What is the natural equivalent of methamphetamine
Illegal Drugs - An Overview (Part 2)
Summary In addition to the socially “accepted” substances such as nicotine and alcohol, illegal drugs are consumed either as mono-substances, but often also in combination. A distinction must be made between “occasional” consumption and regular use (in the context of an addiction). The abuse of illegal drugs at work usually leads to consequences under labor law, since the ability to do the job without endangering others or yourself is usually impaired by the consumption. This is where the company doctor plays a key role. On the one hand, he is committed to occupational safety, but on the other hand, he is also committed to the interests of the employee concerned. This overview is intended to familiarize the occupational physician with the variety of psychotropic substances available on the illegal market. In part 2, as part of the substance overview, the nonselective central nervous depressant substances (gamma hydroxybutyrate, ibotenic acid / muscimol), the psychomotor stimulants (cocaine, amphetamine and its derivatives), the pure opioid agonists as well as some psychedelic substances and hallucinogens (anticholinergic and psychedelic agents ) treated. The naturally occurring active ingredients ("biodrogens") are also taken into account. The clear differences in the risk assessment for the world of work of the individual substances are discussed (duration of action, possibilities of detection, risk of dependency). keywords
· Nonselective central nervous depressants
· Psychomotor stimulants
· Opioid agonists
· Anticholinergic and serotonergic psychedelic agents
· Nonselective sedative substance
· Psychomotoric stimulants
· Opioid agonists
· Anticholinergic and serotonergic psychedelic substances
3.1.1 Gamma hydroxybutyrate (GHB)
GHB is illicitly traded in both liquid and powder form. The active ingredient was originally studied and manufactured as a fast-acting antidepressant in the 1960s. The expectations were not fulfilled. The substance is still used in human medicine (Somsanit®) as an induction hypnotic and sedative in anesthesia and intensive care medicine. This may make it easier to obtain. The synthesis can be carried out in an uncomplicated manner using raw materials that are easy to obtain (corresponding recipes can be found on the Internet): Gammabutyrolactone is heated and sodium hydroxide is added slowly while controlling the pH value. The salt forms in the pH-neutral range. The end product is a 50 percent solution of water and GHB. In the 1980s, the substance was abused by body pictures (GHB stimulates growth hormone). Some scene names like Liquid Ecstasy, Gamma, Liquid Ecstasy, Cerry Menth, Georgia Home suggest that it would be a liquid form of the corresponding dimethoxyamphetamine. However, GHB acts analogously to the natural agonist in the area of GABAergic transmission; there are indications that a specific GHB receptor exists. The effect (dose: 1 to 2 g) is described as balancing, euphoric (increased sensory impressions, increased need for contact, greater physical sensitivity) and compared to a “champagne rush”. The effect of intoxication slowly subsides, followed by slight tiredness without a hangover. Overdosing (more than 4 g orally) leads to impaired motor coordination, headaches, nausea and vomiting, a drop in pulse and blood pressure and myoclonus. In combination with other substances (e.g. alcohol) the unpleasant side effects are increased. Very high doses inhibit the respiratory center and cardio-circulation and lead to unconsciousness and cramps. Physostigmine (Anticholium®) is available as an antidote. The potential for dependence seems to be rather low, psychological dependence is known (regular intake of GHB three to four times a day in low doses). Detection is difficult (more than 90% of GHB is absorbed after oral administration and broken down into water and carbon dioxide without the formation of active metabolites), there are no rapid tests. Evidence in the urine is no longer possible after about four to five hours.
3.1.2 Ibotenic acid / muscimol
These isoxazoles are the actual active substances of the fly agaric (Amanita muscaria) and each contain 0.1% in the mushroom meat.26 Because of its very low concentration, muscarin has no part in the pharmacological effect of the fungus. The fly agaric is a native coniferous and deciduous forest mushroom that should not be confused. The globally widespread toadstool only grows in symbiosis with birch or pine, in a so-called "mycorrhizal partnership". It is often found in our regions from August to November under birches, pines and larches in deciduous and coniferous forests, both individually and in groups. The hat has white lamellas, the pulp is also white and only has a yellow to reddish tint directly under the hat skin. The spores are white and wide, oval in shape. Its use as a shamanistic drug is undisputed, which probably goes back to the Stone Age and was widespread in large parts of Europe and Asia. In North America and Siberia it is said to be used in shamanistic healing and conjuring ceremonies to this day. In Siberia it was the most popular intoxicant before the spread of alcohol. It was available in large quantities free of charge, could simply be preserved by drying and did not lose its effectiveness even after long storage
The isoxazoles are very similar to the neurotransmitter GABA and develop their predominantly inhibitory effect at the corresponding synapses in the central nervous system (direct GABA agonist). The total content of isoxazoles in the dried mushrooms varies between 30 mg and 180 mg per 100 g of dried mushrooms. Ibotenic acid is converted into muscimol, which is ten times more effective, by drying. A single dose of 1 to 2 dried mushrooms after minutes (smoking) to two hours (oral intake) leads to the so-called pantherina syndrome: severe fatigue, vivid dreams (in higher doses, alternation between deep sleep and physical expression of inner experiences, delirious states can occur) in combination with mydriasis, tachycardia, dry mouth (or also salivation and bradycardia depending on the muscarinic content), vomiting, unsteady gait, muscle paralysis. When ingested orally for psychoactive purposes, vomiting is common. Despite the vomiting, the psychological effect occurs (in contrast to mescaline). The duration of action is strongly dose-dependent and is four to eight hours (up to days). Excretion is practically unchanged via the kidneys. 27
