No other class of psychotropic compounds stirs up as much fear and disdain as the deliriants. They are a pariah among drug users and frequently given the epithet of the world’s most dangerous drugs—which with their steep dosage curve and history intertwined with murder and madness, is not far from the truth. That is what fascinated me with these substances and prompted me to research them further. While never safe, I found that there are less dangerous methods of use and a more nuanced picture to be painted.
This essay is dedicated first and foremost to my morbid curiosity, but it is also an attempt at information and harm reduction. I am not in any way, shape, or form encouraging the recreational use of these powerful compounds, but if you, for whatever reason, will do it regardless, at least be as educated on the topic as possible.
“If you dance with the devil, then you haven’t got a clue, for you think you’ll change the devil, but the devil changes you.” – J.M. Smith
Delirium is an organically caused decline from a previous baseline level of mental function, often varying in severity over a short period, including attention deficits and disorganization of behavior, usually involving other cognitive deficits such as changes in arousal, hyperactive, hypoactive, or mixed perceptual deficits, altered sleep-wake cycle, and psychotic features such as hallucinations and delusions.
Delirium is one of the oldest forms of mental disorder known in medical history. The cause might be an underlying disease, overconsumption, or withdrawal from psychoactive compounds—particularly anticholinergic or central nervous system depressants such as alcohol, benzodiazepines, and opioids.
Although hallucinations and delusions are sometimes present in delirium, these are not required for the diagnosis. The symptoms of delirium are clinically distinct from those induced by psychosis or hallucinogens, except for deliriants. An organic process must, by definition, cause delirium, which is a physically identifiable structural, functional, or chemical disturbance in the brain. Delirium requires both sudden change mentation and a natural cause for this.
The core features are disturbances of consciousness, that is reduced clarity and awareness of the environment, with diminished ability to focus, sustain, or shift attention, change in cognition, that is problem-solving, impairment of memory, or other perceptual disturbances, hallucinations, the onset of hours to days, and a tendency to fluctuate. The behavior might either be overactive or under-active, and sleep is often disturbed, with loss of normal circadian rhythm, thinking is slow and muddled, but the content often complex. Other clinical features include disorganized thinking, poor memory, delusions, and mood lability.
Memory impairment occurs and is linked to inattention, reducing the formation of new long-term memory, which, by definition, survives the withdrawal of attention. It is typical in delirium because the initial construction of new long-term memories generally requires an even higher degree of focus than do short-term memory tasks. Since old memories are retained without the need for concentration, previously formed long-term memories created before the onset of delirium are usually preserved in all but the most severe cases.
Delirious hallucinations are often visual, though they can be tactile, auditory, or olfactory. Abnormalities of effect which might attend to the state of delirium may include many distortions to perceived or communicated emotional states. Emotional states might also fluctuate, for example, terror, sadness, and jocularity.
The pathophysiology of delirium is not well understood. Early rodent models of delirium used an antagonist of the muscarinic acetylcholine receptors, atropine, to induce cognitive and electroencephalography changes similar to delirium. Other anticholinergic drugs such as scopolamine have also produced delirium-like effects. These models and clinical studies of drugs with anticholinergic activity have contributed to a hypocholinergic theory of delirium.
Treatment of delirium requires treating the underlying cause, and multi-component interventions are thought to be the most effective. The two main strategies address the underlying acute cause or causes and then optimize conditions for the brain, including ensuring adequate oxygenation, hydration, nutrition, and normal levels of metabolites, minimizing drug effects, treating constipation, and treating pain, etcetera.
Detection and management of mental stress are also essential. Therefore, treating the cause is not adequate. All factors which might disrupt brain function should be analyzed. Non-medication treatments are the first measure of delirium unless there is severe agitation that places the person at risk of harming oneself or others. Examples are avoiding unnecessary movement, involving family members, having recognizable faces at the bedside, having means of orientation available, such as a clock and a calendar, which might stabilize the situation. Otherwise, verbal and non-verbal de-escalation techniques might be required to offer reassurances and calm the person experiencing delirium.
If these measures are insufficient, or if de-escalation techniques are inappropriate, pharmacological treatment is indicated. Physical restraints are occasionally used as a last resort in cases with severe delirium. The use of restraint should be avoided as it can increase agitation and risk of injury.
A chemical compound is a substance composed of many identical molecules, or molecular entities, composed of atoms from more than one element held together by chemical bonds. A chemical element bonded to an identical chemical component is not a chemical compound since only one element is involved. There are four types of compounds, depending on how the constituent atoms are held together, molecules held together by covalent bonds, ionic compounds held together by metallic bonds, certain complexes held together by coordinate covalent bonds.
A chemical formula expresses information about the proportions of atoms constituting a particular chemical compound, using standard abbreviations for the chemical elements and subscripts to indicate the number of atoms involved. A compound can be converted to a different chemical composition by interaction with a second chemical compound via a chemical reaction. In this process, bonds between atoms are broken in both interacting compounds, and then bonds are reformed so that new associations are made between the atoms.
Chemical compounds have a unique and defined chemical structure held together in a defined spatial arrangement by chemical bonds. Chemical compounds can be molecular compounds held together by covalent bonds, salts held together by ionic bonds, intermetallic compounds held together by metallic bonds, or the subset of chemical complexes held together by coordinate covalent bonds.
Deliriants are a class of hallucinogenic chemical compounds unique in that they offer solid hallucinations that merge seamlessly with waking consciousness, similar to fully formed dreams of delusions. In contrast, classical psychedelics and dissociative have progressive levels of sensory distortion before reaching the level of concrete hallucinations.
Typical deliriants are those who block the muscarinic acetylcholine receptors. These are called anticholinergics. Many of which are biosynthesized in the nightshade family of plants, such as Datura, Brugmansia, henbane, and mandrake. These alkaloids are also found in other plants such as corkwood and garrya. These tropane alkaloids are poisonous and can cause death due to heart failure and hyperthermia, even in small doses. Examples of anticholinergic tropane alkaloids are scopolamine, daturine, and atropine.
Another class of deliriants is the antihistamines, which also exhibit anticholinergic effects. Examples are diphenhydramines, dimenhydramine, doxylamine, and mirtazapine. Compounds eliciting deliriant effects without strictly being anticholinergics are the nonsteroidal anti-inflammatory drug benzydamine, the isoxazole muscimol, and the phenylpropenes myristicin and elemicin.
Despite the legal status of several common deliriant plants and drugs, substances in this class are unpopular as recreational drugs due to the severe and unpleasant nature of the hallucinations produced. In addition to their potentially dangerous mental and physical effects, accidents during deliriant experiences are common, and certain deliriants are poisonous and can cause death due to tachycardia-induced heart failure or hyperthermia, even in small dosages.
An anticholinergic agent is a substance that selectively blocks the neurotransmitter acetylcholine from binding to its receptor in the nerve cells of the central and peripheral nervous system, thus inhibiting parasympathetic nerve impulses.
Nerve fibers of the parasympathetic system are responsible for the involuntary movement of smooth muscles in the gastrointestinal and urinary tract, lungs, and other parts of the body. Anticholinergics are divided into categories by what subtype of receptor they bind to. The most common are antimuscarinic agents, which bind to the muscarinic acetylcholine receptors. Others are antinicotinic agents that attach to the nicotinic acetylcholine receptors.
Anticholinergics are used to treat a multitude of conditions, and diseases, including vertigo, motion sickness, extrapyramidal symptoms, gastrointestinal disorders, peptic ulcers, diarrhea, pylorospasm, diverticulitis, ulcerative colitis, nausea, vomiting, genitourinary disorders on a short-term basis, respiratory ailments like asthma, chronic bronchitis and chronic obstructive pulmonary disease, sinus bradycardia due to a hypersensitive vagus nerve. Anticholinergics are also used in situations where a decrease in saliva is advantageous, for example, surgical procedures.
Among recreational users, anticholinergics are commonly referred to as deliriants and are usually considered the least enjoyable class of drugs because of the unpleasant side effects while not generally inducing euphoria. Thus, the risk of addiction is low, and recreational use is uncommon.
Side effects, many of which resemble those in delirium, include poor coordination, dementia, decrease mucus production, decreased sweating leading to increased body temperature, pupil dilation and consequent sensitivity to light, decreased ability to focus, blurred vision, cycloplegia, double-vision, increased heart rate, tendency to be easily startled, urinary retention, urinary incontinence while sleeping, decreased bowel movement, ileus, and increased intraocular pressure which is dangerous in people with narrow-angle glaucoma, confusion, agitation, euphoria or dysphoria, respiratory depression, problems with memory, inability to concentrate, wandering thoughts, in inherent speech, wakeful myoclonic jerking, illogical thinking, visual disturbances, periodic flashes of light, periodic changes in visual field, visual snow, restricted or tunnel vision, visual, auditory, other sensory hallucinations, warping or waving of surfaces and edges, textured surfaces, dancing lines, spiders, insects and form constants, lifelike objects indistinguishable from reality, phantom smoking, hallucinated presence of people, seizures, coma, and death, severe drop in systolic blood pressure when suddenly standing up.
Long-term use of anticholinergics might accelerate mental and physical decline; while it is unclear if they increase the risk of death in general, they do in older populations.
Anticholinergic syndrome subsides once all the causative agents are excreted. Physostigmine can be used, and a reversible acetylcholinesterase inhibitor and antidote in life-threatening cases but come with the side effects associated with cholinergic excess. Racetams and choline activate the cholinergic system and alleviate the cognitive symptoms associated with long-term anticholinergic use. Nicotine also counteracts anticholinergics by activating nicotinic acetylcholine receptors. Moreover, although an adenosine receptor antagonist, caffeine can neutralize the anticholinergic symptoms by reducing sedation and increasing acetylcholine activity.
Plants of the Solanaceae or nightshade family, such as henbane, belladonna, Datura, Brugmansia, and mandrake, contain various anticholinergic tropane alkaloids, for example, scopolamine, daturine, and atropine. Other plants rich in these compounds are garrya and corkwood.
Opiate-containing drug preparations, such as those containing hydrocodone and codeine, are combined with an anticholinergic to deter misuses.
Antihistamines are drugs that treat allergies and alleviate symptoms such as nasal congestion, sneezing, hives from pollen, dust, mites, animal allergy, and are used as a short-term, inexpensive, generic, over-the-counter drug with few side effects. They oppose the activity of histamine receptors in the body and are classified according to which receptor they act on.
