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Jul 6, 2021
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LSD (d-Lysergic Acid Diethylamide) is a semisynthetic psychoactive substance from the family of Amides of Lysergic Acid. At the moment it is the most well-known and the most studied psychoactive hallucinogenic substance, which can cause altered perception, thinking and feeling in low doses, without the effects of psychomotor stimulation and depression. Other names include: Lysergide, Cid, Blotter, Tabs, LSD-25, LSD, L, Lucy and Acid.

Total synthesis of Lysergic Acid

Synthesis of LSD-25 from Lysergic acid monohydrate


Physicochemical properties and forms of the substance.
LSD is a semisynthetic substance, made from Lysergic Acid found in a parasitic fungus that infects rye C. Purpurea. The molecule consists of an indole system with a tetracyclic ring (C20H25ON3). IUPAC name: (6aR,9R)-N,N-Diethyl-7-methyl-4,6,6a,7,8,9-hexahydroindolo-[4,3-fg]quinoline-9-carboxamide. Carbons 5 and 8 are asymmetric: therefore, there can be four isomeric optically active LSD isomers, which are well-known. They are d-LSD, l-LSD, d- isolisergic acid diethylamide and l-isolisergic acid diethylamide. Only d-LSD isomer has psychoactive properties. LSD is crystallized from benzene in the form of pointed prisms. It is water-soluble, its melting point is 83 °C. LSD is usually stabilized in a solution of tartaric acid. The molar mass is 323.42 g/mol. LSD is unstable when pH is less than 4. After 4 weeks of storing the substance at a temperature of 45 degrees Celsius, about 45% of the substance is lost. Due to LSD base instability, it needs to be stabilised in form of salts, usually in form of tartrate. In its pure form the substance has the appearance of colorless, odorless prismatic crystals, has moderate or high sensitivity to oxygen, ultraviolet radiation and chlorine, decomposes at room temperature (the effect is lost proportionally), and if there is an appropriate temperature regime (from minus five to plus five degrees Celsius) and the place of storage is dry and dark, the substance can be stored for a long time (up to several years).


The most common form of LSD is Blotter – which is a small square sheet of perforated "blotting" paper, submerged in the solution of LSD. These blotters are placed on the tongue or under the tongue with a temporary exposure, chewed or swallowed. Sometimes the solution of LSD is used, which can be taken with a pipette and dripped on the mucous membrane of the mouth or nose. Tablets or microdots are usually intended for oral use, which can be swallowed or chewed. If LSD is in the form of powder, it is best diluted in a liquid solution and put on a blotter to control the dose. Another form of this substance is "gel tablets", which are taken orally and are elements of gelatin containing LSD.

After oral administration, LSD is completely absorbed in the digestive tract. When taking 100-250 mcg of LSD orally, psychoactive and sympatomimetic effects are present during 30-45 minutes, reaching their peak after 1,5-2,5 hours. Nowadays, there is no full LSD metabolism model. Most of the studies were conducted on animals, mostly on rats. It is assumed that the metabolic rate of LSD varies from one type of rats to another, as well as it is dependent on the nature and number of metabolites formed. After oral administration of LSD, it is metabolized intensively, which explains why only 1% of the dose is excreted unchanged in the urine. LSD is mainly metabolized in the liver tissue to form structurally similar and inactive metabolites after the processes of N-dealkylation and/or oxidation. In humans, LSD undergoes metabolic N-demethylation at position 6 to form N-demethyl-LSD (Nor-LSD), even though it is a secondary metabolic pathway. The main metabolites of LSD are: 2-oxo-LSD, 2-oxo-3-hydroxy-LSD (oh-LSD), N-demethyl-LSD(Nor-LSD), Lysergic Acid N-ethylamide (LAE) 13- and 14-hydroxy-LSD. At plasma concentrations of 0.1 and 20 mg/l, in vitro experiments on guinea pigs showed, that about 65-90% of LSD binds to non-diffusive plasma components. It was researched that LSD causes psychoactive effects on a person (at a dose 1 mcg/kg orally) at a concentration of 0,005 mcg/g of brain tissue.