Cocaine is a psychostimulating alkaloid from the leaves of the coca bush (Erythroxylon coca, Figure 6a). There is reason to believe that coca has been cultivated in Peru for at least 4,500 years. All pre-Columbian cultures in the Andes have left evidence that they were familiar with the use of coca leaves. They were (and are) used by the Indians for medicinal and mystical-ceremonial purposes because of their intoxicating and stimulating effect. In 1859 the individual alkaloids of the coca plant were isolated by Albert Niemann (including the main alkaloid cocaine, Figure 6b). It was first used medicinally as a local anesthetic (Karl Moller). A little later, the substance was used as a stimulant and additive in soft drinks (Vin Mariani, Coca-Cola). Sigmund Freud recommended cocaine for states of physical and mental exhaustion, for depression and catatonic stupor, as well as for alcohol and morphine addiction.10 The powder form of the substance offered on the illegal market as “coke” or “snow” is extracted and mixed with cocaine hydrochloride (Figure 6c ) further processed form.28 The “fashion drug” of the twenties of the last century was usually snuffed. The intravenous form of application of the water-soluble cocaine hydrochloride is also possible, but is rarely practiced. Cocaine is also offered modified as "crack" (and therefore smokable). Crack (Figure 6d) is produced either by extraction in ether or by boiling cocaine hydrochloride in baking powder solution, with cracking noises (crack) forming the free and pyrolysis-resistant (smokable) base as residue. 29
Cocaine is (like other local anesthetics) a tertiary amine and, as a weak base, only soluble in water as an acid salt (hydrochloride). Mode of action: In addition to the local anesthetic effect, the (dose-dependent) inhibition of the active presynaptic reuptake of dopamine, noradrenaline and serotonin from the synaptic gap is the main focus. This ultimately results in a sustained and increased transmitter concentration in the synaptic gap with a correspondingly prolonged and intensified effect of these transmitters on the postsynaptic receptors. In addition to the pronounced psychostimulatory effect, this also explains the strong sympathomimetic effects of cocaine. In addition to these effects, various directly toxic effects of the substance are observed, which, however, can hardly be clinically differentiated from the effects of sympathomimetic activation: cardiotoxicity (increased electrical instability of the myocardium with a tendency to arrhythmias; sudden cardiac death from coronary spasms), cerebrovascular damage, mesenteric ischemia, acute pulmonary edema and central respiratory depressive effect. Cocaine is directly neurotoxic. The picture of toxic-paranoid psychosis after long-term or high-dose use of cocaine is explained by the profound interventions in the neurotransmitter system29 on the one hand and also the morphologically detectable neurotoxic effects in the CNS.9 The rapid development of tolerance is known with considerable psychological dependency development.
The absorption takes place quickly with smoking (possibly even faster than after intravenous injection), slower with nasal application. The substance is eliminated through hepatic metabolism or hydrolytic cleavage, partly unchanged renally (in the case of intravenous injection even to a very high degree). The metabolites are still detectable in the urine after days. The effective elimination half-life varies between 30 and 90 minutes depending on the type of application.
The psychogenic effect of cocaine takes place in two phases (Figure 7). After ingestion of 25 to 150 mg cocaine, the intoxication phase occurs quickly (euphoria, compulsion to speak, restlessness, subtle tremor, preconvulsive movements; tactile auditory, color-visual, olfactory and / or gustatory hallucinations, possibly sexually accentuated. With gradual decrease in the direct effect With cocaine, this state passes into an intense second phase (pronounced feelings of fear to paranoid delusions, depression, exhaustion, drowsiness). In this phase, the so-called hunger for substances arises, which leads to the almost compulsive reuse of the drug to compensate for these negative effects.29 the psychological changes of partly pronounced clinical symptoms: increase in blood pressure (approx. 20% above normal), bradycardia, subsequently arrhythmia and tachycardia and increase in respiratory rate. Psychotic reactions with paranoid hallucinations, headaches, hyperthermia, nausea and vomiting are known. At higher doses (over 2 mg / kg body mass) serious psychological damage occurs initially (toxic paranoid psychosis), which is characterized by disturbances in the perception of reality, paranoia, increased aggressiveness and even killing intentions. The transition to general toxic phenomena is then fluid and dose-dependent:
· Decreased reaction to external stimuli, hyperreflexia, athetotic movements, convulsions (tonic-clonic), status epilepticus, incontinence
Further increase in blood pressure and heart rate (risk of vascular ruptures, e.g. mass hemorrhage)
Heart or mesenteric infarction, aortic dissection
· Increasing arrhythmia, drop in blood pressure
→ central cyanosis
· Dyspnea with transition to Cheyne-Stoke breathing
→ progressive hypoxia
Failure of circulatory and respiratory regulatory functions (ventricular fibrillation, cardiac arrest)
· Cocaine shock
· Respiratory arrest and / or pulmonary edema with agonal gasping
Paralysis of vital brain centers with coma (fixed and dilated pupils)
The cocaine withdrawal syndrome results from the omission of the drug after long-term use due to a lack of transmitter dopamine in the CNS. The symptoms are characterized by an affective mood with depression, anxiety and irritability, exhaustion, occasionally insomnia or psychomotor agitation, undernourishment and malnutrition. The complications are depressive syndrome and suicidality. Cocaine psychosis is similar in nature to both delirium tremens and schizophrenia. Tactile hallucinations, clouding of consciousness, restlessness, delusional experiences and fear-filled optical-acoustic hallucinations occur independently of the consumption of cocaine (paranoid-hallucinatory psychosis). Because of its price, cocaine in its “classic form” is considered a drug of the “elite”: “Cocaine is more widespread than most people assume. All professional groups are affected, with the image professions such as actors, models, managers and stockbrokers developing a real subculture. The use of cocaine is considered good form in some circles, and it is almost exclusively sniffed. () This procedure requires some practice and utensils that are imposing according to the preciousness of the drug: Dosing spoons made of gold, rolled up banknotes as suction tubes, exclusive storage containers. Quinine, yohimbine.