The H1-antihistamines act on the histamine H₁ receptors in the mast cells, smooth muscle, endothelium, the tuberomammillary nucleus in the brain, and are used to treat insomnia and allergic reactions in the nose, for example, itching, runny nose, and sneezing, as well as motion sickness or vertigo cases by problems with the inner ear. H1-antihistamines can reduce inflammation through the expression of NF-κB, the transcription factor that regulates inflammatory processes, by promotion from both the receptors constitutive activity and agonism through, for example, histamine binding at the H₁ receptor.
These effects, in combination, and some cases, metabolic ones included, give most first-generation antihistamines an analgesic-sparing or potentiating effect on opioid analgesics and to some extent with other ones as well. Some antihistamines might have analgesic properties of their own, for example, orphenadrine.
The H2-antihistamines act on the histamine H₂ receptors in the upper gastrointestinal tract, primarily in the stomach, and are used to treat gastric acid conditions like peptic ulcers and acid reflux. Second-generation antihistamines primarily affect peripheral histamine receptors by crossing the blood-brain barrier to a much lower degree than first-generation antihistamines. Higher dosages can still cause drowsiness through acting on the central nervous system. Some second-generation antihistamines can interact with CNS psychoactive drugs. H2-antihistamines are among the first-line therapy in gastrointestinal conditions like peptic ulcers and gastroesophageal reflux disease.
H3-antihistamines are used for inhibiting the H₃ receptors, inhibitory autoreceptors located at the histaminergic nerve terminals in the brain, which modulate histamine release. In the brain, histamine triggers a secondary release of excitatory neurotransmitters such as glutamate and acetylcholine via stimulation of the H₁ receptors in the cerebral cortex. Unlike the sedating H1-antihistamines, H3-antihistamines have stimulant and cognition-modulating effects. H3-antihistamines and H4-antihistamines are experimental agents without any defined clinical use, although some are in human trials.
Histamine receptors exhibit constitutive activity, and antihistamines can function as either a neutral receptor antagonist or an inverse agonist at histamine receptors, as for a few currently marketed H1-antihistamines.
The classic symptoms of an allergic reaction are caused by a histamine-induced increase in vascular permeability, causing fluid to escape from capillaries into tissues while promoting angiogenesis. Antihistamines suppress the reaction by blocking the binding of histamine to its receptor or reducing histamine receptor activity. Most side effects form cross-reactivity with unintended receptors.
Antihistamines can vary significantly in cost. Those newer and still under patent are generally more expensive, while many older variations are available in generic form. The newer drugs are not necessarily safer or more effective. Not much-published research exists which compares the efficacy and safety of the various antihistamines available.
Phenylpropene is the scaffold for a class of derivatives called phenylpropenoids, or phenylpropenes, propenylphenols, alkenylbenzenes, or allylbenzenes. In plant biochemistry, phenylpropenes is derived from the general shikimate, phenylpropanoid synthesis pathway and belong to the diverse and essential class of phenylpropanoids, which have been used as precursors for a variety of effective insecticides. The phenylpropenes, including eugenol, chavicol, safrole, and estragole, are derived from the monolignols, the primary constituents of various essential oils.
Phenylpropenes are extensively used as flavors insignificantly low doses. However, in high doses such as in medical use, it can be a concern, as phenylpropene compounds readily are metabolized by P450 sulfotransferase to reactive intermediate carcinogens that bind DNA, which is also rapidly metabolized to the less toxic dihydrodiol or glutathione conjugates, and excreted.
Isoxazole is an azole with an oxygen atom next to the nitrogen, and also the name of the class of compounds containing this ring. Isoxazolyl is the univalent radical derived from isoxazole. Isoxazole rings are found in some natural compounds, such as ibotenate and muscimol. Isoxazoles also form the basis for many drugs, including the COX-2 inhibitor valdecoxib and the neurotransmitter agonist AMPA. The derivative, furoxan, is a nitric oxide donor.
An isoxazolyl group is found in many beta-lactamase-resistant antibiotics, such as cloxacillin, dicloxacillin, and flucloxacillin. Examples of AAS containing the isoxazole ring include danazol and androisoxazole.
Nonsteroidal anti-inflammatory drugs or NSAIDs are a class of drugs that decrease pain, fever, prevent blood clots, and in higher doses reduces inflammation. Their side effects depend on the specific drug but generally include an increased risk of gastrointestinal ulcers and bleeds, heart attack, and kidney disease. The term nonsteroidal distinguishes these drugs from steroids, which have similar eicosanoid-depressing, anti-inflammatory action, and a broad range of other effects.
Most NSAIDs are weak acids that are absorbed well from the stomach and intestinal mucosa and are highly protein-bound in plasma, mostly to albumin so that their volume of distribution typically approximates to plasma volume.
NSAIDs work by inhibiting the cyclooxygenase enzymes, COX-1 and COX-2, which are involved in the synthesis of biological mediators such as prostaglandins involved in inflammation, and thromboxanes, which are involved in blood clotting.
There are non-selective, which are the most common and thins the blood, and COX-2 selective NSAIDs that have less gastrointestinal effects but promote thrombosis and increase the risk of a heart attack. All NSAIDs increase the risk of renal disease. This is because the COX enzymes catalyze the formation of prostaglandins and thromboxane from arachidonic acid, derived from the cellular phospholipid bilayer by phospholipase A2. Prostaglandins act as messenger molecules in the process of inflammation.
NSAIDs are generally used for the symptomatic relief of conditions such as osteoarthritis, rheumatoid arthritis, mild-to-moderate pain due to inflammation and tissue injury, lower back pain, inflammatory arthropathies, psoriatic arthritis, reactive arthritis, tennis elbow, headache, migraine, acute gout, menstrual pain, metastatic bone pain, postoperative pain, muscle stiffness and pain due to Parkinson’s disease, fever, ileus, renal colic, and macular edema.
The use of NSAIDs increases the risk of a range of cardiovascular complications, but the primary adverse drug reactions associated with NSAIDs use is related to irritation of the gastrointestinal tract. The acidic molecules directly irritate the gastric mucosa. Simultaneously, inhibition of COX-1 and COX-2 reduces the levels of protective prostaglandins, and inhibition of prostaglandin synthesis causes increased gastric acid secretion, reduced mucus secretion, diminished bicarbonate secretion, reduced mucus secretion, and diminished trophic effects on the epithelial mucosa.
While most NSAIDs penetrate poorly into the central nervous system, the COX enzymes are expressed constitutively in some areas of the CNS, but even the limited penetration causes adverse effects such as sleepiness and dizziness. NSAIDs’ interaction with the endocannabinoid system and its endocannabinoids by COX using these as substrates might play a crucial role in both the therapeutic and adverse effects of NSAIDs.
Most NSAIDs are metabolized in the liver by oxidation and conjugation to inactive metabolites usually excreted in the urine and partially in bile.
Scopolamine, also called hyoscine, levo-duboisine, devil’s breath, and barundunga, is among the secondary metabolites of plants from the Solanaceae or nightshade family: henbane, Datura, Brugmansia, belladonna, mandrake, garrya, and corkwood. Scopolamine is in the antimuscarinic family of medications and works by blocking acetylcholine’s effects within the nervous system. Although it is usually referred to as a nonspecific antimuscarinic, there is indirect evidence for m1-receptor subtype specificity. Scopolamine can be taken orally, ophthalmically, intravenously, and transdermally.
It has many medicinal uses, such as to treat postoperative nausea, vomiting, motion sickness as a transdermal patch, gastrointestinal spasms, renal or biliary spasms, irritable bowel syndrome, hypersalivation, bowel colic, eye inflammation, and sometimes used to reduce respiratory tract secretions before surgery. Scopolamine has been used to potentiate opioids to increase analgesia, which is profound enough to allow higher doses to be used as a form of anesthesia, called twilight sleep.
While scopolamine has occasionally been used recreationally for its deliriant hallucinogenic properties, the experiences are often unpleasant both mentally and physically, as well as dangerous. Repeated use is rare. Overdose symptoms include tachycardia, arrhythmia, blurred vision, photophobia, urinary retention, drowsiness, Cheyne-Stokes respiration, dry mouth, flushing, inhibition of gastrointestinal motility, hallucinations, delirium, coma, and death.
The biosynthesis of scopolamine begins with the decarboxylation of L-ornithine to putrescine by ornithine decarboxylase. Putrescine is methylated to N-methylputrescine by putrescine N-methyltransferase.
A putrescine oxidase that explicitly recognizes methylated putrescine catalyzes this compound’s deamination to 4-methylaminobutanal, which then undergoes a spontaneous ring formation to N-methyl-pyrrolium cation. In the next step, the pyrrolium cation condenses with acetoacetic acid yielding hygrine. No enzymatic activity could be demonstrated to catalyze this reaction. Hygrine further rearranges to tropinone.
Subsequently, tropinone reductase I convert tropinone to tropine, which condenses with phenylalanine-derived phenyllactate to littorine. A cytochrome P450 classified as CYP80F1 oxidizes and rearranges littorine to daturine aldehyde. In the final step, daturine undergoes epoxidation catalyzed by 6beta-hydroxyhyoscyamine epoxidase yielding scopolamine.
Scopolamine has been used as a research tool to study the involvement of acetylcholine in cognition. Results in primates suggest that acetylcholine is involved in the encoding of new information into long-term memory. Scopolamine has also been investigated as a rapid-onset antidepressant, with some small studies finding positive results.
Daturine, also known as hyoscyamine, is a tropane alkaloid and secondary metabolite found in certain plants of the Solanaceae, or nightshade family, including henbane, mandrake, Datura, and belladonna. It is the levorotary isomer of atropine, known as levo-atropine, and is a direct precursor in the plant biosynthesis of scopolamine, synthesized via the same metabolic pathway.
Daturine has anticholinergic activity on the muscarinic acetylcholine receptors and thus is an antimuscarinic. It blocks acetylcholine’s action at parasympathetic sites in sweat glands, salivary glands, stomach secretion, heart muscle, sinoastrial node, smooth muscle in the gastrointestinal tract, and the central nervous system. Increasing cardiac output and heart rate lowers blood pressure and dries secretions while possibly antagonizing serotonin.
