Gamma hydroxybutyric acid. Butyratomania: the effect of butyrate on the body, the consequences of use and the treatment of addiction. How GHB manifests its narcotic effect in humans
Butyrate sodium- once a purely medicinal product with a strange fate. Initially, it was obtained for medical purposes and was used in anesthesiology for breath-sustaining anesthesia. In recent years, it has become widespread among young people in large cities as a powerful synthetic drug. Butyrate is the slang word for sodium oxybutyrate. The formation of dependence occurs extremely quickly and, unfortunately, for a long time, close people do not see the problem. About 3-4 years ago there was an opportunity to legally buy sodium hydroxybutyrate in the network of pharmacies in Russian cities. At the moment, the sale of this drug is discontinued.
History of the manufacture of sodium oxybutyrate
For the first time gamma-hydroxybutyric acid (GHB) was obtained in 1874. Initially, the substance was not of any interest to scientists; the French physician Labori played an important role in the study of biology and the distribution of the substance. The drug was introduced into clinical practice in 1960 almost fifty years ago, an interesting fact is that its formula was originally calculated on paper, and the synthesis was made after that. In just one year, Laborie received the results of almost 8 thousand cases of clinical use of the substance. It was found that it has some effects that are not typical for this class of substances. Subsequently, the effect of GHB on the human body was carried out by many foreign and domestic researchers. Many articles are devoted to the possibilities of using sodium hydroxybutyrate in psychiatry and in the treatment of alcoholism. GHB has long been referred to as sleeping pills, and then to nootropic drugs that improve brain activity. Until 1989, all articles about butyrate were positive, noting the good physiological effects of the drug and the absence of long-term negative effects. At the same time, the anabolic effect of this substance was also discovered - when using these drugs by bodybuilders and athletes, muscle mass quickly increased. Also, the tool was widely used as a dietary supplement, it was used uncontrollably and without prescriptions. But soon the over-the-counter sale of the drug was banned, and medical data were accumulated on the complications and poisoning associated with the use of butyrate. This was considered by scientists as a possible threat to public health and there were strict restrictions on circulation. Despite the illegality, oxybutyrate is actively consumed by young people, its synthesis takes place underground and is distributed on the “black market”.
The use of sodium hydroxybutyrate in medicine
In medical practice, the drug is used in neurology for the treatment of sleep disorders due to narcolepsy, and in psychiatry - in patients suffering from neuroses. In therapeutic doses, the substance shows an increase in the body's resistance to oxygen deficiency. It is also used in medical practice as a mildly acting sleeping pill. Research is underway to treat Parkinson's disease, schizophrenia, and chronic fatigue syndrome. In some European countries, oxybutyrate is used to get rid of alcohol addiction. Animal experiments and clinical studies have shown that the drug softens the manifestations of a hangover syndrome and causes an improvement in well-being. In ophthalmology, the drug has proven itself to improve vision in patients with glaucoma. In some countries, there are practices using sodium hydroxybutyrate as a non-narcotic agent for shallow anesthesia during simple operations, and even for basic anesthesia for anesthesia in obstetrics, as well as in pediatric surgery, for the elderly. In this way, application oxybutyrate sodium perspective in medicine.
Drug butyrate: effects, action
Action butyrate enhances the effects of other drugs and painkillers, while the substance itself does not have a calming or psychostimulating effect. Effects begin to appear 15-20 minutes after ingestion, and last an average of an hour or two hours, in some cases longer. In a small dose, butyrate causes relaxation, uplifting, a feeling of euphoria, and a desire to communicate a lot. The condition resembles alcohol intoxication with no hangover effect. Therefore, often many do not want to stop at the first dose and continue to take butyrate, as a result, addiction to the substance appears. With an average dose, relaxation of the whole body and inconsistency of speech occur, you want to dance. Sometimes nausea is possible. Increasing the dose leads to deep sleep for several hours. The concentration of the drug in the liver after a couple of uses reaches a critical value, the body is not able to cope with a large amount of toxins and the inhibition reaction begins. Constant drowsiness, inability to sleep, apathy and indifference to others - all this is a negative reaction of inhibition. In the youth environment, a stereotype is imposed, as if butyrate helps to feel directly and freely, overcome communication complexes, and improves mood. To some extent, this is true, sodium oxybutyrate removes barriers, but the barriers of decency, a person simply loses control, begins to behave thoughtlessly and stupidly. With the constant use of the drug, personal degradation quickly develops. A person becomes aggressive and commits inadequate actions, which he would not have dared to do in a normal state. For example, stories of walking or jogging in the nude are not uncommon. Memory lapses are possible. Nine times out of ten, the use of butyrate along with alcohol produces unexpected results instead of a positive effect. At the same time, it is easy not to calculate the required dose, if for the first time a person did not receive the expected effect in the form of euphoria due to a weak solution, perhaps the next time he will receive a real concentration, which may well lead to a painful death.