3.2.2 Amphetamine and its derivatives (Figure 8)
These compounds are also dopamine releasing agents. Amphetamine and derivatives were first produced by Lazar Edeleanu at the University of Berlin in 1887. He called the substances "Phenylisopropylamine". It was a series of substances that are related to the plant ingredient "ephedrine", which was isolated by Nagayoshi Nagai two years earlier. For a long time there was no medical use for amphetamine until it became available as pharmaceutical amphetamine in many countries. Amphetamine, both D-amphetamine and L-amphetamine (or a racemic mixture of both isomers), is believed to have an effect on binding to the corresponding transport protein for monoamines and in this way the extracellular concentrations of dopamine, adrenaline and Serotonin will be increased. It is believed that D-amphetamine mainly affects the dopaminergic transmission system and L-amphetamine affects more the adrenergic systems. The stimulating effects are more related to the activity of the dopanic system, predominantly in the limbic system (“reward center”). Amphetamine binds to the transport protein for dopamine (DAT) and in this way inhibits the transport of dopamine back from the synaptic gap into the cell. Amphetamine also gets into the cell, which leads to a dopamine efflux from the cell (dopamine is transported from the cell into the synaptic cleft by the opposite transport via DAT) .31 The amphetamine derivatives with psychedelic active components (mescaline, DOM, MDA, MMDA , TMA, DMA etc.) are chemically very similar, but their effects are clearly different from those of amphetamine (and hallucinogens). They are therefore referred to as entactogens and are shown separately.
Amphetamine (alpha-methylphenetylamine; synonyms: Speed, Pep, Amph) was launched on the market in 1930 as a drug against runny nose (Benzedrin®). The stimulating properties showed up quickly and the further developed dextroamphetamine was produced as a stimulant for soldiers and pilots in World War II and used particularly by the American, Japanese and German armies.30 The medical indications for this group of substances are rather rare - structurally related compounds are used in some Diseases still used (e.g. methylphenidate = Ritalin®). The latter is and has occasionally been misused as an amphetamine derivative.
Metamphetamine can be produced illegally relatively easily and has been increasingly consumed in the rave subculture as "crank", "crystal", "speed" or "meth" since the 1980s. The smokable form: d-methamphetamine ("ice") is particularly popular. Due to its purity, this substance can produce effects similar to intravenous amphetamine when smoked.
Resorption from the gastrointestinal tract is rapid and extensive, with maximum blood levels after one to two hours. The mode of action is characterized by the centrally and peripherally dose-dependent dopaminergic and potent adrenergic properties; In very high doses, additional inhibition of the release of serotonin and inhibition of the re-uptake of biogenic amines in the synaptic gap ("speed syndrome") with depletion of the stores and reduced effectiveness. In the case of oral administration, the effects appear after approx. 30 minutes. The consumer feels empowered and powerful (freed from worries).Considerable physical (and mental) performance is possible for a few hours afterwards ("doping"). Methamphetamine has a more euphoric effect with a feeling of “sharpened” intellect and increased energy (similar to cocaine). After a few hours, the stimulating effect diminishes and a feeling of exhaustion and tiredness comes to the fore, but at this stage it is practically impossible to sleep. This increases the temptation to take amphetamines again or to force sleep by taking sedatives / hypnotics. Significant mood swings (irritability, aggressiveness) can occur.30 In general, there is an appetite-suppressing side effect that was previously also used therapeutically (use of amphetamine derivatives as appetite suppressants, e.g. Amphetaminil = Aponeuron®). Amphetamines are still used regularly outside of sport to improve performance! Paranoid amphetamine psychosis can occur with the use of large amounts or prolonged use. The patients feel persecuted and threatened, complain of visual-acoustic hallucinations and are referred to inpatient psychiatric treatment because of endangering themselves and others.
The elimination takes place predominantly hepatically (rate amphetamine> metamphetamine) and the metabolites are excreted renally. After a single application, about 90% of the active ingredient is excreted within three to five days. Correspondingly, it can be detected in the urine within this period without any problems.
Kath (Kathee), also called Qat, Quaat, Gat, Jaad, Chat, Chad, Chaad and Miraa, from the African Kath shrub (Catha edulis), is a luxury food from the Arab world.