Daturine has 98% of the anticholinergic potency of atropine, while scopolamine has 92% the anticholinergic potency of atropine. It is used to provide relief from spasms caused by various lower abdominal and bladder disorders, including peptic ulcers, irritable bowel syndrome, diverticulitis, pancreatitis, colic, and intestinal cystitis. It is also used in relieving some heart problems, controlling some symptoms of Parkinson’s disease, and controlling abnormal respiratory symptoms and hyper-mucus secretions in patients with lung disease.
It is also useful in pain control for neuropathic pain, chronic pain, and palliative care for intractable pain from treatment p-resistant, untreatable, and incurable diseases. Combined with opioids, it increases analgesia, or pain relief obtained; several mechanisms contribute to this effect. When used in combination with opioids or other antiperistaltic agents, there is an increased risk of constipation and paralytic ileus.
Side effects include dry mouth and throat, increased appetite leading to weight gain, eye pain, blurred vision, restlessness, dizziness, arrhythmia, flushing, and faintness. An overdose will cause headaches, nausea, vomiting, and central nervous system symptoms, including disorientation, hallucinations, euphoria, sexual arousal, short-term memory loss, and possible coma in extreme cases. The euphoric and sexual effects are stronger than those of atropine but weaker than those of scopolamine.
The biosynthesis of scopolamine begins with decarboxylation of L-ornithine to putrescine by ornithine decarboxylase. Putrescine is methylated to N-methylputrescine by putrescine N-methyltransferase.
A putrescine oxidase that explicitly recognizes methylated putrescine catalyzes this compound’s deamination to 4-methylaminobutanal, which then undergoes a spontaneous ring formation to N-methylpyrrolium cation. In the next step, the pyrrolium cation condenses with acetoacetic acid, yielding hygrine. No enzymatic activity could be demonstrated that catalyzes this reaction. Hygrine further rearranges to tropinone.
Subsequently, tropinone reductase I convert tropinone to tropine, which condenses with phenylalanine-derived phenyllactate to littorine. A cytochrome P450 classified as Cyp80F1 oxidizes and rearranges littorine to hyoscyamine aldehyde.
Atropine is an enantiomeric mixture of d-hyoscyamine and l-hyoscyamine, with most of its physiological effects due to l-hyoscyamine. First isolated in 1833, it is on the World Health Organization’s list of the most effective and safe medicines needed in a health system. It is an anticholinergic of the antimuscarinic subtype that antagonizes the muscarinic acetylcholine receptors of type M1, M2, M3, M4, M5, and inhibit the parasympathetic nervous system. Atropine is used as a medication to treat certain nerve agents and pesticide poisoning, slow heart rate, and decrease saliva production.
Although not an actual antidote, atropine can, by blocking acetylcholine’s action at muscarinic receptors, serve as a treatment for organophosphate poisoning with insecticides and nerve gases such as tabun, sarin, soman, and VX. Some nerve agents destroy acetylcholinesterase by phosphorylation so that the action of acetylcholine becomes excessive. Atropine can reduce the effect by blocking muscarinic acetylcholine receptors, which would otherwise be overstimulated by excessive acetylcholine accumulation.
Atropine is typically given through intravenous and intramuscular injections, transdermally, or as eye drops. Intravenously, it begins working within a minute and lasts from half an hour to an hour. Atropine is used to paralyze the accommodation reflex temporarily and to dilate the pupils. These effects typically wear off within 7 to 14 days. Atropine is sometimes added to potentially addictive drugs such as opioids used against diarrhea to deter misuse, and wherein its secretion-reducing effects act synergistically.
Adverse reactions to atropine include ventricular fibrillation, constipation, urinary retention, dizziness, nausea, blurred vision, vertigo, fast heart rate, dilated pupils, photophobia, dry mouth, and potentially deliriant hallucinations and excitation. Because of the hallucinogenic properties, some use the drug recreationally, though this is potentially dangerous, as atropine is poisonous in overdoses and often unpleasant. Atropine is incapacitating at dosages of 10 to 20 milligrams orally. Its median lethal dose via the same route is estimated to be 453 milligrams, with a probit slope of 1.8. The antidote is physostigmine and pilocarpine.
Atropine is found in many members of the Solanaceae or nightshade family, such as belladonna, Datura, Brugmansia, mandrake, and henbane. Both atropine and the genus Atropa belladonna derive their name from Atropos, one of the three Fates who, according to Greek mythology, chose how a person was to die.
The biosynthesis of atropine starting from l-phenylalanine first undergoes a transamination forming phenylpyruvic acid, which is then reduced to phenyl-lactic acid. Coenzyme A then couples phenyl-lactic acid with tropine forming littorine, which then undergoes a radical rearrangement initiated with a P450 enzyme forming hyoscyamine aldehyde. A dehydrogenase then reduces the aldehyde to a primary alcohol making (−)-hyoscyamine, which upon racemization forms atropine. Atropine can otherwise be synthesized by letting tropine react with tropic acid in the presence of hydrochloric acid.
Diphenhydramine is a first-generation antihistamine and anticholinergic, mainly used to treat allergies and insomnia, symptoms of common cold, tremors in Parkinsonism, anxiety, and nausea. Also having local anesthetic properties, it has been used as an alternative to common local anesthetics. It can be used by mouth, injected into a vein or muscle, or topically as creams, lotions, gels, and sprays with less systematic effects. The maximal effect is typically around two hours after a dose and lasts for up to seven hours.
George Rieveschl discovered diphenhydramine and came into commercial use in 1946. It is among others sold under the trade name Benadryl. In addition to epinephrine, it is used in injections for anaphylaxis. Because of its sedative properties, diphenhydramine is widely used in nonprescription sleep aids, either alone or combined with compounds such as acetaminophen or paracetamol. A typical dose creates driving impairment equivalent to a blood-alcohol level of 0.10, which is higher than the 0.08 limit of most drunk driving laws.
The potent anticholinergic activity of diphenhydramine is responsible for the side effects of dry mouth and throat, increased heart rate, pupil dilation, urinary retention, constipation, and at high doses, hallucinations, and delirium. Other side effects include motor impairment, flushed skin, blurred vision akin to cycloplegia, sedation, difficulty concentrating, short-term memory loss, visual disturbances, irregular breathing, dizziness, irritability, itchy skin, abnormal sensitivity to bright light, increased body temperature. Diphenhydramine can cause minor physical dependence. Alcohol may increase the drowsiness caused by diphenhydramine.
Symptoms of an overdose might include dysphoria, hallucinations, heart palpitations, extreme drowsiness, severe dizziness, abnormal speech, flushed skin, severe mouth, and throat dryness, tremors, seizures, inability to urinate, vomiting, motor disturbances, anxiety or nervousness, disorientation, abdominal pain, delirium, coma, and death.
Acute poisoning can lead to cardiovascular collapse and death within 2 to 18 hours. Diphenhydramine can block the delayed rectifier potassium channel and, consequently, prolong the QT interval, leading to cardiac arrhythmias, such as was torsades de pointed. There is no specific antidote, but the anticholinergic symptoms can be alleviated with physostigmine. Benzodiazepines can be administered to decrease the likelihood of psychosis, agitation, and seizures in people with such proneness. Diphenhydramine is used recreationally as a potentiator of opioids and deliriant. Recreational users report calming effects, mild euphoria, and hallucinations.
Diphenhydramine acts as an inverse agonist of the histamine H₁ receptor and is a member of the ethanolamine class of antihistaminergic agents. By reversing the effects of histamine on the capillaries, it can reduce allergic symptoms. Its ability to cross the blood-brain barrier and inversely agonize the H₁ receptors causes drowsiness. It also has potent antimuscarinic activity as a competitive antagonist of the muscarinic acetylcholine receptor.
Its actions as a local anesthetic come from blocking the intracellular sodium channels. Diphenhydramine also inhibits the reuptake of serotonin. While it potentiates the analgesia induced by morphine, it does not potentiate endogenous opioids. Diphenhydramine acts as an inhibitor of histamine N-methyltransferase.
Oral bioavailability is in the range of 40% to 60%, and peak plasma concentrations occur approximately 2 to 3 hours after administration. The primary route of metabolism is two successive demethylations of the tertiary amine. The resulting primary amine is further oxidized to a carboxylic acid. The elimination half-life appears to range between 2.4 and 9.3 hours in healthy adults.
Doxylamine is a first-generation antihistamine, discovered in 1949 and primarily used as the succinic acid salt, doxylamine succinate. It is used as a short-term sedative or combined with other drugs to provide night-time allergy and cold relief. It can also be used in combination with paracetamol, acetaminophen, and codeine as an analgesic and calmative preparation. Additionally, it is used in conjunction with pyridoxine to prevent morning sickness in pregnant women.
The drug primarily acts as an antagonist of the histamine H₁ receptor, and this is responsible for its antihistaminergic and sedative effects. It is also, to a lesser extent, an antagonist of the muscarinic acetylcholine receptors. This action is responsible for the anticholinergic side effects of dry mouth, ataxia, urinary retention, drowsiness, memory problems, inability to concentrate, hallucinations, increased sensitivity to external stimuli, and at high doses, delirium.
Doxylamine should not be combined with other antihistamines, such as cetirizine and diphenhydramine, as this combination increases the risk of severe side effects. On a side note, unlike diphenhydramine, doxylamine has have been reported to be the cause of both coma and rhabdomyolysis.
The median lethal dose is estimated to be 50-500 mg/kg in humans. Symptoms of an overdose might include dry mouth, dilated pupils, insomnia, night terrors, euphoria, hallucinations, seizures, rhabdomyolysis, delirium, and death, with fatalities having been reported from doxylamine overdose. These have been characterized by coma, tonic-clonic or grand mal seizures, and cardiorespiratory arrest.
The bioavailability of doxylamine is 24.7% for oral administration and 70.8% for intranasal administration. The Tmax of doxylamine is 1.5 to 2.5 hours, and its elimination half-life is 10 to 12 hours. Doxylamine is metabolized in the liver primarily by the cytochrome P450 enzymes CYP2D6, CYP1A2, and CYP2C9. The primary metabolites are N-desmethyldoxylamine, N,N-didesmethyldoxylamine, and doxylamine N-oxide. Doxylamine is eliminated 60% in the urine and 40% in feces.
