 AM.
Posted 01 November 2006 - 01:34 AM
these are not really prescription drugs. they are legal drugs we buy from the internet. i don't think they are all powerful substances either. a lot of people describe find them subtle. and yes, of course, nootropics with more powerful effects should probably not be combined with other drugs.
but you think it's dangerous to combine many powerful prescription drugs?? look at people's "stacks". how many drugs are combined there... 5, 20 at once?
Posted 01 November 2006 - 01:43 AM
Posted 01 November 2006 - 01:56 AM
Posted 01 November 2006 - 02:12 AM
Posted 02 November 2006 - 05:39 AM
Posted 02 November 2006 - 08:53 AM
how do nootropics interact with other commonly used drugs such as weed, alcohol and lsd?
Posted 02 November 2006 - 04:36 PM
Posted 05 November 2006 - 10:00 AM
Posted 05 November 2006 - 10:38 AM
The monoamine oxidase-B inhibitor L-deprenyl protects against 3,4-methylenedioxymethamphetamine-induced lipid peroxidation and long-term serotonergic deficits.
* Sprague JE,
* Nichols DE.
Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, Indiana, USA.
3,4-Methylenedioxymethamphetamine (MDMA)-induced serotonergic neurotoxicity was assessed in the striatum, hippocampus and frontal cortex of rats by using [3H]paroxetine binding to label serotonin (5-HT) uptake sites and 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels as markers of serotonergic function. NMDA (40 mg/kg) induced a significant decrease in both [3H]paroxetine binding Bmax and 5-HT and 5-HIAA levels 7 days after treatment. The monoamine oxidase-B inhibitor L-deprenyl (2 mg/kg) administered 30 min before MDMA blocked these decreases. MDMA (40 mg/kg) also maximally increased the formation of thiobarbituric acid reactive substances (an indicator of lipid peroxidation) 12 hr after treatment in all three brain regions studied. This increase in malondialdehyde formation was also blocked by pretreatment with L-deprenyl. Tryptophan hydroxylase (TPH) activity was also significantly reduced 18 hr after MDMA. L-Deprenyl reversed this decrease in TPH activity. Another experiment confirmed that a significant fraction of [3H]dopamine uptake into hippocampal synaptosomes was blocked by 500 nM fluoxetine, a selective 5-HT uptake inhibitor. These data suggest that the deamination by monoamine oxidase-B of excessive dopamine within the 5-HT terminal generates hydrogen peroxide that may lead to membrane lipid peroxidation, and perhaps other oxidative insults, resulting in selective 5-HT terminal degeneration subsequent to MDMA treatment.
PMID: 7538579 [PubMed - indexed for MEDLINE]
Inhibition of MAO-B protects against MDMA-induced neurotoxicity in the striatum.
* Sprague JE,
* Nichols DE.
Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, IN 47907, USA.
The effects of the MAO-B inhibitors, L-deprenyl and MDL-72974 on MDMA-induced serotonergic neurotoxicity in rats were examined. MDMA alone produced a significant decrease in the number of 5-HT uptake sites, measured as a decrease in the Bmax for binding of [3H]paroxetine, and in 5-HT and 5-HIAA levels in the striatum. L-Deprenyl and MDL-72974 attenuated this MDMA-induced decrease in serotonergic markers. The data suggest a key role for MAO-B in the expression of the neurotoxicity produced by MDMA in the striatum.
PMID: 7542394 [PubMed - indexed for MEDLINE]
Patterns of use and harm reduction practices of ecstasy users in Australia.
* Allott K,
* Redman J.
Department of Psychology, Monash University, Vic. 3800, Australia. kelly.allott@med.monash.edu.au
Harm reduction refers to the use of strategies to prevent or reduce harmful consequences associated with illicit drug use. There is a paucity of research concerning the harm reduction practices employed by ecstasy users. This study aimed to explore the prevalence, nature and factors associated with harm reduction practices employed by ecstasy users in Australia, with a specific focus on the practice of preloading and postloading--the use of pharmaceuticals and natural products prior and subsequent to ecstasy use. One hundred and sixteen Australian residents aged 18 years and over who had used ecstasy at least once in their lifetime were recruited via convenience sampling, 'snowballing' and via web-based advertisements and completed an anonymous questionnaire. Participants reported using a wide range of strategies for minimising ecstasy-associated harm. The most common strategies used for reducing negative side effects, 'comedown' or neurotoxicity were drinking water, limiting or reducing ecstasy use, taking breaks and taking vitamins or other natural substances. Forty percent of the sample had tested their ecstasy pills for the presence of MDMA. Forty-one percent and 47% of participants had engaged in pre- and postloading, respectively, with the most common pre- and postloading substances being multivitamins, 5-HTP, magnesium and fruit or fruit juice. Younger mean age and 'high' total occasions of ecstasy use was significantly associated with preloading, and 'high' total use and frequency of use was associated with postloading. The results indicate that ecstasy users are aware of the potential for harm associated with ecstasy use and attempt to minimise harm by actively employing strategies. By exploring the pattern of harm reduction practices among ecstasy users, this study has highlighted the need for further research into the efficacy and potential clinical drug interactions associated with such practices, as well as the need for investigation of how such practices may affect patterns of ecstasy use.
PMID: 16226850 [PubMed - indexed for MEDLINE]
Posted 05 November 2006 - 02:35 PM
Posted 05 November 2006 - 11:05 PM
how do nootropics interact with other commonly used drugs such as weed, alcohol and lsd?
Posted 06 November 2006 - 02:21 AM
Edited by mitkat, 06 November 2006 - 02:40 AM.
Posted 06 November 2006 - 06:27 PM
Posted 12 November 2006 - 03:12 PM
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