When the leaves of the plant are chewed, they create a stimulating and euphoric effect. Catha edulis is an evergreen shrub or tree and grows up to 3 m tall with oval, 10 cm long leaves (Figure 8d, e). The flowers are small, white and have five petals. The fruit is an elongated triangular capsule with one to three seeds.
Khat contains more than 40 alkaloids, glycosides, tannins, amino acids, vitamins and minerals. It is believed that the two phenylalkylamines - cathinone and cathine - which are structurally related to amphetamines, are responsible for the psychoactive effects. The presence of amphetamines and caffeine in khat has been ruled out. A number of other substances such as cathidine, edulin and ephedrine have been identified, but these are not likely to play a role in the khat effects. The effective alkaloid (Figure 8c) is D-norpseudoephedrine (cathine). The effect consists in suppressing the feeling of hunger, increasing physical performance and reducing the need for sleep. Mild hallucinations (from the metabolite methcathionine) have also been reported. 10
3.2.3 Amphetamine derivatives with psychedelic active components - entactogens (Table 6)
The synthesis of 3,4-methylene-dioxy-N-methylamphetamine (MDMA) was registered for a patent in 1912 by the Merck company in Darmstadt. However, the effects in humans were not described until the 1970s. At that time it was used as an aid in psychotherapy ("heart-opening-anti-aggression"). The abuse as a recreational drug (ecstasy) at the techno parties to enable hours of dancing under the strongest sensory overload (sometimes with fatal consequences) began as early as the 1980s. The special mode of action (“sacred” attunement) of ecstasy and the numerous analogous substances led to the designation as entactogens (empathogens). The perception-distorting effects of hallucinogens and the stimulating effects of amphetamines are more or less in the background (substance-specific). There are a large number of tablets or capsules in illegal trade, although it is not always clear which active ingredient is packaged and how (Figure 9). An (incomplete) overview of the various substances in this group of active ingredients is provided in Table 7.
The already indicated changes in perception occur 40 to 60 minutes after oral administration. Egoism, hostility and irritation take a back seat. Thinking is more concerned with questions of relationships, questions of life and the aesthetics of perception. A deep trust in life is established without the formal thinking being significantly impaired. With a higher dose, sensory impressions are increasingly experienced aesthetically and with pleasure (similar to the effect of cocaine - "colors become more colorful"). With a further increase in the dose, however, formal thinking becomes slower and less critical (“state of unconditional love”).
The further effect is then described as stimulating, ecstatic and life-affirming ("rave party") or (in the case of introspective consumption) as calming and exhilarating.30,31 The duration of action is three to four hours. As a rule, the after-effects have subsided about six hours (after a single application), the impairment of fine motor skills and coordination is usually only regained on the following day.
Many users report balance and strength the day after the last intake, but others feel rather weak and energetic. In the case of frequent and prolonged abuse, reports have been made of a considerably depressed post-parental leave phase. Changes in the serotonergic system are probably responsible for this. Corresponding morphological findings are available. 9
Ecstasy and its related compounds are eliminated hepatically and most of the metabolites are excreted renally. Corresponding rapid tests for urine are available on the market. In some of these tests, the methylendixoy skeleton does not react, so that the results in the “amphetamine field” appear negative. If in doubt, a GC / MS analysis of the urine should be carried out. The metabolites are detectable three to four days after the last consumption.
3.3 Pure opioid agonists (Figure 10)
A basic distinction is made between the (naturally occurring) opiate morphine (from raw pium), the semi-synthetic heroin (semi-synthetic opioid) and the synthetically produced opioids (fentanyl and its derivatives). The mode of action can mainly be explained by binding to different classes of opiate receptors. First of all, a decrease in the sensitivity of the respiratory center to the CO2 tension or the H + ion concentration in the blood results in increasing paralysis of the respiratory center. This leads to hypoxemia with initial excitation of the vagus center (bradycardia), the oculomotor nucleus (miosis) and the trigger zone of the vomiting center. The elimination takes place differently, in principle relatively quickly and predominantly hepatically. The metabolites are excreted renally and enterally. Sometimes there is a high first-pass effect (heroin, morphine). The accumulation in renal insufficiency is known (e.g. convulsive pethidine metabolites).
The history of the consumption of narcotic or euphoric natural opiates dates back to around 3000 BC. BC to ancient Egypt and leads to the opium caves of China until modern times. Pharmacists and chemists became aware of the pain-relieving, calming, but sometimes also stimulating effects of natural opioids as early as the beginning / middle of the 19th century and tried to find a synthetic equivalent to the natural substance extract opium and to develop a remedy that could and could be produced quickly could also be marketed accordingly. In 1873 the English chemist Charles Wright developed a process for the synthesis of diacetylmorphine, a synthesis product from morphine and acetic anhydride. On June 26, 1896, the Aktiengesellschaft Farbenfabriken (today Bayer AG) took up the process and had it protected under the name "Heroin". A little later, on August 21, 1897, the chemist Felix Hoffmann employed at Bayer also succeeded in synthesizing diacetylmorphine using the same process. The Bayer Group then started production in 1898. Heroin (synonyms: poison, H, substance, tar, Hong Kong rocks) is produced semi-synthetically, the starting substance is morphine. Morphine is obtained as an extract from raw opium, the dried milky sap of the opium poppy (Papaver somniferum). To produce heroin, morphine is acetylated on the two hydroxyl groups using acetic anhydride. Monoacetylated morphine can be produced as a by-product (e.g. 6-MAM). Pure heroin, both as a base and as a hydrochloride, is a colorless crystalline solid.
