Personally, the times I've done cocaine whilst on MDMA just took me out of my roll and into a coke high for about 30 min before picking back up with the roll, but weaker. In my opinion, coke and alcohol are both bully drugs that will take over from whatever else you might be doing. YMMV.
I'm pretty sure NHTSA or similar has done a study ...
The study was conducted in accordance with the Declaration of Helsinki, approved by the local Institutional Review Board (Comité Ètic d’Investigació Clı́nica -Institut Municipal d’Assistència Sanitària), and authorized by the Dirección General de Farmacia y Productos Sanitarios (98/112) of the Spanish Ministry of Health. All volunteers gave the written informed consent before to inclusion in the study and were paid for their participation.
3,4-Methylenedioxymethamphetamine (MDMA) is frequently consumed in association with alcohol. The effect of this combination in humans has not been previously investigated. Nine male healthy volunteers received single oral doses of 100 mg of MDMA plus 0.8 g/kg ethanol, 100 mg of MDMA, 0.8 g/kg of ethanol, and placebo in a double blind, double dummy, randomized crossover trial. Measurements included psychomotor performance, subjective effects, and pharmacokinetics.
Plasma concentrations of MDMA showed a 13% increase after the use of alcohol, whereas plasma concentrations of alcohol showed a 9 to 15% decrease after MDMA administration. The MDMA-alcohol combination induced longer lasting euphoria and well being than MDMA or alcohol alone. MDMA reversed the subjective sedation induced by alcohol but did not reduce drunkenness feelings. MDMA did not reverse the actions of alcohol on psychomotor abilities. Combined use of MDMA and alcohol causes dissociation between subjective and objective sedation. Subjects may feel euphoric and less sedated and might have the feeling of doing better, but actual performance ability continues to be impaired by the effect of alcohol. Confirmation of these findings in further studies will be highly relevant in terms of road safety.
To our knowledge, results of this study provide the first information in humans about the pharmacodynamics (psychomotor performance and subjective effects) and pharmacokinetics of MDMA and alcohol interactions. The administration of 100 mg of MDMA, a dose in the range of doses used recreationally (Gamella et al., 1997), produced subjective effects similar to own observations in a previous study in which 75 and 125 mg were used (Camı́ et al., 2000a). Similar feelings of euphoria, stimulation,
Our previous studies consistently showed that MDMA-induced locomotor hyperactivity is dramatically increased by coadministration of ethanol (EtOH) in rats, indicating possible potentiation of MDMA abuse liability. Thus, we aimed to identify the brain region(s) and neuropharmacological substrates involved in the pharmacodynamics of this potentiation.
We first showed that potentiation of locomotor activity by the combination of ip administration of EtOH (1.5 g/kg) and MDMA (6.6 mg/kg) is delay sensitive and maximal when both drugs are injected simultaneously. Then, we used the 2-deoxyglucose quantitative autoradiography technique to assess the impact of EtOH, MDMA, or their combination on local cerebral metabolic rates for glucose (CMRglcs). We showed a specific metabolic activation in the ventral striatum (VS) under MDMA + EtOH versus MDMA or EtOH alone. We next tested if reversible (tetrodotoxin, TTX) or permanent (6-hydrodoxyopamine, 6-OHDA) lesion of the VS could affect locomotor response to MDMA and MDMA + EtOH. Finally, we blocked dopamine D1 or glutamate NMDA receptors in the VS and measured the effects of MDMA and MDMA + EtOH on locomotor activity. We showed that bilateral reversible inactivation (TTX) or permanent lesion (6-OHDA) of the VS prevented the potentiation by EtOH of MDMA-induced locomotor hyperactivity. Likewise, blockade of D1 or NMDA receptors in the VS also reduced the potentiation of MDMA locomotor activity by EtOH. These data indicate that dopamine D1 and glutamate NMDA receptor-driven mechanisms in the VS play a key role in the pharmacodynamics of EtOH-induced potentiation of the locomotor effects of MDMA.
