Medical Sciences Stack Exchange is a question and answer site for professionals in medical and allied health fields, students of those professions, related academics, and others with a sound understanding of medicine and healthcare-related sciences. It only takes a minute to sign up.
Sign up to join this community
Many drugs that will kill you in high quantities are used recreationally in low doses. (e.g. alcohol or heroine).
I wonder if you diluted a military grade nerve agent in a lot of water. Would the resultant drink be pleasant? Sort of like alcohol?
Obviously this is a hypothetical question. But hypothetically could you create a drink with a tiny amount of nerve agent in it and say a mixer to make a pleasant after dinner drink? What would be the effects do you imagine?
Okay, this is the closest you're going to get to a "military grade" nerve agent that elevates your mood: using botox as an antidepressant.
Botulinum toxin A (botox) is a nerve agent. In fact, it's the most potent toxin known, and could potentially be used as a bioweapon.
Botulinum toxin: Bioweapon & magic drug (Dhaked, et al. 2010)
Botulinum neurotoxins, causative agents of botulism in humans, are produced by Clostridium botulinum, an anaerobic spore-former Gram positive bacillus. Botulinum neurotoxin poses a major bioweapon threat because of its extreme potency and lethality; its ease of production, transport, and misuse; and the need for prolonged intensive care among affected persons. A single gram of crystalline toxin, evenly dispersed and inhaled, can kill more than one million people. The basis of the phenomenal potency of botulinum toxin is enzymatic; the toxin is a zinc proteinase that cleaves neuronal vesicle associated proteins responsible for acetylcholine release into the neuromuscular junction. As a military or terrorist weapon, botulinum toxin could be disseminated via aerosol or by contamination of water or food supplies, causing widespread casualties. A fascinating aspect of botulinum toxin research in recent years has been development of the most potent toxin into a molecule of significant therapeutic utility. It is the first biological toxin which is licensed for treatment of human diseases. In the late 1980s, Canada approved use of the toxin to treat strabismus, in 2001 in the removal of facial wrinkles and in 2002, the FDA in the United States followed suit. The present review focuses on both warfare potential and medical uses of botulinum neurotoxin.
However, if you injected, say, 40 units of botox into your procerus and corrugator supercilii frown muscles, you would get a drug with a robust antidepressant effect. The effect size is quite impressive and the antidepressant effect may be greater than what is typically seen from conventional antidepressants:
Botulinum toxin A (BTA) injection into the glabellar region is currently being studied as a treatment for major depressive disorder (MDD). Here we explore efficacy data of this novel approach in a pooled analysis.A literature search revealed 3 RCTs on this topic. Individual patient data and clinical end points shared by these 3 trials were pooled and analyzed as one study (n=134) using multiple regression models with random effects.In the pooled sample, the BTA (n=59) and the placebo group (n=75) did not differ in the baseline variables. Efficacy outcomes revealed BTA superiority over placebo: Improvement in the Hamilton Depression Rating Scale or Montgomery-Asberg Depression Rating Scale 6 weeks after baseline was 45.7% for BTA vs. 14.6% for placebo (p<0.0001), corresponding to a BTA response rate of 54.2% (vs. 10.7%) and a BTA remission rate of 30.5% (vs. 6.7%). Equalling the status of a meta-analysis, this study increases evidence that a single treatment of BTA into the glabellar region can reduce symptoms of MDD. Further studies are needed to better understand how BTA exerts its mood-lifting effect.
The proposed mechanism of action is quite interesting. It's thought that afferents in the face can influence your mood by sending feedback to the amygdala. In short, botox works by paralysing the frown muscles in your face. And if you can't frown, then perhaps you can't feel so down:
We develop the concept of emotional proprioception, whereby the muscles of facial expression play a central role in encoding and transmitting information to the brain’s emotional circuitry, and describe its underlying neuroanatomy. We explore the role of facial expression in both reflecting and influencing depressed mood. The circuitry involved in this latter effect is a logical target for treatment with botulinum toxin, and we review the evidence in support of this strategy. Clinical trial data suggest that botulinum toxin is effective in treating depression. We discuss the clinical and theoretical implications of these data. This novel treatment approach is just one example of the potential importance of the cranial nerves in the treatment of depression.