The bioavailability depends on the type of application. The absorption takes place rapidly (less morphine) gastrointestinally and parenterally (e.g. from tissue). The opium alkaloids are exhaled through the lungs practically unchanged during smoking. The intravenous application of heroin has lost popularity; it is smokable (often in combination with crack). Heroin is much more lipophilic than morphine and therefore reaches the CNS quickly, which leads to a rapid surge to the site of action; therefore, an intravenous injection of heroin triggers an initial “kick” (also called a flash). With all forms of consumption other than intravenous injection, this effect is at least greatly weakened, if at all, due to the slower influx according to the current state of science. The reasons for this are the slower absorption, the premature hydrolysis and the first-pass effect. However, this does not apply to smoking the pyrolysis-resistant substance.
Until recently it was assumed that heroin itself only works as a prodrug: According to this consideration, it does not bind itself to the opiate receptors, rather it is the active metabolites that are responsible for its effects. However, recent studies have come to the conclusion that under certain conditions heroin can dock itself to opiate receptors.
It is worth mentioning the high intrinsic activity of 6-MAM at the µ-receptor, it is higher than that of morphine and therefore a decisive factor for the strong expression of the "kick" after intravenous heroin injection.
The doses consumed by a heroin addict often exceed 10 to 30 times the original therapeutic dose of the active ingredient. If one takes into account the average purity of illegally traded heroin, which in Europe - with the exception of the Netherlands - is usually between 5 and 15% for end customers, rarely more than 20%, an average long-term intravenous heroin user gets by with a quantity which corresponds to 100–200 mg of the pure substance. The case law in the Federal Republic of Germany based the determination of the not insignificant amount of heroin within the meaning of § 29a Narcotics Act on the fact that a dose of 50 mg is lethal for a non-drug addict, although this figure is most likely not the truth and some studies are far assume higher human LD50. This number seems to apply more to mixed use, which is very common and is not recognized in many hospital toxicity reports after fatal overdoses, especially if the substances cannot be detected with a standard drug screening or if it is the much more widespread mixed use, namely those with ethanol , acts.
The stronger effect of heroin in contrast to morphine is explained by the fact that heroin (and the primary metabolic product monoacetylmorphine) crosses the blood-brain barrier more easily than morphine due to its higher fat solubility. The effects of heroin last six hours to often more than 24 hours in non-tolerant users, with after-effects sometimes lasting several days after the first consumption. On the other hand, the effects of heroin on an addict, if he consumes an average high dose, do not last longer than six to eight hours, after which the withdrawal symptoms slowly set in again. Opioids such as the heroin substitute methadone have a half-life of up to 24 hours. The dose tolerance of opioids increases rapidly with daily consumption, which is why many addicts constantly increase the dose within the scope of the availability of the substance, since with daily consumption the amount that led to the desired effect on the previous day to 1.5 to Must be increased 2 times to achieve a comparable effect. However, since most addicts quickly exhausted their financial possibilities, most of them are mostly on the hunt for money in order to achieve a reasonably constant dosage ("steady state") and to prevent withdrawal symptoms. Heroin can be detected as 6-MAM in the blood for a few hours, metabolic residues in the urine for one to four days and in the hair for several months.
Similar to morphine, heroin has a euphoric and analgesic effect. Normal sleep is more likely to be disturbed by its application. Depending on the form of application, it has a half-life of four to six hours and is not organotoxic. Further (dose-dependent) effects in the opioid-naïve organism are the emetic and respiratory depressive effects. The side effect of constipation is not subject to any tolerance formation - the active ingredient was used as a remedy for diarrhea around the turn of the century. In the case of intoxication, respiratory depression is mainly dangerous, which can be fatal, especially if other sedating psychotropic substances such as alcohol, benzodiazepines or barbiturates are added in the sense of polytoxicomania.
In the 1960s, the substance class of fentanyls (anilinopiperidines) was introduced as analgesics in Europe and gained great importance in clinical anesthesia. Starting with Meperidine (ethyl-, 1-methyl-4-phenyl-4-piperidinecarboxylate, Pethidin®), newer and more effective structural analogues were discovered in the 1970s and 1980s and traded on the black market as heroin substitutes. The synthesis did not require any illegal starting products, the production was carried out from nicotinic or isonicotinic acid or piperidine derivatives. Today there are fentanyl derivatives (Table 8) that are several thousand times more effective than morphine. 3-methyl-fentanyl is about 3000 times more effective than morphine, other substances from the group of fentanyl derivatives have an even stronger effect. The extreme potency is explained by a particularly high affinity for the corresponding receptors. As a result, it is hardly possible (for the inexperienced) to dose the active ingredient exactly, which very easily leads to fatal overdoses. The intoxication is often perceived as a sleep-like state, as many sensations are simply switched off by the strong effects of the drug. On the other hand, it is reported that the high is extremely "overwhelming" (repeated ejaculations, uncontrolled bowel movements with indescribable euphoria). It is sold on the black market as a heroin substitute or as alleged heroin or used as an additive for low-quality heroin. The detection of fentanyl derivatives in the blood is only possible for a short time and is technically very demanding in the urine. Rapid tests do not exist.