Half-life of Nor-LSD is about 10 hours, which is longer than half-life of LSD. The presence of potential glucuronides, apparently, is an important stage of detoxification, which is the most frequent and most important phase II reaction in humans. Both LSD metabolites Nor-LSD and hydroxy-LSD have a longer half-life period than LSD. After incubation of the human microsomal liver with LSD, 2 more metabolites of LSD were identified: after dealkylation reaction - Lysergic Acid ethylamide (LAE), and 2-oxo-LSD –after reaction of oxidation. CYP3A4, CYP1A2 and CYP2C19 play an important part in LSD metabolism. The use of the CYP1A2 inhibitor alpha-naphthoflavone and the CYP3A4 inhibitor ketoconazole confirmed the importance of both enzymes after a significant decrease in the formation of metabolites. CYP2D6, CYP2E1 and CYP3A4 are significantly involved in the metabolism of LSD into Nor-LSD, whereas CYP1A2, CYP2C9, CYP2E1 and CYP3A4 make a significant contribution to O-H-LSD formation.


Registration of LSD in urine after single use (200 mg orally) in humans shows that elimination rate of LSD reaches the maximum after 4-6 hours since use. Half-life of LSD elimination is 3.6 hours. It is reported that LSD and its metabolites can be detected in urine during 4 days after oral use. When using screening radioimmunoassay (RIA) (threshold value of 0.1 ng/ml), the detection limit is 100 micrograms of LSD orally is about 30 hours. Each doubling of the initial amount adds about 5 hours. LSD or its cross-reactive metabolites were detected within 34-120 hours at concentrations in urine of 2-28 mcg/l (n = 7,300 mcg LSD orally.

Since LSD enters the body in very small quantities, the LSD found in biological samples is also very small. The period of detection of LSD in body, depends on the test used, the detection limit, the collection point, the type of liquid sample and the amount of LSD administrated. Conventional forensic methods of confirmatory and quantitative testing of LSD include high-performance thin-layer chromatography (HPTLC) and various forms of gas chromatography / mass spectrometry (GC/MS) with detection limits set at about 0.4 micrograms/l. Practical (forensic) detection limits are 0,1 and 0.25 ng/ml for LSD and N-demethyl-LSD respectively. Average detection time of LSD in blood samples is estimated at 6-12 hours and 2-4 days in urine samples. In most LSD-positive urine samples, 2-oxo-3-hydroxy-LSD metabolite is present in higher concentrations, and can be detected for a longer period of time, than LSD itself. LSD detection in hair samples is now available even for small doses and single dosages, but it is not available for LSD metabolites.

Complex receptor interactions of LSD are an important topic of experimental work and reflections on its mechanisms of action. The prevailing hypothesis about how indole hallucinogens affect serotonin is summarized in the context of precisely suppressing the activation of serotonergic cells while simultaneously protecting postsynaptic serotonergic receptors from secondary autoactivation. Non-hallucinogenic LSD counterparts do not inhibit the activation of receptors.

Serotonin (5-hydroxytryptamine; 5-HT) is produced by a few neurons (1000), each of which innervates up to 500,000 other neurons. For the most part, these neurons originate in the raphe nuclei (RN) of the midbrain. One of their main targets is the blue spot (LC), which controls the release of norepinephrine, which regulates the sympathetic nervous system. The LC also has neurons that extend into the cerebellum, thalamus, hypothalamus, cerebral cortex and hippocampus. The PH expands its projections into the brain stem and upwards into the brain. It has been suggested that neurons in this area of the brain can suppress sensations, thereby protecting the brain from sensory overload.


In general, 5-HT can be considered basically as an inhibitory transmitter; thus, when its activity decreases, the next neuron in the circuit is released from inhibition and becomes more active. This point of view is limited by the fact that some 5-HT receptors are excitatory ion channels (5-HT 3), and some subtypes may have excitatory effects depending on the binding of the G-protein in specific neurons. Since the serotonergic systems seem to be directly involved in the control of sensations, sleep, attention and mood, it is possible to explain the actions of LSD and other hallucinogens by their disinhibition of these critical systems.