Mirtazapine is an orally taken tetracycline atypical antidepressant, with four interconnected atom rings. In addition to its antidepressant properties, mirtazapine had anxiolytic, sedative, animatic, and appetite stimulant effects and is sometimes used to treat anxiety disorders, insomnia, nausea, vomiting, and to produce weight gain. It acts as an antagonist of specific adrenergic and serotonin receptors and is also a potent antihistamine. It is occasionally described as a noradrenergic and specific serotonergic antidepressant.
Mirtazapine is primarily used in the treatments of major depressive disorder and other mood disorders. It has also been found useful in alleviating generalized anxiety disorder, social anxiety disorder, obsessive-compulsive disorder, panic disorder, post-traumatic stress disorder, low appetite or underweight, insomnia, nausea and vomiting, itching, headaches, and migraine.
Side effects include constipation, dry mouth, sleepiness, increased appetite and subsequent weight gain, weakness, confusion, dizziness, peripheral edema, elevated transaminases, elevated serum triglycerides, and high total cholesterol. Mirtazapine is considered relatively safe in the event of an overdose, and as much as 30 to 50 times the standard dose is relatively nontoxic.
Concurrent use with inhibitors or inducers of the cytochrome, CYP, P450 isoenzymes CYP1A2, CYP2D6, and CYP3A4 can result in altered concentrations of mirtazapine, as these are the primary enzymes responsible for its metabolism. The drug should not be used within two weeks of any monoamine oxidase inhibitor usage, and monoamine oxidase inhibitors should not be administered within two weeks of discontinuing mirtazapine.
Mirtazapine has antihistamine, a2-blocking, and antiserotonergic activity, and is a potent antagonist or inverse agonist of the α2A-, α2B-, and α2C-adrenergic receptors, the serotonin 5-HT2A, 5-HT2C, and 5-HT3 receptors, and the histamine H₁ receptor. It does not inhibit the reuptake of serotonin, norepinephrine, or dopamine, nor does it inhibit monoamine oxidase. Mirtazapine has weak or no activity as an anticholinergic and blocker of sodium or calcium channels. Mirtazapine has been found to act as a partial agonist of the κ-opioid receptor at high concentrations, EC50 = 7.2 μM.
It is an extremely potent H₁ receptor antagonist, and as such, it can cause powerful sedative and hypnotic effects and might alleviate allergies, pruritus, nausea, insomnia, and weight gain. Mirtazapine has a low affinity to the muscarinic acetylcholine receptors, although anticholinergic side effects such as dry mouth, constipation, and dilated pupils might be seen.
The oral bioavailability of mirtazapine is about 50%, and it is mostly bound to plasma proteins, approximately 85%. The liver primarily metabolizes it by demethylation and hydroxylation via cytochrome P450 enzymes, and one of its primary metabolites is desmethylmirtazapine. The elimination half-life is 20 to 40 hours, and about 15% is eliminated through feces and 75% through urine.
Myristicin is a psychoactive anticholinergic phenylpropene found in the essential oil of nutmeg, parsley, and dill, among others. It is insoluble in water but soluble in ethanol and acetone. Myristicin is used as a precursor in the synthesis of the psychedelic empathogenic drug MMDA.
While myristicin is the primary psychoactive component of nutmeg, along with elemicin, the subjective differences in effect between nutmeg and pure myristicin, combined with myristicin, is not a significant component of the seed, suggest it does not fully explain the effects of consuming raw nutmeg. Raw nutmeg consists of 5 to 15% essential oil by mass. The amount of myristicin found in nutmeg essential oil is 4 to 8.5%, and in fresh nutmeg 0.2 to 1.3%. 20 grams of raw nutmeg contains 210 milligrams myristicin, 70 milligrams elemicin, and 39 milligrams safrole.
The effects of nutmeg or myristicin intoxication are nausea, dizziness, dry mouth, bloodshot eyes, memory disturbances, visual distortions, and in high doses, hallucinations, and delirium. At least in the case of raw nutmeg, it might take several hours before the maximum effects are reached, and the effects can last for several days. Myristicin might alter the toxicity and metabolic pathways of some compounds by being a weak monoamine oxidase inhibitor. It might also be neurotoxic.
When myristicin is heated with potassium hydroxide in alcohol and the distillate is crystallized upon cooling, colorless needles of isomyristicin are formed.
Elemicin is a phenylpropene found in several species of plants. It is found in the oleoresin, and essential oil of Canarium luzonicum, also referred to as elemi, from which the name elemicin is derived. Elemicin comprises 2.4% of Canariums luzonium’s essential oil and 2.4% in nutmeg oil, another plant containing the compound, and 10.5% in the oil from its mace.
Elemicin was first isolated from elemi oil by vacuum distillation at 162 to 165 °C and a reduced pressure of 10 Torr. Elemicin has been used to synthesize the alkaloid mescaline. The anticholinergic-like effects caused by eating raw nutmeg is attributed to elemicin and myristicin.
It can be synthesized from syringol and allyl bromide using Williamson ether synthesis and Claisen rearrangement. The electrophilic aromatic substitution entering the para-position was made possible by secondary Cope rearrangement. This is due to syringol’s allyl aromatic ether being blocked by ethers in both ortho-positions. When blocked, the allyl group migrates to the para-position, in this case, with yields above 85%.
Muscimol, also known as agarin or pantherine, is one of the psychoactive agents in Amanita muscaria, Amanita pantherina, and related species. It is a potent, selective agonist of the GABAA receptors and displays sedative-hypnotic, depressant, hallucinogenic, and deliriant psychoactivity. This colorless white solid is classified as an isoxazole.
Ibotenic acid, a neurotoxic secondary metabolite of Amanita muscaria, serves as a prodrug to muscimol, as when the mushroom is ingested or dried is converted via decarboxylation. Muscimol is a potent GABAA agonist, activating the receptor for the inhibitory neurotransmitter GABA, altering neuronal activity in multiple regions, including the cerebral cortex, hippocampus, and cerebellum. Muscimol is also a partial agonist at the GABAA-rho receptor.
The psychoactive dose of muscimol is around 10 to 15 milligrams for an average person. When consumed, some muscimol goes un-metabolized and thus excreted in the urine, a phenomenon exploited by practitioners of the traditional entheogenic use of Amanita muscaria.
Tests involving rabbits dosed with muscimol and connected to an Electroencephalograph showed distinctly synchronized EEG tracing, which is different from serotonergic psychedelics in which brainwave patterns tend to show a desynchronization. In higher doses of 2 mg/kg intravenously, the EEG shows characteristic spikes.
The effects of Amanita mushrooms begin 30 to 120 minutes after consumption, and the effects last for 5 to 10 hours. Effects include euphoria, dream-like lucid states of mind, out-of-body experiences, synesthesia, dizziness, clumsiness, nausea, stomach discomfort, increased salivation, muscle twitching or tremors, and in large doses, dissociation and delirium.
Many of muscimol’s effects are consistent with its pharmacology as a GABAA receptor agonist, presenting many depressant or sedative-hypnotic effects, atypical of the effect profile of sedative drugs generally; however, muscimol, like Z-drugs, can cause hallucinogenic changes in perception. The hallucinogenic effect produced by muscimol is most closely comparable to the hallucinogenic side effects produced by some other GABAergic drugs such as zolpidem.
It can be produced synthetically from the lithium acetylide derived from propargyl chloride. Treatment with ethyl chloroformate afford ethyl 4-chlorotetrolate, which condenses with hydroxylamine to give the chloromethylisoxazole. Anhydrous ammonia converts this chloride to muscimol. The overall yield achieved in the literature was 18.7%.
The LD50 via injection in mice is 3.8 mg/kg subcutaneously, 2.5 mg/kg Intraperitoneally, while the LD50 in rats is 4.5 mg/kg intravenously and 45 mg/kg orally.
Benzydamine is a locally-acting nonsteroidal anti-inflammatory drug or NSAID, with anesthetic, analgesic, and anti-inflammatory properties used to treat conditions of the mouth and throat. It is primarily used for gingivitis, stomatitis, glossitis, aphthous ulcers, glandular fever, pharyngitis, tonsillitis, dental surgery due to radiation therapy, post-tonsillectomy, and radiation or intubation mucositis. As a prostaglandin synthetase inhibitor, benzydamine selectively binds to inflamed tissues while, unlike other NSAIDs, not inhibiting cyclooxygenase or lipooxygenase and without being ulcerogenic.
Benzydamine can be used alone or in combination with other medication to increase the likelihood of therapeutic effect with little risk of interaction. There are no contraindications to the use of benzydamine except for known hypersensitivity, and benzydamine is generally well tolerated. However, occasionally oral tissue numbness or stinging sensations might occur, as well as itching, skin rashes, swelling or redness, difficulty breathing, and wheezing.
In vitro studies indicate that benzydamine has antibacterial activity and acts synergistically with other antibiotics, especially tetracyclines, against antibiotic-resistant strains of Ptaphylococcus aureus and Pseudomonas aerugiosa.
Benzydamine can be used recreationally in high dosages, as it acts as a deliriant and central nervous system stimulant. Even though it exhibits many side effects like those of anticholinergics, they are distinctly different, producing a delirium with minimal confusion, despite visual, auditory, and tactile hallucinations. Benzydamine also manifest hallucinations resembling those of psychedelics.
The synthesis starts with the reaction of the N-benzyl derivative from methyl anthranilate with nitrous acid to give the N-nitroso derivative. Reduction utilizing sodium hydrosulfite or dithionite leads to the transient hydrazine, which undergoes spontaneous internal hydrazide formation. Treatment of the enolate of this amide with 3-chloro-1-dimethylamino propane gives benzydamine.
An alternative synthesis starts with a subsequent reaction of N-benzylaniline with phosgene and then with sodium azide to produce the corresponding carbonyl azide. The nitrogen is evolved on heating, and a separable mixture of nitrene insertion product and the desired ketoindazole # results. The latter reaction appears to be a Curtius rearrangement type product to produce an N-isocyanate #, which then cyclizes. Alkalytation of the enol with sodium methoxide and 3-dimethylaminopropyl chloride gives benzydamine. Alternately, the use of chloroacetamide in the alkylation step, followed by acid hydrolysis, produces bendazac instead.