3.4.1 Anticholinergic psychedelic substances (Solanaceae alkaloids)
The first mind-altering substances came from nature. The actual meaning of the word “drug” takes on a meaning of its own with psychedelic substances from nature. The term "drug" comes from the Middle High German "dröge", d. H. dried. This actually meant dried medicinal plants. In recent years there has been an increasing interest in native plants with a psychoactive effect. This is likely to include This is because ecstasy is widespread in the techno scene and consumers are very interested in hallucinogens, trance and ecstasy experiences. Plants from the nightshade family (Solanaceae) have been used for intoxication for thousands of years
With thorn apple (Datura stramonium and others), deadly nightshade (Atropa belladonna L.), henbane (Hyoscyamus niger and others), angel's trumpet (Brugmansia suaveolens and others) or mandrake (Mandragora officinarum), the number of psychotropic nightshade plants is by no means exhausted. On the contrary, so far psychoactive species have been detected in a total of 34 genera of the Solanaceae family, some of which are suspected of having a mind-altering activity. The individual plants not only contain the tropane alkaloids, which are typical of the nightshade, atropine (D- and L-hyoscyamine; Figure 11a) and scopolamine (L-hyoscine; Figure 11b), but also other compounds such as coumarins, pyrrolidine and other alkaloids, withanolides , Diterpenes, triterpenes and many more. Mandrake (Figure 11c) is the common name for species of the genus Mandragora from the nightshade family (Solanaceae). Their roots are sometimes forked at the end, reminiscent of the shape of a human body with two legs. The deadly nightshade, native to Europe and Asia (Figure 11d), is a perennial herb that branches at a height of about 1 m and can reach a height of up to 1.5 m. The hairy, elliptical leaves can be up to 20 cm long in the first year, but then shrink again. The color of the bell-shaped flowers varies from blue-violet to a dull red. After blooming, the berries ripen, which first turn green and then shiny black. The fruits are tasty and not bitter, which can be confused with cherries (by children). The black henbane (Hyoscyamus niger; Figure 11e), sometimes referred to as the smelly aftershade, belongs to the nightshade family that originate in Eurasia.The black henbane grows as an annual or biennial and is an herbaceous plant up to 75 cm high with hairy, 8 to 20 cm long leaves. The eye-catching terminal flowers are 2.5 cm in diameter and are greenish-yellow with red veins. Black henbane blooms from June to September. The seed pod contains many black, tiny, pitted seeds. Brugmansia is also a genus of the nightshade family and comprises six flowering species that are native to the subtropical areas of South America along the Andes from Colombia to northern Chile and southeastern Brazil. They are known as angel's trumpets (Figure 11 f) and g) and share this name with the closely related thorn apple family (Datura). The genus Brugmansia has pendent rather than upright flowers like Datura and is perennial and woody, while Datura has herbaceous, usually annual or only short-lived perennials (Figure 11h).
The leaves and / or flowers are used orally as a tea infusion. Angel's trumpet flowers can also be placed in milk. Dried leaves and flowers are smoked. The plants are available in every well-stocked flower shop, the seeds are easy to get by mail order. After ingestion, rapid and complete absorption takes place. Elimination takes place mainly hepatically with a longer half-life (12 to 38 hours!). The pharmacological effect is based on the competitive displacement of acetylcholine as a central and peripheral transmitter (mainly parasympatholytic effects, especially recognizable on the eye, cardiovascular system and glandular secretions). After a single dose of two to four leaves or one or two flowers (oral) or 0.3 g of the seeds (approx. 50–100 pieces), the onset of action can be expected after about 60 minutes. Depending on the dose, the duration of action is three hours to two days!
These herbal drugs are highly psychoactive. Ingestion of Datura induces symptoms such as spectral illusions, delirium, dilated pupils, thirst, dry oral mucous membranes, and uncontrolled muscle movements (Bernhard-Smith 1996). The pharmacological effect is caused by tropane alkaloids in the plant, the most active of which is scopolamine (also hyoscine). Depending on the subspecies and part of the plant, hyoscyamine (atropine), norhyoscyamine, tropine or other ingredients can also occur. The parasympatholytic effect manifests itself in hyperthermia, hypertension, tachycardia, bronchodilation, delirium, hallucinations (acoustic, visual or haptic), blurred vision, drowsiness, dizziness, slowed reactions, restlessness and persistent memory disorders that can lead to amnesia. It is reported that when the substance is taken, time seems to pass more slowly and sensory perception is disturbed.10 Clinically, this state corresponds to the central anticholinergic syndrome known from anesthesia. The psychological effect is characterized by feverish dream-like visions and illusions that quickly turn into hallucinations; scenic and often frightening hallucinatory experiences (violent and physically strong acting behaviors with considerable danger to oneself and others). The detection of tropane alkaloids and their metabolites has practically only forensic significance and is technically complex.