LSD firmly binds to human serotonin (5-hydroxytryptamine (5-HT)), 5-HT1A, 5-HT2A, 5-HT2C,dopamine D2 and α2-adrenergic receptors and is less active with α1 adrenergic receptors D1, and D3 receptors. LSD also activates the trace amino-bound receptor 1 of rats and mice (TAAR1), but not human TAAR1, is a partial agonist of 5-HT2A the receptor, which causes the main hallucinogenic effect. Subjective LSD effects in humans can be blocked by pretreatment (inactivation or pronounced single stimulation with a decrease in density) with a 5-HT2A receptor antagonist. A key mechanism of action of LSD and other serotonergic hallucinogens is the activation of the transmission of frontal cortex glutamate, secondary to the stimulation of the 5-HT2A receptor.

LSD acts as an agonist of 5-HT autoreceptors on 5-HT1A receptors in the LC, RN and cerebral cortex. It suppresses arousal and the release of serotonin from these cells. It also acts as a partial agonist of the 5-HT1A postsynaptic site. LSD has a high affinity for other subtypes of 5-HT1:5-HT1B, 5-HT1D and 5-HT1E.

LSD effect on the 5-HT2C, 5-HT5A,5-HT6 and 5-HT7 receptors is described, but its role remains uncertain. However, the hallucinogenic effect of LSD was associated with its affinity for the 5-HT2 receptor, where it acts as an agonist of 5-HT2, since this property is shared by hallucinogens of the phenethylamine group (mescaline, 2,5-dimethoxy-4-iodamphetamine, etc.). A strong correlation was described between the psychoactive doses of these hallucinogens and their corresponding effectiveness on the 5-HT 2 receptor. Most data indicate a specific mechanism of 5-HT2A, although the effect of 5-HT2C cannot be excluded.

LSD, presumably, can be characterized as a partial agonist of mixed 5-HT2/5-HT1 receptors. Nowadays, LSD is considered a partial agonist of 5-HT2A receptors. Especially those that are expressed on the pyramidal cells of the neocortex. Activation of 5-HT2A also leads to an increase in the level of cortical glutamate, probably mediated by thalamic afferents, but this increase in the release of glutamate can lead to changes in corticocortical and cortical-subcortical transmission.


In studies of regional distribution in brain tissues, it is demonstrated that cellular structures contain more LSD than the rest of brain structures. The highest LSD concentration is found in the hippocampus, basal ganglia, periventricular gray matter and the frontal-parietal cortex. The structures of the limbic system (hippocampus, amygdala, arch and septum) contain 2-3 times more LSD than cortical structures. The brain stem contains concentrations of LSD similar to the cortex, and LSD is distributed relatively evenly between the white and gray matter.

When studying the influence of LSD on cerebral blood flow, it was concluded that total cerebral blood flow (measured by the method of nitrous oxide load tests), cerebral vascular resistance, oxygen consumption by the brain and glucose utilization did not have any significant changes. Studies of neurophysiological action of LSD shows that there is a dose-dependent hyperreflexia and mild ataxia, which are the main neurological effects of LSD. Thus, light or low-specific signs of activation with an increase in the average frequency of alpha waves were identified on the EEG indicators, and there is also often a progressive desynchronization with a change in normal lateralization patterns.

In a study where healthy people were given orally from 0.5 to 1 mcg/kg of LSD as an experiment there was a decrease in the release of inorganic phosphate, also, the excretion of dopamine in the urine was significantly reduced (up to 476 mcg in 24 hours). However, it did not affect the excretion of norepinephrine, serotonin, comovanillin acid, vanillylmindal acid and 5-hydroxyndoleacetic acid in any way. Moreover, LSD causes a decrease in creatinine clearance, but does not affect calcium clearance and serum calcium levels in general. There are no effects on transaminases, lipid levels, sodium, chloride, urea, cholesterol. There is some experimentally confirmed data that LSD significantly reduces the level of prolactin in plasma at rest in rats (at a dose of 0.05 and 0.2 mg/kg), however, there are no changes in the concentrations of luteinizing hormone and follicle-stimulating hormone. In humans, LCD increases the growth hormone in the blood serum with a peak at 120 minutes, but does not change the level of prolactin. There is evidence of a significant increase in the excretion of 17-ketosteroids.