References
Dhaked, R. K., Singh, M. K., Singh, P., & Gupta, P. (2010). Botulinum toxin: bioweapon & magic drug. The Indian journal of medical research, 132(5), 489. PMCID: PMC3028942
Finzi, E., & Rosenthal, N. E. (2016). Emotional proprioception: treatment of depression with afferent facial feedback. Journal of psychiatric research, 80, 93-96. DOI: 10.1016/j.jpsychires.2016.06.009
Magid, M., Finzi, E., Kruger, T. H. C., Robertson, H. T., Keeling, B. H., Jung, S., ... & Wollmer, M. A. (2015). Treating depression with botulinum toxin: a pooled analysis of randomized controlled trials. Pharmacopsychiatry, 25(06), 205-210. DOI: 10.1055/s-0035-1559621
"Recreational drugs" have "psychotropic effects," which means they affect the mood and perception of stimuli in the brain. Both alcohol and heroin are psychotropic drugs. Alcohol acts mainly on the GABA and glutamate receptors in the brain resulting in disinhibited behavior. Heroin acts on the opioid receptors in the brain, which results in euphoria.
Military nerve gases, even if they have some effects on mood, they mainly have unpleasant physical effects by increasing the activity of the neurotransmitter acetylcholine in the parasympathetic nerves and between the nerves and muscles, which results in vomiting, diarrhea, increased salivation, stopping breathing and heart beating and eventually death. So, by decreasing the dose of a nerve gas you would still likely have more unpleasant toxic effects than pleasant psychotropic effects.
UPDATE:
Nerve gases may actually have some psychotropic effects in the brain as a "side effect" (as apposed to their "main effects" in the peripheral nerves and muscles). But, by decreasing the dose to a non-lethal dose, they would still likely have more unpleasant main effects than pleasant psychotropic effects, so there would be no point to use them. You can think of organophosphate pesticides as a much weaker ("diluted") form of organophosphate nerve gases. You can further dilute pesticides, but it is not likely you'll get an acceptable ratio of pleasant/unpleasant effects from them.
Contra to Jan's answer, "so they do not have psychotropic effects"... actually they do. First, acetylcholine is a CNS neurotransmitter as well. Second, nerve agents aren't that selective (like many psychiatric drugs actually):
Nerve agents cause excessive stimulation of the cholinergic system, with stimulation of muscarinic receptors at autonomic effector organs, stimulation then depression of skeletal muscle and autonomic ganglia, and stimulation of cholinergic receptors in the CNS [...]. They also bind to nicotinic, cardiac muscarinic and glutamate NMDA (N-methyl-D-aspartate) receptors directly and antagonize GABA (γ-aminobutyric acid) neurotransmission.
The CNS effects of nerve agents [are] (same source):
Headache, anxiety, irritability, ataxia, fatigue, amnesia, hypothermia, lethargy, unconsciousness, central respiratory depression, convulsions, coma.
Additionally you get all the non-CNS effects (they're specified for each type of receptor in the source, but I've compressed them below):
Miosis, eye pain, glandular hypersecretion (salivary, bronchial and lachrymal), sweating, bradycardia (QT prolongation or atrioventricular block), bronchoconstriction, vomiting, diarrhoea, urination, Tachycardia, hypertension (adrenal medulla), Fasciculations, weakness, muscular paralysis, rhabdomyolysis, depressed ventilation
Probably most of these and some of the CNS effects would be (very) undesirable for a recreational drug. There's also the fact that possessing a nerve agent would be seen possibly as terrorism threat and so forth... So, why bother when you get most of those (listed) CNS results with alcohol?