The sad consequences of taking sodium butyrate
There is not a single drug or potent substance that would have such an effect on the mental state and make a person more and more crazy, strong, and, unfortunately, often, irreversible changes occur in his brain. The whole organism as a whole also suffers: the liver, lungs, reproductive system. Therefore, the desire to present butyrate as a safe option for entertainment on the Internet or in a company is, at its core, a deception or an attempt to mislead. Sodium butyrate gives disastrous results. DVRs constantly record road accidents in which many people are under butyrate died, they just suddenly fell asleep at the wheel and crashed to death. Even without taking the statistics of accidents, due to the sudden loss of control over their bodies when using butyrate in excess doses, many were injured as a result of falling from stairs or windows, while working with various complex technical devices. Many, considering such a drug harmless, exceeded the permissible dose and fell into a medical coma, very young people stopped breathing and heart. The teenager fell into a deep sleep and died, choking on vomit. In the United States alone, over 60 deaths have been officially recorded in recent years. Sodium hydroxybutyrate is a dangerous drug that is both psychologically and physically addictive, shortening life and contributing to early death. The consequences of taking the drug are terrifying and develop very quickly. The drug is produced in an artisanal way, often using extremely toxic substances in the synthesis, while suppliers advertise it as a "purified" and "chemically modified" product, i.e. disseminate deliberately false information about legal and new types of butyrate. The harm done to the body, especially to the fragile psyche of a teenager, is catastrophic, and the consequences are unpredictable. There are extremely rare cases when a teenager, having taken the first dose, would be limited only to her. Sodium hydroxybutyrate and drugs similar in chemical composition do not contribute to the development of severe physical addiction, however, their regular use forms a persistent psychological dependence. The withdrawal syndrome manifests itself very clearly in the form of severe dizziness, anxiety, insomnia and chest pains that do not go away. Below is a good example - a video of human behavior under butyrate.
Systematic (IUPAC) name: 4-hydroxybutanoic acid
Legal Status: Prohibited Substance (S9) (AC) Schedule III (CA) Class C (UK), Class B (New Zealand), Schedule I and III (US)
Usage: usually oral; intravenous
Bioavailability: 25% (oral)
Metabolism: 95%, mainly in the liver, but also in the blood and tissues
Half-life: 30-60 minutes
Excretion: 5%, kidneys
Synonyms: γ-hydroxybutyric acid; γ-hydroxybutyrate
Formula: C4H8O3
Mol. mass: 104.10 g/mol (GHB)
126.09 g/mol (sodium salt)
142.19 g/mol (potassium salt)
γ-hydroxybutyric acid (GHB), also known as 4-hydroxybutanoic acid, is a natural substance found in the human central nervous system, as well as in wine, beef, small citrus fruits, and in small amounts in the bodies of almost all animals. In many countries of the world, GHB is classified as a prohibited drug. Currently, the circulation and use of the drug is regulated in Australia and New Zealand, Canada, most European countries and the United States. GHB in the form of sodium salt, known as sodium oxybate or under the trade name , is used to treat and treat excessive daytime sleepiness in patients with. GHB is used medicinally as a general anesthetic, to treat conditions such as insomnia, depression, narcolepsy and alcoholism, and to improve athletic performance. It is also used as an intoxicant and a so-called "rape drug". GHB is naturally produced in the cells of the human body and is structurally related to the ketone body beta-hydroxybutyrate. As a dietary supplement or drug, GHB is usually used in the form of a salt such as sodium gamma-hydroxybutyrate (Na. GHB, sodium oxybate or Xyrem) or potassium gamma-hydroxybutyrate (K. GHB, potassium oxybate). GHB is also synthesized during fermentation and is found in small amounts in some beers and wines. Succinate semialdehyde dehydrogenase deficiency is a disease that contributes to the accumulation of GHB in the blood.
Usage
Medical use
GHB is used in medicine only for the treatment of narcolepsy, and less often for alcoholism. GHB is the active ingredient in the prescription drug sodium oxybate (Xyrem). Sodium oxybate is approved by the US FDA for the treatment of cataplexy associated with narcolepsy and excessive daytime sleepiness associated with narcolepsy. GHB increases the duration of non-REM sleep.