Clinical effects.
In modern placebo-controlled studies using psychometric visual analog scales, the effects of LSD were mostly positive, and the average group ratings of "good effect of the drug "and "sympathy for the drug" reached 90%. However, when taking more than 200 mcg orally, the assessment of "more negative effects" was in 50% of the volunteers, which determines the appropriate recommended dose of the substance. The preliminary action of the 5 HT2A antagonist ketanserin completely leveled the effects of LSD. Music has been proven to enhance the emotional response while using LSD, it also enhances and transforms images with closed eyes or scenes from the past of individual's life.

Physical effects of LSD include: spontaneous bodily sensations, or “body high”, - a general tingling sensation throughout the body, completely in unpredictable places during the whole trip, or in its first half; stimulation - low or moderate stimulation without the effect of agitation and without a subsequent sedative effect due to the depletion of neurotransmitters; euphoria - moderate euphoria or intense empathogenia, often with the presence of cognitive illusions of mood (euphoria together with dysphoria); analgesic effect; increased body temperature; nausea may occur; appetite suppression; rarely-violation of urination, excessive yawning, hypersalivation, bruxism, muscle spasms/tremor.


Cognitive effects include: analysis enhancement - the transformation of the course of thought with the predominance of "new" objectivity, "unusual ideas", is one of the main criteria for choosing this substance by artists, marketologists and people whose profession requires creativity; anxiety and paranoia – at doses more than 170 mcg the chances of such effects increase. At low doses they are practically inexistent, or light anxiety can be present, which is insignificant to the trip; conceptual thinking and cognitive euphoria - according to studies using visual analog scales, this type of euphoria was only 20-25% of the one induced by intake of psychoactive substances like MDMA and cocaine. However, conceptual thinking, which is characteristic for LSD, is more pronounces compared to other known hallucinogens and psychostimulants; personal bias suppression; creativity enhancement; Introspection; novelty enhancement; focus enhancement; immersion enhancement, personal meaning enhancement and emotion enhancement – these effects, as a rule, they have a constant wave-like pattern throughout the trip, they are also called “recreational LCD” or recreational LSD effects” because they are the main cognitive positive effects that are often used for the purpose of conservative therapy of various mental disorders; other uncommon effects of this group: empathy, affection and sociability enhancement, delusion, deja vu, increased libido/music appreciation and sense of humor, laughter fits, memory suppression, effects «ego death»; suggestibility enhancement, thought acceleration, thought connectivity and time distortion – these effects take place in the middle of a trip, practically at its peak, the predominance of one effect over another depends solely on the type of personality, neural connections, activity of the limbic system and other factors at the level of the central nervous system; wakefulness; auditory enhancement/distortion/hallucination; multisensory synaesthesia; "existential self-realization"; "spirituality enhancement"; "unity and interconnectedness»;


