Alcohol & NBOMe
Alcohol, specifically ethanol, potentiates the effects of gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the brain. Ethanol functions as a positive allosteric modulator, particularly of receptors containing the δ subunit. Similar to benzodiazepines and barbiturates, it enhances the GABA system's inhibitory effect. This leads to a general slowdown in sensory information processing, inhibition of cognitive processes, and suppression of normal bodily and cognitive functions. Unlike other GABAergic drugs that consistently induce neurological suppression regardless of dosage, ethanol, especially in moderate amounts, may counterbalance some of these inhibitory effects, making its neurological activity somewhat distinct.
In addition, alcohol mediates its effects through:
- 5-HT3 Serotonine Receptor Agonism
- Interaction with Glycine and Nicotinic Acetylcholine Receptors
- Adenosine Uptake Inhibition: Ethanol inhibits the nucleoside transport system in bronchial epithelial cells, blocking adenosine uptake. This leads to increased extracellular adenosine, potentially affecting airway homeostasis.
- Glutamate Suppression: It reduces the effectiveness of glutamate, an excitatory neurotransmitter. Alcohol does this by interacting with and blocking glutamate from binding to NMDA receptors.
- Dihydropyridine Effects: Ethanol's direct influences lead to secondary effects involving various neurotransmitter and neuropeptide systems, contributing to the behavioral and symptomatic effects seen in alcohol intoxication.
The NBOMe family of drugs, which includes compounds like 25I-NBOMe, 25C-NBOMe, and 25B-NBOMe, represents a class of potent synthetic hallucinogens. These substances are known for their strong psychedelic effects, even at very low doses.
The primary mechanism of NBOMe compounds is their strong agonistic action on the 5-HT2A serotonin receptor. This receptor is key in modulating perception, cognition, and mood. The intense activation of 5-HT2A receptors is primarily responsible for the hallucinogenic effects of these substances.
While 5-HT2A is the primary target, NBOMe compounds can also interact with other serotonin receptors, though with less affinity. This can contribute to their complex psychopharmacological profile.
Combining alcohol with NBOMes presents a complex and potentially dangerous interaction due to their distinct pharmacological profiles and the risks associated with their combined effects.
Alcohol's GABAergic and dopaminergic effects might be paradoxically modulated by NBOMe's serotonergic activity, leading to unpredictable mental states. Combining alcohol's vasodilatory effects with NBOMe's actions can strain the cardiovascular system, increasing risks of hypertension and arrhythmias. Both substances impair judgment, but in different ways; the combination can lead to heightened risk-taking behaviors.
With poor timing and chaotic use, the user may encounter strong anxiety, paranoia, confusion, nausea, headaches, and dizziness. This is the most harmless. If the dosages are not observed, states of psychosis with unpleasant and frightening hallucinations are possible.
We have not come across confirmed data on acute, rapid, and fatal conditions associated with this combination.
Small doses of alcohol can be used before using psychedelics to relieve anxiety and facilitate "entry". Also, small doses of alcohol can play the role of a light sedative at the final stages of the trip or after it. It is important to take into account individual tolerance, and susceptibility, stick to really small doses, and proper timing.
Considering the above, we recommend treating this combination with great caution.
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