3.4.2 Serotonergic Psychedelic Substances
Lysergic acid diethylamide (LSD) is a synthetic product of the not so hallucinogenic, but far more toxic lysergic acid (naturally occurring ergot alkaloid), belongs to the hallucinogens and is usually a white, crystalline substance (structural formula - Figure 12a). For dosage, LSD is dissolved in water and then dripped onto small pieces of blotting paper (cardboard) or felt pads printed with colorful symbols, but also impregnated in gelatine corners (micros) (Figure 12b). LSD is one of the most powerful hallucinogens known. Even in very small doses, it produces long-lasting pseudo-hallucinogenic effects. The chemist Albert Hofmann produced lysergic acid diethylamide for the first time on November 16, 1938 as part of his research on ergot. On April 16, 1943, Hofmann decided to test the possible effects of LSD; he suspected that he had missed something in the first few attempts. During his work with LSD, Hofmann noticed a hallucinogenic effect in himself that he could not explain at first. He suspected that LSD had been absorbed into his body through unclean work through the skin. He repeated this experience on April 19, 1943 by taking 250 micrograms of LSD. Compared to the effectiveness of the ergot alkaloids known at the time, this corresponded to the smallest amount at which one could still have expected an effect. It turned out, however, that this amount already corresponded to ten times the normally effective dose (from approx. 20 µg) of lysergic acid diethylamide. LSD was made available under the trade name Delysid® by the pharmaceutical manufacturer Sandoz for psychiatric treatment and for research purposes. It wasn't until the 1980s that LSD regained popularity as a party drug in the techno scene. After illegal consumption had declined at the beginning of the last decade according to estimates by the drug commissioner of the federal government, there has been a slight increase in first-time users since 2008 (drug and addiction report of the federal government 2009). Something similar is reported from the USA (http://www.drugabuse.gov/infofacts/hallucinogens.html). LSD is very highly concentrated and for this reason it is dissolved in liquid and then dripped onto small blotting paper or felt pads. Each plate contains around 20 to 100 µg of LSD. LSD works after half an hour to an hour, very long (six to twelve hours) and is difficult to control (half-life approx. Three hours)!
The psychoactive one of the four possible stereoisomers acts as a partial agonist with great affinity at the 5-HT2A receptor, to which all classic hallucinogens bind. In contrast to mescaline and psilocin, LSD also acts directly on the D2 receptor. LSD has a massive impact on our feelings (see Figure 12 c). The sense of time is slowed down and the boundaries between oneself and others are described as relaxed or dissolved. Self-esteem is extremely high. Balance disorders and gait disorders are present after about half an hour to an hour. Usually, while intoxicated, the user is aware that the hallucinations are triggered by the drug. Perhaps just because of a little something, sudden feelings of fear and panic can break out. Sometimes it is then impossible to tell the difference between reality and intoxication. The consumers then report of distorted, frightening images during the intoxication, a massive and frightening intervention in the perception of time, short-term and abrupt changes in the emotional state and physical discomfort.30 The effects are strictly dose-dependent: psychological effect - up to about 100 µg euphoria, visual pseudo-hallucinations, Distortions of faces and objects; up to approx. 200 µg abolition of the space-time feeling, relaxed associative thinking (mystical, religious); from approx. 200–300 mg hallucinations (fantastic scenes, landscapes or film-like experiences) sometimes experienced as wonderful, sometimes as frightening, synesthesia, alternation between euphoria and dysphoria; over 300 µg ego-dissolving and “cosmic” perceived hallucinations, persecution and impairment delusions, megalomania). Accidents due to incorrect reactions to hallucinations and hallucinations that are not recognized as such are possible. In extreme cases it can lead to self-destructive acts, e.g. B. because you think you can fly. After the effects have subsided, after-effects such as nausea, tiredness and flashbacks are still noticeable for a few days. Even with a single use, the consumer's performance can be disturbed in the long term.35 A turning away from the real world can also be observed, which can lead to severe psychosis. With repeated use within a few days, tolerance to the substance quickly develops. Physical dependence is not known. Psychological dependence is rare and manifests itself in internal and external motor restlessness, and sometimes anxiety. LSD can be detected in the urine about one to four days after ingestion.
Dimethyltryptamine (DMT) is a hallucinogenic tryptamine alkaloid that can be found in a number of plants, both in the skin secretions of the cane toad and in traces in humans and mammals. Smoked or injected in high doses, it is one of the most powerful hallucinogens known. An effect with oral intake is only achieved with simultaneous or previous intake of monoaminooxidase inhibitors (MAO-inhibiting beta-carbolines occurring in various plants; alternative synthetic MAO-inhibitors from the pharmacy = "Pharmahuasca"), because DMT very quickly (First -Pass effect) is broken down by the body's own monoamine oxidase.10 DMT acts as an agonist on the 5-HT2A receptor and also interacts with the 5-HT2C receptor. In contrast to structurally related hallucinogens LSD, psilocin and mescaline, DMT does not develop tolerance, the reason for this is unclear. However, this would be a further indication that it plays an important role as an endogenous neurotransmitter and for this reason does not lead to the development of tolerance.39 DMT is the main active ingredient of ayahuasca, a cultic drink used by South American Indians. The types of application: smoking, intramuscular, oral (Business Man‘s LSD) in the form of powder, crystals and parts of plants. The effect is similar to LSD, mostly associated with nausea, vomiting and reduced activity up to falling asleep.