Visual effects of LSD: visual acuity enhancement/сolour enhancement – these effects are almost always present when taking 50-75 mcg LSD, and are considered positive desirable effects, they can last within 2 hours after leveling the main effects of LSD; pattern recognition enhancement, magnification, frame rate enhancement – some objects may seem bigger, than they actually are, increase in sharpness and clarity of details, altered perception of proportions of objects and images, these effects are wave-like, transient and controlled drifting (melting, breathing, morphing and flowing) - drifting (melting, breathing, morphing and flowing) – the sensation of actions and surrounding objects moving slowly smoothly, as of "fleeting" images and essence, which leaves the impression of watching a cartoon; tracers and after images (palinopsia) - they are "traces" of objects that remain after change of their location or even disappearance from the view, sometimes you can see a full-fledged object or person even after he disappeared from the view, and this "image" of a person's movement can be repeated recursively for several seconds;
Vegetative effects and side effects: LCD moderately increases blood pressure, heart rate, body temperature and pupil size. Sympathomimetic LSD effects at doses 100 and 200 mcg are similar, but are less pronounced than effects of MDMA and other psychostimulants. Acute but non-threatening side-effects of LSD during 10-24 hours after may occur in the form of dizziness, difficulty concentrating, headache, lack of appetite, dry mouth, imbalance and a feeling of emotional exhaustion.
LSD use causes "flashbacks", characterized as episodic or short replications of elements of previous experience with substances. Clinically significant flashbacks are also defined as persistent perception disorder associated with hallucinogens (HPPD syndrome). AT a dose of 75 mcg LSD can increase the subjective assessment of cognitive disorganization and delusional thinking, however, in 90% of cases this is due to a negative mood before use. Patients with schizoaffective disorder or schizophrenia may have a deficit of sensorimotor gating, which is reflected in the pre-pulse inhibition of the flinching reaction (PPI).

Methods of use and doses
The most important thing while using LSD is not the dose of the substance, but preparation for this act. It is necessary that the following principles of preparation are observed:
1. Make sure that you can spend the following hours in a calm and comforting environment. LSD-trip lasts a while, for 100 mcg – up to 6-7 hours. After that, the effects remain and decrease for another couple of hours. Sort out your affairs in advance to be sure that you will not need to rush somewhere and that no one will bother you. It is better to use LSD no later than 12 hours before going to sleep because there may be problems with falling asleep. Buy some light food in advance to eat after. During the trip, food will not be especially enjoyable, however it will not be repulsive either.
2. Calculate the correct dose for yourself. If it is your first time using, start with a minimum dose, if you have positive experience using LSD at a certain dose – you can repeat it with increasing the dose by 10-15% of the initial one, but no more! If you want to try, but you are worried about the process, you can try the dose of 50 mcg, you will feel light but distinctive change in mood and perception, but your consciousness will not be altered.

Low dose - 50-75 mcg; medium dose- 75-150 mcg; high dose- more than 150 mcg.

3. Place blotter on your tongue and leave for 10 minutes until it dissolves or until you feel that you have achieved the desired effect for the trip.
4. It is necessary for the first trip to be accompanied by a setter (there should only be positive interactions between this person and you, there shouldn't be any conflict or negative emotions about them because, otherwise, it can induce negative thoughts about the setter during the trip).
5. When the effects manifest, there will be distinct changes in your world perception, your vision can change: rainbow halos around lights, trails behind moving objects, geometric shapes with closed eyes, moving, twisting, crawling patterns on the surface of objects. These effects can be entertaining, but don't let them distract you from your sense of self, your life and the world around you.
6. LSD breaks mental barriers, allowing you to plunge deeper into yourself. You can feel intense feelings like happiness, sadness, become thoughtful or absent-minded, or get carried away with an idea. LSD demonstrated its quality to induce solving problems of science and engineering, allowing you to approach issues with increased creative potential and openness to new solutions. It is important to remember 2 things: you need to be open with your feelings and allow them to flow through you in an easy manner full of love. If you are stuck on a bad thought or emotion, it is better to start thinking about something pleasant, and you will notice, how your condition changes positively; try to remain open to your feelings and ideas.

LSD overdose and first aid.
As a rule, complications associated with the use of LSD are not associated directly with an overdose of the substance. They usually are associated with its effects, hallucinations, in particular, which indirectly, regardless of the dose, cause anxiety. Any psychotic episodes with delirium, mania, psychosis and anxiety can also cause a long-term trauma, called an anxiety disorder, which requires certain therapy; usually, this disorder responds well to treatment, the condition is reversible, and the patient does not notice changes in the condition for a short period of time. As for, the most dangerous complication in the long period is HPPD. If this syndrome is identified in a patient, a mandatory consultation of a qualified specialist is indicated in order to determine the need of pharmacological therapy and psychotherapy.