There are thousands of sources for these deliriant compounds, but I will concentrate on those most common and studied. Most of which are from the plant kingdom, mainly from the nightshade family, some from Myristica, another few are fungi of the family Amanita, the rest are pharmaceuticals, primarily antihistamines, and one NSAID.
Hyoscyamus niger, also known as henbane, black henbane, or stinking nightshade, is a plant of the family Solanaceae. The word henbane dates back to at least AD 1265. Its origins are unclear, but it probably referred to death rather than chickens. Another etymology of the word associates it with bhelena, meaning crazy plant.
Henbane was historically used in combination with other plants such as mandrake, deadly nightshade, and Datura as an anesthetic potion, as well as for its psychoactive properties in magical brews. It was initially used in continental Europe, Asia, and the Arab World, though it spread to England during the Middle Ages. Its cultivation for medicinal use is spread and legal in Central, Eastern Europe, and India. Furthermore, while henbane is considered an endangered species and is on World Conservation Union’s Red List, It is globally distributed and grown for pharmaceutical purposes.
It is used to treat rheumatism, toothaches, asthma, coughing, nervous diseases, and stomach pain. It might also be used as an analgesic, sedative, and narcotic in some cultures. Adhesive bandages with henbane extract behind the ear are reported to prevent travel-sickness, and henbane oil is used for medicinal massage. Henbane material can be bought in pharmacies with a prescription in most western countries, while the sale of henbane oil is not legally regulated and allowed in shops other than pharmacies.
The leaves and herbage without the roots are chopped and dried and then used for medicinal purposes or in incense and smoking blends, making beer or tea, and seasoning wine. Henbane leaves are boiled in oil to derive henbane oil, while the seeds are used in incense blends. In all preparations, the dosages have to be carefully estimated due to the high toxicity of henbane. For some therapeutic applications, a dose like 0.5 and 1.5-3 grams was used. The lethal dose is not known. Scopolamine, daturine, and other tropane alkaloids have been found in the plant’s foliage and seeds. The standard alkaloid content has been reported to be 0.03% to 0.28%.
Henbane ingestion by humans is followed simultaneously by peripheral inhibition and central stimulation. Typical effects include hallucinations, dilated pupils, restlessness, and flushed skin. Less common effects are tachycardia, convulsions, vomiting, hypertension, hyperpyrexia, and ataxia. Initial effects typically last for three to four hours, while after-effects may last up to three days—overdose results in delirium, coma, respiratory paralysis, and death. Low and average doses have inebriating and aphrodisiac effects.
Datura is a family of nine species of poisonous flowering plants belonging to the nightshade, or Solanaceae genus. Commonly known as devil’s trumpets and sometimes called jimsonweed, moonflowers, devil’s weed, hell’s bells, and thorn-apple. It is closely related to the genus Brugmansia and is mainly found in America and Northern Africa.
All species and every part of the plant are poisonous, especially their seeds and flowers, all of which contain tropane alkaloids such as scopolamine, atropine, and daturine, which is named after Datura. There can be a five to one variation in alkaloid content between plants, and there the content can vary in any given plant depending on its age, where it is grown, and the local weather conditions. These variations make Datura hazardous as a drug.
It has been used for centuries as an entheogen by the Navajo and especially the Havasupai tribes having a great deal of experience combined with detailed knowledge about the plant, while it in some parts of India and Europe, has been extensively used as a poison. The State Chemical Laborites in Agra, India, investigated 2,788 deaths caused by Datura between 1950 and 1965. In some places, it is prohibited to buy, sell, or cultivate Datura.
Having a combination of anticholinergic alkaloids, datura intoxication produces effects similar to anticholinergic delirium, with an inability differentiating reality from fantasy, hyperthermia, tachycardia, bizarre behavior, amnesia, and severely dilated pupils with resultant painful photophobia that can last for days. The majority of those who have used Datura recreationally describe their experience as extraordinarily unpleasant, both mentally and physically.
Due to their agitated and confused state, those intoxicated by Datura are typically hospitalized. Gastric lavage and administration of activated charcoal can reduce the stomach’s absorption of the alkaloids. Physostigmine is used to reverse the effects, and benzodiazepines can be used to calm the individual, while supportive care with oxygen, hydration, and symptomatic treatment is provided. The patient remains under observation until the symptoms resolve, circa 24 to 36 hours after ingestion.
Brugmansia or angels trumpet is a family of seven flowering, woody trees and shrubs with large and fragrant pendulum flowers and soft fruit. Native to the tropical regions of South America, from Venezuela to northern Chile and south-eastern Brazil, Brugmansia is grown as ornamental plants worldwide and has become naturalized in tropical areas within North America, Africa, Australia, and Asia.
All parts of Brugmansia are toxic, with the seeds and leaves being the richest in the anticholinergics, scopolamine, daturine, atropine, and several other tropane alkaloids. Effects of ingestion are the same as in other anticholinergic poisonings, with confusion, fast heart rate, dry mouth, paralysis of smooth muscle, visual disturbances, pupil dilation, hallucinations, delirium, and death. Several of the alkaloids found in Brugmansia and other of the nightshades are used in medicine to this day for their anti-asthmatic, anticholinergic, narcotic, and anesthetic properties, although often artificially synthesized.
Brugmansia has a long tradition of use in many South American indigenous cultures in medical preparations and as an entheogen in a spiritual context. As a medicine, it is used transdermally as a poultice, tincture, ointment for the treatment of aches and pains, dermatitis, orchitis, arthritis, rheumatism, infections, and internally, in highly diluted preparations for stomach and muscle ailments, decongestant, inducing vomiting to expel worms and parasite, as well as a sedative.
Atropa belladonna, also known as the deadly nightshade, is a perennial and herbaceous plant in the nightshade family Solanaceae. Native to Europe, North Africa, Western Asia, and introduced to some parts of Canada and the United States. It contains toxic anticholinergic tropane alkaloids, including atropine, scopolamine, and daturine, which in overdose causes delirium and hallucinations. These alkaloids are extensively used as pharmaceutical anticholinergics. Physostigmine and pilocarpine are used as an antidote for belladonna poisoning, the same as for the anticholinergics atropine, scopolamine, and atropine.
Belladonna often grows as a subshrub from a fleshy rootstock. Plants grow two meters tall with ovate leaves 18 centimeters long. The bell-shaped flowers are dull purple with green tinges and faintly scented; the fruits are berries, approximately 1.5 centimeters in diameter, and green before ripening into a shiny-black. There is a pale-yellow flowering form called Atropa belladonna var. lueta, with a pale-yellow fruit.
The name of the genus, Atropa, is derived from the goddess in Greek mythology, Atropos, meaning: she who may not be turned aside. She would determine the course of a man’s life by weaving threads that symbolized his birth, his life events, and finally, his death by cutting the threads. The name belladonna comes from Italian, meaning beautiful lady, originating from its use as a cosmetic. The juice of A. belladonna was applied as a decoction to beautify by inducing pallid skin and used as drops to increase the pupil size in women, which were considered attractive by acting as a muscarinic antagonist, blocking receptors in the muscles of the eye that constrict pupil size. Belladonna is currently rarely used cosmetically, as it carries the adverse effects of causing minor visual distortions, inability to focus on near objects, and increased heart rate. Prolonged usage was reputed to cause blindness.
All parts of the plant contain tropane alkaloids. Roots have circa 1.3%, leaves 1.2%, stalks 0.65%, flowers 0.6%, ripe berries 0.7%, and seeds 0.4% tropane alkaloids. Leaves reach maximal alkaloid content when the plant is budding and flowering, while the roots are most poisonous at the end of the plant’s vegetation period. Bees transform belladonna nectar into honey that also contains tropane alkaloids.
The active agents in belladonna, atropine, scopolamine, daturine, have anticholinergic properties, and thus the symptoms of belladonna poisoning are the same as other anticholinergics. With dilated pupils, sensitivity to light, blurred vision, fast heart rate, loss of balance, staggering, headaches, rashes, flushing, dry mouth and throat, slurred speech, urinary retention, constipation, confusion, hallucinations, delirium, and convulsions. Belladonna has occasionally been used as a recreational drug because of the vivid hallucinations and delirium it produces. However, these effects are commonly described as very unpleasant, and recreational use is uncommon.
The plant has been used in medicine for millennia, and belladonna tinctures, decoctions, powders, and alkaloid salt mixtures are still produced for pharmaceutical use. These are often standardized at 1037 parts daturine to 194 parts atropine, and 65 parts scopolamine. The plant was an essential ingredient in witches flying ointments, a transdermally absorbed hallucinogen with a fatty base. It is reported to produce a deathlike trance with vivid hallucinations.
Mandragora officinarum of the plant genus Mandragora, often known as mandrake, although this name is also used for other plants. It is a perennial herbaceous plant with ovate leaves arranged in a rosette, a thick upright root which is often branched, and bell-shaped flowers followed by yellow or orange berries.
All species of Mandragora contain biologically active alkaloids and tropane alkaloids in particular. More than 80 substances have been identified. There is little difference in alkaloid composition between Mandragora officinarum and Mandragora autumnalis.
The alkaloids are present in all parts of the plant, but the highest consternations are found in the root and leaves. These alkaloids include atropine, daturine, scopolamine, scopine, cuscohygrine, apoatropine, 3-alpha-tigloyloxytropane, 3-alpha,6-beta-ditigloyloxytropane, and belladonnines. Non-alkaloid constituents included sitosterol and beta-methylesculetin. Alkaloid content varies between different plants and parts of the plant.
Many of these alkaloids are poisonous vis anticholinergic activity. Ingestion of these compounds might result in vomiting, blurred vision, pupil dilation, dryness of the mouth, urinary retention, dizziness, headache, flushing, rapid heart rate, hallucinations, delirium, coma, and death.
These deliriant hallucinogenic tropane alkaloids, combined with the shape of the mandrake root that often resembles human features, have associated it with various superstitious practices throughout history. Mandrake was often made up into amulets, which were belied to bring good fortune, increase fertility, etcetera. In one superstition, people who pull up its root will be condemned to hell, and the mandrake would scream as it came out of the ground, killing anyone that heard it.
Although often intertwined with superstition, mandrake has a long history of medicinal use as an anesthetic for surgery or as a remedy for rheumatic pains by applying the juice from finely grated roots. It was also ingested to treat convulsions, treatment of wounds, gout, insomnia, melancholy, and mania, or in large doses to excite delirium. The use of anticholinergic alkaloids such as those in Mandragora in combination with opioids has persisted from ancient times until today.