Psilocin is an indole alkaloid and is one of the tryptamines.30,40 It is the hydrolysis product of psilocybin and as such is actually the psychoactive form. But it also occurs as an alkaloid itself. The free base decomposes spontaneously in air. The effects of consuming it are similar to an LSD high, but are usually shorter. Psilocin is a partial agonist on the 5-HT2A receptor and is therefore one of the classic hallucinogens. Its binding profile (as far as is known) is less complex than that of LSD. The binding of psilocin to the 5-HT2C receptor is probably responsible for side effects (e.g. on blood sugar levels). The two compounds are contained as active ingredients in so-called "magic mushrooms". Psilocybin-containing mushrooms are found worldwide, most of them are in the genus of the bald heads (psilocybe). A total of over 180 species are known. The pointed bald head (Psilocybe semilanceata), which is often found on fertilized pastures, is particularly widespread in Central Europe. Cuban bald heads (Figure 13d) are often offered for sale (legal or illegal). In late summer and autumn, the pointed conical bald head (Figure 13c) often grows on naturally fertilized pastures in Germany and neighboring countries. However, the Blauende Kahlkopf (Figure 13e) has spread strongly over the last 15 years on remains of wood and can be found locally in large numbers, e.g. B. in Central Germany. Their strong blue discoloration with pressure and with age is very characteristic of the fungus and is otherwise only found in the Röhrlingen in Europe, which are not psychoactive.
The effect of the mushrooms is similar to that of LSD, but is of shorter duration. In general, a change in perception and consciousness can be observed. As with many psychedelic drugs, the effects are very individual and can produce a wide variety of effects in different users. Set and setting as well as dose are of decisive importance. The effect occurs about 10–120 minutes after ingestion, peaks after one and a half to three hours and lasts about three to eight hours. In rare cases, the effect can last longer, but the change in the perception of time can make it appear longer. Depending on the dose, in addition to increased perception, more or less pronounced changes in the senses of sight, hearing and touch take place. You experience an increased perception of colors and contrasts, increased visual acuity, lights are perceived as extraordinary. Surfaces appear to be rippling, shimmering, or breathing. Complex "closed eye visuals" and "open eye visuals" of objects or images take place. Objects warp, transform, or change color. A feeling of merging with the environment can arise. Noises are heard more clearly, music can gain rhythm and depth. Synesthesia, seeing tones, tasting colors, etc. is reported in some cases. Consumption of these mushrooms (mostly in dried form, because of the somewhat unpleasant taste in cocoa) is currently experiencing a renewed wave of popularity. The reason for this seems to be the “gentler” effect compared to LSD. Even after the intoxication has subsided, reduced ability to concentrate, delayed readiness to react and reduced concentration as well as increased distractibility persist for many hours. Psilocybin is mainly metabolized in the hepatic to indole acetic acid derivatives and then excreted renally.30 Detection in the urine is possible for one to three days after the last consumption.
Bufotenin (from Bufo toad) is a hallucinogenic tryptamine alkaloid. Bufotenin is an isomer of psilocin. The effect is therefore very similar to psilocin. Optical hallucinations such as flashes of light occur together with dizziness, high blood pressure, and states of confusion. Nausea and tachycardia are also possible. The hallucinogenic effects have long been considered controversial. The first indications were found in the 1950s. Tests on humans in the following decades did not produce a uniform picture. Since the drug was also administered to mentally ill and imprisoned persons against their will, the setting in these cases is likely to have been rather unfavorable. On the other hand, there are numerous reports of a cultic use. Bufotenin is found naturally in various plants (and is one of the few psychoactive drugs that is also extracted from animals). In addition, the substance was found in small quantities in human urine and appears to be a normal breakdown product of human metabolism. Bufotenin is found in the skin secretion of various toads. The cane toad (Bufo marinus) is best known. From Australia in the 1990s there were frequent reports of the newly emerged custom of toad licking. The poisonous secretion is excreted by massaging the toad and then licked up.41 Oral consumption of the secretion is not without risk, as besides bufotenin it contains, among other things, cardiac toxins such as bufotoxin. Their effect is similar to that of digitalis glycosides. To avoid the poisonous effect, the toad secretion is smoked. While the poisonous components of the secretion are supposedly destroyed in the process, the chemically very stable bufotenin is supposed to be preserved.10 In the skin secretion of the Colorado River toad (Bufo alvarius) there is predominantly 5-methoxy-N, N-dimethyl-tryptamine (5- Meo-DMT), a natural neurotransmitter in the human nervous system. If it is smoked, the effect occurs in a flash, is extremely extreme and only lasts ten minutes. 5-MeO-DMT is structurally very similar to bufotenin.10 It is also found in many different plant species and, like DMT, has been used as an entheogen by South American shamans for thousands of years. 5-MeO-DMT was first synthesized in 1936. In 1959, it was isolated as one of the psychoactive ingredients in the seeds of Anadenanthera peregrina found in yopo snuff. It is found in many organisms that contain bufotein (5-hydrox-DMT) and is the O-methyl analog of this substance. Proof of consumption is likely to be difficult because the half-life is extremely short.
Part 1 of this article is in ErgoMed / Prakt. Arb.med. 5/2011 published. Part III (including bibliography) will appear in the next issue.February 15, 2012
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