The most common symptoms of an LSD overdose (with each increase in the starting average dose by 10%, the probability of occurrence of one of the following symptoms increases by 25%): panic attack, paranoia, delusions of persecution, anxiety, disorientation, small-scale tremor, shortness of breath, respiratory arrhythmia, increased sweating.

In case of an overdose non-pharmacological help includes: identifying anxiety, understanding that everything occurring is no more than the substance effect, and it will stop soon, you can try breathing exercises with deep inhale and slow exhale for a short time; it is necessary to immediately free your head of all the thoughts in the head, and try to think of good moments in your life that are associated with the pleasant tones of the color palette (color-associated model); if you are a setter, it is necessary to have a therapeutic conversation with the tripper, explain the situation, change location, if the negative effects are associated with the environment.

As for pharmacological treatment, initially, it is necessary to consider using bare minimum of medications. In patients with light anxiety and worrying, drinking 50-100 ml. of strong alcohol with herbs (but no more) can help. If the situation is not improving within 30 minutes and anxiety persists, as a rule, it is necessary to use benzodiazepine tranquilizers: alprazolam (0.5-1 mg). In severe cases of overdose, when there is intense anxiety with signs of delusions of persecution, paranoia - it is necessary to use neuroleptics, when using LSD, the drug of choice is chlorpromazine (50 or 100 mg).

Alcohol's central depressant effects can be used to reduce some of the anxiety and tension produced by LSD. However, alcohol can cause dehydration, nausea and physical fatigue which can negatively influence the trip. Users are advised to pace themselves and drink a portion of their usual amount if making the decision to drink on LSD. Benzodiazepines are highly effective at reducing the intensity of LSD's effects through the general suppression of brain activity. LSD enhances the cognitive, visual and general hallucinatory effects of dissociatives.
Dissociative-induced holes, spaces, and voids and internal hallucinations become more vivid and intense on LSD. These effects correspond with an increased risk of confusion, delusions, and psychosis.
LSD and MDMA are highly synergistic and mutually enhance each other's physical, cognitive, and visual effects. The synergy between these substances is unpredictable, and it is advised to start with markedly lower doses than one would take for each individually. There is some evidence that suggests LSD increases the neurotoxicity of MDMA. Antidepressant and antipsychotic drugs may block the effect of LSD by acting on the same receptors and outcompeting their ability to bind. Antidepressants mirtazapine and trazodone act on the 5-HT2A and 5-HT2C receptors, where they block serotonin and other molecules from binding. Atypical antipsychotics also act on these receptors in order to decrease hallucinations and cognitive distortion. Lithium is commonly prescribed in the treatment of bipolar disorder; however, there is a large body of anecdotal evidence that suggests taking it with psychedelics can significantly increase the risk of psychosis and seizures. As a result, this combination should be strictly avoided. Tricyclic antidepressants increase physical, hallucinatory and psychological responses to LSD. Since the symptoms are similar to those induced by lithium and LSD, seizures cannot be excluded.
Tramadol is well documented to lower the seizure threshold in individuals, and LSD also has the potential to induce seizures in susceptible individuals. Cannabis can have an unexpectedly strong and unpredictable synergy with LSD. While it is commonly used to intensify or prolong LSD's effects, caution is highly advised as mixing these substances can significantly increase the risk of negative psychological effects like anxiety, paranoia, panic attacks, and psychosis. Anecdotal reports often describe the ingestion of cannabis as the triggering event for a bad trip or psychosis. It is advised to start off with only a fraction (e.g. 1/4th - 1/3rd) of their typical cannabis dose and space out hits to avoid accidental over intake.

To prevent dyspeptic functional disorders of the gastrointestinal tract, 6 hours before they use the consumption of anything other than water is not recommended, and also the consumption of heavy food and large amounts of food is not recommended 12 hours before the use. Pharmacological prevention of dyspeptic functional disorders includes metoclopramide 5-10 mg 2 hours before taking LSD.​
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