Duboisia myoporoides, or corkwood, is a shrub or tree native to high-rainfall areas on the margins of rainforests in eastern Australia. It had a thick and corklike bark, with leaves which are obovate to elliptic in shape, 4-15 centimeters long and 1-4 centimeters wide, small white flowers produced in clusters, and poisonous globule purple-black berries. The leaves are a commercial source of pharmaceutically useful alkaloids, for example, scopolamine that is used to treat motion sickness, stomach disorders, and the side effects of cancer therapy.
Garrya is a genus of flowering plants in the family Garryaceae, native to Mexico, the Western United States, Central America, and the Greater Antilles. Other names include silk tassel and tassel bush. They are evergreen, dioecious wind-pollinated shrubs growing to one to five meters tall. The leaves are arranged in opposite pairs and are simple, leathery, dark green to gray-green, ovate, 3 to 15 centimeters long, with an entire margin and a short petiole. The flowers are gray-green catkins, short and spreading when first produced in late summer. The male catkins becoming long and pendulous in late winter when shedding pollen, 1 to 20 centimeters long. The female catkins are usually a little shorter and less pendulous. The fruit is a round dry berry containing two seeds.
Some species, notably Garrya elliptica, are widely cultivated in gardens for their foliage and the catkins produced in late winter. They are frequently grown against a wall or as a windbreak in coastal areas. Male plants are more widely grown, as their catkins are longer and more attractive; one such cultivar, G. elliptica, James Roof, has catkins up to 35 centimeters long. The hybrids G × issaquahensis, G. elliptica × G. fremontii, and G × thuretii, G. elliptica × G. fadyenii, have been bred for garden planting.
Nutmeg is the spice made from the ground seed of Myristica fragrans, a dark-leaved evergreen tree native to the Banda Islands in the Moluccas or Spice Islands of Indonesia. Its warm and slightly sweet taste is used to flavor many kinds of baked goods, confections, puddings, potatoes, meats, sausages, vegetables, and beverages like eggnog.
The seed is dried gradually in the sun over a period of six to eight weeks, shrinking away the nut from its hard shell, which is then broken, and the nutmeg is removed. The nutmeg is grayish-brown ovals with furrowed surfaces, roughly 20.5 to 30 millimeters long and 15 to 18 millimeters wide, weighing 5 to 10 grams dried. Mace is the similarly tasting spice made from the reddish seed covering, aril, of the nutmeg seed. It is removed from the nutmeg seed, flattened out, and dried in the sun for 10 to 14 days.
The essential oil is obtained from ground nutmeg by steam distillation and is widely used in the perfumery and pharmaceutical industries. This volatile fraction contains 60 to 80% d-camphene by weight, as well as quantities of d-pinene, limonene, d-borneol, l-terpineol, geraniol, safrol, and myristicin. The oil is colorless to light yellow and smells and tastes nutmeg. It is used in baked goods, syrups, beverages, and sweets, instead of nutmeg as it leaves no particles in the product. It is also used in toothpaste and cough syrups.
Nutmeg butter, reddish-Brown semisolid with the taste and smell of nutmeg, is obtained from the nut through expression. Approximately 75% by weight of nutmeg butter is trimyristin, which can be turned into the 14-carbon fatty acid, myristic acid, which can replace cocoa butter, or be used as an industrial lubricant. The compound maceligan isolated from Myristica fragrans might exert antimicrobial activity against Streptococcus mutas.
In high doses, nutmeg might interact with anxiolytic drugs and exert psychoactive derived from anticholinergic-like hallucinogenic mechanisms and monoamine oxidase inhibition attributed to myristicin and elemicin. The effects of intoxicating can vary significantly from person to person but is often associated with side effects such as excitedness, anxiety, confusion, headaches, nausea, dizziness, dry mouth, bloodshot eyes, amnesia, delirium, and possibly death. The effects of nutmeg intoxication might take multiple hours before reaching full effects and several days before subsiding.
Amanita muscaria, or fly agaric mushroom, is native throughout the temperate, boreal regions of the Northern Hemisphere but has been introduced to many countries in the Southern Hemisphere as symbiotic with pine and birch plantations.
It is a large white-gilled, white-spotted, usually red mushroom, but it varies considerably in its morphology. Amanita muscaria is generally common and numerous where it grows, often found in groups in all stages of development. The fruiting bodies emerge from the ground, looking like eggs. After emerging, the cap is covered with small white to yellow warts, remnants of the membrane that encloses the mushroom when it is young. As it grows, the red color appears through the broken membrane, and warts become less prominent. The red collar might fade after rain and in old mushrooms. Fully grown, the caps are 8 to 20 centimeters in diameter. Amanita muscaria forms symbiotic relationships with many trees, for example, pine, spruce, fir, birch, and cedar, and is commonly seen under introduced trees.
It contains several biologically active agents, at least one of which, muscimol, is psychoactive. Another compound, ibotenic acid, a neurotoxin, serves as a prodrug to muscimol, with approximately 10 to 20% converting to muscimol after ingestion. An active dose in an adult is about 6 milligrams muscimol or 30 to 60-milligram ibotenic acid, typically the amount found in one cap. The amount and ratio of chemical compounds per mushroom vary widely from region to region and season to season. Spring and summer mushrooms contain up to 10 times more psychoactive agents than autumn fruitings. The highest concentration is found in the cap. A fatal dose is approximately 15 caps, and the significant toxins are muscimol and 3-hydroxy-5-aminomethyl-1-isoxazole.
The psychoactive agents are water-soluble. Drying the mushroom might increase potency, as the process facilitates the conversion of ibotenic acid to the potent muscimol through decarboxylation. Ibotenic acid and muscimol are structurally similar to each other and two essential neurotransmitters, glutamic acid and GABA, respectively. Muscimol is a potent GABBAA agonist, and ibotenic acid an agonist of NMDA glutamate receptors and specific metabotropic glutamate receptors involved in the control of neuronal activity. It is these interactions that cause psychoactive effects.
Effects can range from nausea and twitching to drowsiness, cholinergic crisis-like symptoms, low blood pressure, sweating and salivation, auditory and visual distortions, mood changes, euphoria, relaxation, ataxia, and loss of equilibrium. In high doses, it causes delirium, similar in effects to anticholinergic poisoning, with confusion, hallucinations, agitation, and central nervous system depression, seizures, coma, and death.
Symptoms usually manifest after approximately 30 to 90 minutes and peak within three hours, but specific effects can last for several days. Although, in the majority of cases, recovery is complete within 12 to 24 hours. Effects vary highly between individuals, with similar doses causing entirely different reactions. The wide range of psychoactive effects has been described as depressant, sedative-hypnotic, psychedelic, dissociative, and deliriant. Perceptual effects such as synesthesia, macropsia, and micropsia might occur. Some users report lucid dreaming under the influence of its effects.
Amanita pantherina, also known as the panther cap, and false blusher, is a species of fungus found in Europe and Western Asia. It is an ectomycorrhizal fungus, living in root symbiosis with a tree, deriving photosynthesized nutrients from it while providing soil nutrients in return. Amanita pantherina contains the psychoactive compound muscimol but is used as an entheogen much less often than its much more distinguishable relative Amanita muscaria.
Its gills are 4 to 11 centimeters wide, first hemispheric and then convex to plano-convex, deep brown to hazel-brown to pale ochraceous brown, with densely distributed warts that are pure white to sordid cream; its flesh is white and unchanging when injured. Its gills are free and white to grayish. Its volva is white, becoming gray with age. The panther cap smells like raw potatoes. Other than the brownish cap with white warts, distinguishing features of Amanita pantherina include the collar-like roll of volva tissue at the top of the basal bulb.
It is found in both deciduous, mainly beech, and less frequently, coniferous woodland and rarely meadows throughout Europe and Western Asia in late summer and autumn. It has also been recorded in South Africa, where it was accidentally introduced with trees imported from Europe. There are also reports of Amanita pantherina on Vancouver Island, in British Columbia, Canada.
Amanita regalis, commonly known as the royal fly agaric or the king of Sweden Amanita, is a fungus common in Scandinavia but is also found in Eastern and Northern Europe, Alaska, and Korea. The mushroom resembles the fly agaric, Amanita muscaria, but differs in being larger, with a liver-brown cap bearing numerous scabs, and in having a stem which is yellow-ochre at the base, with white patches. Amanita regalis contains the psychoactive compounds ibotenic acid and muscimol.
It is typically found in mountainous forests, both deciduous and coniferous. It exists in a symbiotic relationship with birch, Scots pine, mountain pine, and Norway spruce. The mycelium envelopes the roots of the trees and supplies them with minerals, trace elements, and water, while the tree, in return, provides the fungus with food.
The cap of regalis is 10 to 25 centimeters broad, and depending on the state of development, ranges in shale from spherical, convex to somewhat flattened. The color is yellowish-brown and is densely covered with yellow to light ochraceous scabby warts arranged in almost regular concentric rings, which are a remnant from the volva. The gills are white with a creamy yellow tinge, unattached to the stem, and close together. The stem of a mature individual is typically 10 to 20 centimeters long and 1.5 to 2 centimeters wide. The flesh does not change color in the air and has insignificant taste and smell.
This will be a monumental chapter both of size and importance. At first, I wrote it under the title, Dosages, but then I decided to change it into something less enticing that better describes what we are going to explore here, as this chapter is about not dying, and for those that skipped it, the joke’s on you. This will be the most controversial section of this essay. There are no well-studied guidelines to follow for recreational doses, and while the territory is not unexplored, it is unmapped.
Nothing in this chapter should be taken as medical advice, and this is nothing more than wild speculations about effective dosages for deadly chemicals in the microgram-range. I will not be touching on specific doses to use. Instead, I will distinguish what doses not to use and how to avoid ingesting said toxic doses. I will give you the tools but not show you how to use them. I will not tell you what to do. I will tell you what not to do. For simplicity’s sake and easier comparisons, I will refer to all doses in micrograms.
I will be concentrating on scopolamine, daturine, atropine, and the plants containing these alkaloids. Especially the nightshades, as they are the ones most commonly used, in combination with being most variable in alkaloid content, thus most dangerous. Pharmaceuticals offer the advantage of a definite amount of the compound in accordance with their label.
If there is one bit of advice to be taken from this chapter, regardless of which compounds or route of administration you might choose, it is to start low, even lower than what you would think is low, and then increase the doses incrementally from there. It is always possible to redose, but never to undose. Yes, it will take you a while to reach the effective doses, but keep in mind that there is no effective dose for the dead.
All parts of the nightshades, henbane, Datura, Brugmansia, and belladonna, contains the desired alkaloids. With roots and seeds generally containing the highest amounts. There is high variability in alkaloid content depending on the time and environment, time of lifecycle, year, and even day. The alkaloid profiles and content of the different nightshades and subtypes also vary. One diploid seed of Datura innoxia contains on average 1904 micrograms scopolamine and 1134 microgram daturine, for a total of 3038 micrograms with a ratio of 1.679, making it the one with the highest total amount of alkaloids. While in comparison, one diploid seed of Datura stramonium contains 135 micrograms of scopolamine and 1043 micrograms of daturine, for a total of 1178 micrograms with a ratio of 0.129. Do keep in mind the possibility of other unknown yet active alkaloids unaccounted for.
In the case of Datura, this discrepancy makes for mistakes, as one seed of one genus is not necessarily the same as another and thus cannot be taken in comparable dosages. This makes emulating what others have done extremely risky. Instead, one should always calculate the total amount of alkaloids administered to avoid fatal mistakes.
Another point to be made is the difference in scopolamine to daturine alkaloid ratios. 1.678 for innoxia and 0.129 for stramonium. While scopolamine and daturine exhibit similar effects, they are not the same. At comparable doses, daturine has 98% of the anticholinergic power of atropine, while scopolamine has 92% of the anticholinergic power of atropine. The euphoric and sexual effects of daturine are stronger than those of atropine but weaker than those of scopolamine.
Scopolamine hydrobromide, or the acid salt form most commonly used in medicine, differs strikingly from atropine in that it does not stimulate the medullary centers and therefore does not increase respiration or elevate blood pressure. It frequently appears to act as a cerebral depressant and tends to promote sleep. A striking effect of large doses of scopolamine hydrobromide is the loss of memory for events that happened while the patient was under the influence of the drug. The vagolytic action of scopolamine is less than that of atropine, as is its effect in producing mydriasis. Besides, whereas atropine produces stimulation of the central nervous system, scopolamine depresses the cerebral cortex. Scopolamine possesses a more intense drying effect than atropine.
With the lowest anticholinergic potency in combination with the highest euphoric and sexual effects, scopolamine could be considered the most desirable of these, all in all, similar alkaloids. For simplicity’s sake, I will from here treat it as such. Next is what part of the plant to use; as there is high variability in alkaloid content, we want one with the highest scopolamine to another tropane ratio, and most stable alkaloid profile, or maybe least unstable profile.
For a comparison made with dry plant material, the flower of Hyoscyamus niger contains 0.1294% scopolamine and 0.0945% daturine, the seed 0.1887% scopolamine, and 0.1097% daturine, the root 0.0097% scopolamine and 0.0189% daturine, and the stem 0.0386% scopolamine and 0.0518% daturine.
While the flower has the highest scopolamine to daturine ratio, the seeds exhibit the lowest variability in total alkaloid content, and over time, thus could be considered the best choice. To complicate things even further, the nightshades exhibit polyploidy, meaning they can take on forms with more than two paired sets of chromosomes, which changes them quite a lot in morphology. I will compare henbane or Hyoscyamus niger seeds with different ploidy.
One diploid seed of Hyoscyamus niger is circa 1.77 millimeters long, weighs circa 970 micrograms, contains approximately 42 micrograms scopolamine, and 14 micrograms daturine for a total alkaloid content of 55 micrograms.
One tetraploid seed of Hyoscyamus niger is circa 1.92 millimeters long, weighs circa 1420 micrograms, contains approximately 107 micrograms scopolamine and 54 micrograms daturine for a total alkaloid content of 159 micrograms.
Usually, they are in the diploid form, but occasionally they come in the tetraploid form, which more than three times as potent, with a higher daturine to scopolamine ratio. Be observant. To discern the most suitable source, I will compare some of the most common. First, I will calculate the alkaloid content of diploid seeds from the different commonly used species, Datura innoxia, Datura stramonium, and Hyoscyamus niger.
One diploid seed of Datura innoxia contains on average 1904 micrograms of scopolamine and 1134 micrograms of daturine for a total of 3038 micrograms of said alkaloids with a ratio of 1.679.
One diploid seed of Datura stramonium contains on average 135 micrograms of scopolamine and 1043 micrograms of daturine for a total of 1178 micrograms of said alkaloids with a ratio of 0.129.
One diploid seed of Hyoscyamus niger contains on average 42 micrograms of scopolamine and 14 micrograms of daturine for a total of 56 micrograms of said alkaloids with a ratio of 3.701.
In this case, the genus truly matters in dosing and for acquiring the desired alkaloid ratio. The smaller and less potent seeds and favorable alkaloid ratio of henbane could be considered better because the higher number having to be ingested results in a lower variability of the dosage from some seeds being weaker or stronger or miscalculations when counting the seeds. With seeds like this, new batches can be added to the same airtight and light-free container with old seeds and shaken. Differences in median potency will be minimized. Any variations will be so slight that the danger of something going wrong would be minimized, and future dosages can be adjusted.
There are four practical routes of administration, oral, transdermal, nasal, and rectal. The oral bioavailability of scopolamine, daturine, and atropine are highly variable, with a number ranging from approximately 10 to 50%. Taking into the equation the variability in alkaloid content of these plants, the dosages could change many folds. While transdermal administration faces similar concerns as oral, rectal, and nasal administrations have a higher bioavailability. For practical reasons, I will concentrate on the intranasal route.
In intranasal administration of scopolamine, peak plasma concentrations are reached within one hour of dosing, showing a similar magnitude of effects to intravenous administration. Absolute intranasal bioavailability, calculated from the area under the drug concentration versus time curve, was found to be significantly higher than that of orally administered scopolamine at 83% versus 3.7%.
Scopolamine could be extracted by crushing the seeds with a pestle and mortar before being soaked in distilled water mixed with alcohol to deter bacterial growth. Vodka would be suitable for this purpose, but keep in mind, the higher the ethanol content, the higher the daturine content, due to daturine being more soluble in ethanol than scopolamine. Calculate the potency of the solution to avoid overdose before starting as low as possible and titrating up from there. The administration could be done intranasally with a nasal spray bottle.
It is yet to be established if this medium is suitable for long-term storage. There is a high probability of the alkaloids degrading faster than if stored dry. To keep the alkaloid content stable, swap no more than half of the old plant material for crushed fresh at a time.
Keep in mind that the solubility of the alkaloids depends on the temperature of the water, with higher temperatures meaning more alkaloids dissolved, and at a lower temperature, they will precipitate out of the solution, meaning that the potency will change.
The water solubility at room temperature for scopolamine is approximately 100,000 mg/L, and 3,560 mg/L for daturine. Or 100 mg/ml for scopolamine, and 3.56 mg/ml for daturine. This can be taken advantage of to change the scopolamine to daturine ratio further in favor of scopolamine and to establish a definitive highest possible alkaloid content in any specific amount of water.
In other words, the total amount of scopolamine dissolved in water at 25 °C cannot exceed 10% of the solution’s total mass, and that amount for daturine is 0.0036%.
While it varies, and you have to research this yourself, a standard nasal spray bottle of 17 grams or 17,000 milligrams, with 1,700 milligrams scopolamine, administers approximately 142 milligrams with each press, which with a saturated solution means 14,2 milligrams or 14,200 micrograms of scopolamine, with an additional amount of daturine not exceeding 511 micrograms. In reality, the scopolamine content will be lower due to ethanol. If a 40% ethanol solution is used, the total amount of scopolamine will be reduced to maybe 8,520 micrograms, while the amount of daturine will increase.
I have given you the source, alkaloid, and route of administration, which I believe is the least dangerous, but I will not give you a safe dosage to use, for there are non. I will end this chapter with some studies and case reports regarding the dangers of anticholinergics, from which you can draw your own conclusions. Good luck.
An oral dose of 50,000 micrograms atropine sulfate in humans has been reported to be fatal, but exact data on lethal doses of scopolamine are lacking. Ingestion of 10,000 micrograms has been reported to be fatal in children, whereas adults have survived more than 100,000 micrograms.
A dose of 450 micrograms of scopolamine has caused toxic psychosis, which lasted ten days. However, it is not clear if this involved oral or ocular administration. Also, the source of this statement cannot be verified.
In a study involving 115 patients following acute poisoning from over the counter sleep preparations containing scopolamine in combination with an antihistamine. The lowest ingested dose producing life-threatening symptoms, for example, convulsions, arrhythmias, hallucinations, was 2,000 to 4,000 micrograms.
There is also a case report of a ten-year-old boy with acute onset of confusion and visual hallucinations subsequently confirmed to be due to scopolamine toxicity following ingestion of travel sickness medication. The amount of scopolamine hydrobromide ingested was 2,400 micrograms. Van Sassenbrocck and colleagues describe three patients who received 10,000 micrograms of scopolamine hydrobromide as an accidental overdose due to compounding errors instead of scopolamine butylbromide. In some cases, symptoms persisted for months, and in one case, the patient had been mistakenly diagnosed as suffering a stroke.
For scopolamine, hallucinations have been reported with doses as low as two mcg/kg.
While so-called “set and setting” is considered paramount by contemporary users of psychotropics, and unfortunately quite unexplored avenue is techniques for controlling the mind such as trance, hypnosis, and lucid dreaming. The biggest danger with deliriants is the mind wandering to places where the user does not want it to go. With these techniques, the mind can be controlled and steered in the desired direction. Thus diminishing distraction and unpleasant experiences.
Interestingly enough, trance is a widely used concept in indigenous populations using psychotropic plants. It seems like somewhere on the way, between the past when these substances were commonly used, through the centuries when it was frowned upon by the broad masses, to today when it is reemerging, these practices were lost in time.
First, we have to understand how these concepts work. How we can implement them and what they can do and what they cannot do. They are in no way a safeguard against accidents, mistakes, or sheer stupidity. They are not a substitute for a safe setting, a watcher, nor a sane mind.
Hypnosis is a state of human consciousness involving focused attention and reduced peripheral awareness, and an enhanced capacity to respond to suggestions. The term may also refer to art, skill, or act of inducing hypnosis. Hypnosis is a state of focused attention and increased suggestibility, where the hypnotized individual appears to heed only the communications of the hypnotist and typically responds uncritically and automatically while ignoring all aspects of the environment other than those pointed out by the hypnotist.
In a hypnotic state, the individual feel, see, smell, and otherwise experience the hypnotist’s suggestions even though they might contradict the actual stimuli present in the environment. These effects are not limited to sensory change, as suggestion meat alters the subject’s memory, awareness of self, or be extended post hypnotically into the subject’s subsequent waking activity.
Hypnosis typically involves an introduction to the procedure, during which the subject is told that suggestions for imaginative experiences will be presented. The induction is an extended initial suggestion for using one’s imagination and might contain further elaborations of the introduction. The procedure is used to encourage and evaluate responses to suggestions. In hypnosis, the subject is guided by the hypnotist to respond to suggestions for changes in subjective experience, perception, sensation, emotion, thought, and behavior. Self-hypnosis, in which the administration of the hypnotic procedure is done by oneself, is possible.
Changes in brain activity have been found in highly responsive subjects. These changes vary depending on the type of suggestion given. Light to medium hypnosis, where the body undergoes physical and mental relaxation, is associated with a pattern of mostly alpha waves. In contrast, enhanced theta wave patterns are observed when there is a task performance or concentrative hypnosis. In brain scans, regions of the brain associated with specific sensory input are activated following the suggestion. Hypnotic induction might affect the activity in brain regions that control intention and conflict processing.
Comparing highly and weakly susceptible subjects, task results are consistent regardless of the subjects’ mental state. However, under hypnosis, the highly susceptible subjects showed significantly more brain activity in the anterior cingulate gyrus, an area in the brain that responds to errors and evaluate emotional outcomes. The highly susceptible group also showed much higher activity in the prefrontal cortex’s left side, a region involved with higher-level cognitive processing and behavior.
During a lucid dream, the dreamer is aware that they are dreaming and might be able to exert control over the narrative and environment. Time perception during lucid dreaming is about the same as during waking life. Lucid dreaming can be used as a treatment to alleviate recurrent nightmares.
The first step to lucid dreaming is recognizing that one is dreaming; this might happen in the dorsolateral prefrontal cortex, which is one of few areas deactivated during rapid eye movement sleep, and where working memory occurs. When this area is activated, and the recognition of dreaming occurs, the dreamer must be cations to let the dream continue, yet be conscious enough to remember that it is a dream. While maintaining this balance, activation in the amygdala and parahippocampal cortex might be lessened. To continue the dream hallucinations the pons, and parieto-occipital junction stays active.
Lucid dreams begin in the rapid eye movement phase of sleep; successively higher amounts of the beta-1 frequency band, 13-19 hertz, are exhibited during lucid dreams. Hence, there is increased activity in the parietal lobes, making lucid dreams a conscious process. Thus, lucid dreams might not be as much a state of sleep as brief wakefulness, as the dreamers experienced their lucid dreams during REM sleep, which might mean lucid dreaming is a twilight state between waking and dreaming. While dream control and dream awareness are correlated, neither requires the other. One can be exhibited without the capacity of the other. Sometimes the dreamer is aware they can exercise control but chooses not to.
Trance is a state of awareness or consciousness other than the ordinary waking consciousness. The use of repetitive rhythms to induce trance is an ancient phenomenon, shamanistic practitioners have been employing this method for millennia, and there are striking similarities of shamanistic use of auditory stimulus among different cultures. Entrainment is the synchronization or different rhythmic cycles. Breathing and heart rate are affected by an auditory stimulus, as is brainwave activity, especially theta waves. This is the essential and the cause behind the altered states of consciousness it can induce.
These techniques, by themselves or in conjunction can, and should be used when entering delirium. Do not forget to exercise common sense, good judgment, and stay calm; your mind is a mirror image of your emotions, and they a mirror image of your mind. Again, these techniques do not make this venture safe, just less dangerous.
Drank three Shots of Datura Tea
A young male describes having hazy memories from the incident but claims he patched them together by talking to others present at the time. He looks back at the event as something, Terrifying, incredible, and life-changing. He also says he still has trouble dealing with the emotions he experiences when looking back. A friend of his had made a tea out of Datura, of which the protagonist drank four shots. It tasted foul.
Then came the thirst, and he tried to drink a glass of apple cider, but it was difficult as his throat seemed to close up with every sip. His thirst did not subside. Instead, he felt the urge to urinate but could not. He then describes feeling like he was talking normally to his friends, but without them understanding. To them, it sounded like gibberish. He smoked phantom cigarettes, something that he would continue doing for three days.
Again he tried to urinate, but neither this time; he believed it to be possible, but it was possible in reality, and he made a mess. He also took all the family’s toothbrushes and put them in his pocket. When they went outside the house to smoke cannabis, he wandered off, and later they found him talking to a pine tree. This he did not remember. From this point on, his memory became better.
They all went to a party where he had a fear for the balloons; someone tried to talk with him, but the gibberish that came out made them understand he was on something, and he was taken home. When he walked home, every piece of sidewalk seemed to shatter under his step and disappear. He tried to run, but jolts of electricity coursed through his body.
They rushed him to the hospital, where the staff appeared like monsters to him, and he tried to get away. One of the doctors, whom the protagonist thought was a wizard, handed him a portion of activated charcoal, which he vomited up again. Soon after this, his kidneys began shutting down, and they put in a catheter while he tried to resist.
He remembers believing he was tied to a bed, with Chewbacca by his side. Again, he smoked phantom cigarettes. He dropped one on the bedsheet, and when he tried picking it up, it had transformed into the stick shift of his car, and he was sitting in it, driving down the street. He tried hitting the brakes, but they were gone, and he was back in the hospital room. Behind a small fan, a miniature girl sat crouched, staring at him. He asked Chewbacca to take the fan out, and he complied. Later he found out Chewbacca was his father.
He stayed at the hospital for multiple days, with malfunctioning kidneys and a heart rate fluctuating between being dangerously high or low. After he had been omitted, he felt frail for multiple days more. During his stay at the intensive care unit, the doctors had given him a 50% chance of survival.
Ate 150 Datura Seeds
Another young male describes it as a life-changing experience. Shortly after eating the seeds, his stomach cramped, and he vomited. He felt drunk and could barely walk. Then he felt insects crawling under his skin; in a panic, he clawed at his skin, trying to rip them out. The last thing he remembers was running out the door before everything became black. It was like a dream, with entities swirling around him while feeling the presence of people. From here on, his memories are hazy.
In the morning, he woke up naked on the floor of his apartment, not remembering how he got there. His eyes were dry as a desert, and his contact lenses were stuck. Everything looked fuzzy through them. He felt energized and happy. Then he saw the two policemen looking at him. They asked him questions to which he answered, wrapped him in a bedsheet, and took him to the police station, where they continued to ask questions.
He was put in a cell, where he slowly started to come back to reality, wondering what had happened, what he had done. He was taken to the courtroom, where he was charged with Disorderly Conduct before being let go. Then he realized that he was still in delirium. Spirits revolved around him while he walked aimlessly and talked to people that were not there.
He became more and more dehydrated as the day went by; he drank out of water sprinklers and the gutter before falling asleep under an overpass. He woke up at dawn and continued walking. Remembering the address to a friend, he took the long walk there before passing out on the floor.
It took him four days to get back to normal, and he had to use a cane to walk for a week. His body was cut and bruised from allegedly jumping in and out of a pool for most of the night.
Drank an Unknown Amount of Datura Tea
First, he only felt extreme muscle tiredness and almost being unable to stand. Then in the next instant, he was at his friend’s apartment having a nonsensical conversation with his friend. Then, he was at home, and his memories slowly began coming back to him; he remembered having smoked phantom cigarettes and that the apartment had been his home, and the friend his mother. He later found out he had been crawling on the floor when he initially drank the datura tea, thinking he was eating bugs, while his friend was convulsing with foam coming out his mouth.
His family had taken him home, where he rolled imaginary joints, snorted imaginary lines while talking to imaginary people. Two days later, he still had problems seeing.
Ate Two Tablespoons of Datura Seeds
Within an hour, all colors turned into shades of pink and red. He felt stupid and slightly scared. His mouth and throat became parched, and when he tried to pick up a soda can to drink from, he could not lift it. He then raised it with both hands, and while spilling a lot, he drank the rest before going to sleep.
He woke up still feeling weird, described as half-dead, and not knowing what is happening. Needing to urinate, he crawled to the edge of his bed and tried standing up, but fell onto his face. After falling about ten times, he made it to the bathroom. Next, he remembered being in the emergency room, where the doctors and nurses asked him what kind of drugs he had taken. He could not speak nor walk anymore.
They tried intubating him to pump his stomach, but he pulled out the tube fought the nurses and doctors. They sedated him with Valium through an IV after he had broken the first needle in his arm. Then they pumped his stomach. He had a temperature of 41° C and a pulse of 140. They believed he would have died if he had come later. He remained delirious for over two days and stayed one more recovering.
Drank Tea From 10 Datura Leaves
His body felt drunk, but his mind was coherent. From here on, he lost track of all time. Hallucinations of spiderwebs in the corners of the walls. His eyesight worsened, and it was a monumental task to get out of the couch and to the bathroom, where he noticed his pupils were very dilated and his skin red.
He tried regurgitating, but little came up before his throat began closing up, extremely dry, making breathing difficult. When he tried to drink, he felt like he was going to choke. To find a remedy for his problems, he searched the internet for what he, in retrospect, estimate as multiple hours, unable to comprehend the symbols on the screen. Instead, he went to talk to his daughter before realizing she was not at home. She was away with her mother.
Later, when they returned, they found him standing in the smoke-filled house, staring into nothingness while the stove with another pot of tea was on fire. He insisted that nothing was wrong, and they left again. When they returned, he sat at the computer again, while the front door was open, and their pets were gone.
Two months later, he still did not feel the same as before. His throat was permanently damaged, and unable to maintain a train of thought.