recreational use
GHB is a central nervous system depressant and is used as an intoxicant, but at lower doses it produces a stimulant effect due to its effect on the GHB receptor. The substance has many unofficial names, including "G", "Liquid X", "Liquid E", "Juice", "Mills", "Liquid G" and "Fantasy". Its effects are described as comparable to alcohol and ecstasy and include euphoria, disinhibition, hypersensitivity, and empathic states, among others. At higher doses, GHB can cause nausea, dizziness, drowsiness, agitation, visual disturbances, respiratory depression, amnesia, unconsciousness, and death. The action of GHB can last from 1.5 to 3 hours, or longer (when taking large doses). GHB is not recommended to be combined with alcohol because the side effects of these depressants (vomiting combined with drowsiness) can potentially be deadly. For recreational purposes, doses in the range between 500 mg and 3000 mg are most commonly used. When used as a recreational agent, GHB can be used as a sodium or potassium salt (white crystalline powder), or as a GHB salt dissolved in water to form a clear solution. GHB sodium salt has a salty taste. Other salts such as GHB calcium and GHB magnesium are also used, however the sodium salt is by far the most common form of the substance. Some chemicals are synthesized into GHB in the stomach and blood. Examples of such prodrugs are gamma-butyrolactone () and 1,4-butanediol (1,4-B). An additional risk of toxicity may be associated with the use of these precursors. 1,4-B and are usually clear liquids, although they may be mixed with other, more harmful industrial solvents such as paint or varnish removers. GHB can be easily made with very little understanding of chemistry, since all of its synthesis is as little as mixing two precursors, and an alkali metal hydroxide such as sodium hydroxide. Due to the ease of manufacture and the availability of precursors, GHB is often produced not in illegal laboratories, but in the private homes of manufacturers. Available by prescription in some countries (most of Europe) for the treatment of rare and severe forms of sleep disorders such as narcolepsy, GHB has been a banned substance in the US since the 1990s. However, on July 17, 2002, GHB was approved as a treatment for cataplexy, often associated with narcolepsy. GHB is a "colorless and odorless" substance.
Use in clubs and raves
GHB is often used in clubs, raves and parties; in small doses, GHB can act as a stimulant and aphrodisiac. GHB is sometimes referred to as liquid ecstasy because it can induce euphoria and promote sociability. However, GHB differs from (ecstasy) in its chemical and pharmacological modes of action.
Sports and athletics
Some athletes also use GHB, due to the fact that the substance increases levels naturally. One study showed that GHB doubled secretions in healthy young men. This action of GHB is mediated by muscarinic acetylcholine receptors and can be reversed by prior administration of pirenzepine, which blocks muscarinic acetylcholine receptors.
GHB and incidents of violence
IN THE USA
Along with alcohol and potent benzodiazepines such as flunitrazepam (Rohypnol), GHB is a so-called "rape drug". The sodium form of GHB tastes extremely salty, but because it is colorless and odorless, it is very easy to mix it into a drink to mask its taste. GHB can also be obtained in the form of various salts, some of which may not have a pronounced taste, for example, in the form of a sodium salt, or in an unstable free acid form. GHB is also often used in cases of sexual abuse related to intoxication. In such cases, the victim is usually vulnerable as a result of intoxication with sedatives such as alcohol. T1 is found in the victim's hair, so hair testing can be used to confirm rape. For detection of GHB in urine, the sample must be taken within 8-12 hours of ingestion of GHB. The content of GHB in the hair can be detected within a month after taking GHB. Other drugs, such as muscle relaxants (eg Carisoprodol), are sometimes used in combination with GHB. Thus, a hair sample can be tested for several drugs. Several high-profile rapes have been linked to GHB use. These cases received wide publicity in the United States. In early 1999, 15-year-old Samantha Reid of Rockwood, Michigan, died as a result of GHB poisoning. Reed's death prompted the creation of a 2000 statute that placed GHB on Schedule 1 of a controlled substance.
In other countries
A 2006 study suggested that there was "no evidence of widespread use of rape substances" in the UK, and that less than 2% of cases were associated with GHB and 17% were associated with cocaine.
Side effects
Combination with alcohol
GHB inhibits the rate of alcohol elimination in the human body. This may explain the respiratory arrest effect observed after ingestion of GHB and alcohol. A review of the details of 194 deaths associated with GHB over ten years showed that the majority of these cases were associated with respiratory arrest caused by drug interaction with alcohol.
Registered deaths
One report suggests that an overdose of sodium oxybate can be fatal. This conclusion was made on the basis of the deaths of three patients who were prescribed the drug. However, in two of the three cases, post-mortem GHB concentrations were 141 and 110 mg/L, and are within the expected range of GHB concentrations after death. The third case involved a patient who had tried to poison himself by drug overdose in the past. One publication examined 226 deaths associated with the use of GHB. Of the 226 cases, 213 were associated with death due to cardiac and respiratory arrest. In 71 cases (34%), the victims did not take additional intoxicants. Post-mortem blood concentrations of GHB were 18-4400 mg/l (median = 347). GHB is produced in very small amounts in the body, and blood levels can increase to 30-50 mg/L after death. Levels above this range are associated with deaths. The UK Parliamentary Committee notes that the use of GHB is less dangerous than the use of tobacco and alcohol in terms of such indicators as harm to society, physical harm and drug addiction.
Overdose treatment
An overdose of GHB is difficult to treat due to the many effects the substance can have on the body. At doses above 3500 mg, GHB can cause rapid loss of consciousness, with a single dose over 7000 mg often causing life-threatening respiratory depression. Higher doses cause bradycardia and cardiac arrest. Other side effects include seizures (especially when combined with stimulants) and nausea/vomiting (especially when combined with alcohol). The most dangerous result of an overdose of GHB (with or without other substances) is respiratory arrest. Other relatively common causes of death associated with GHB use are vomiting, positional asphyxia, and insensitivity to injury while intoxicated (which can lead, for example, to traffic accidents while driving under the influence of GHB). The risk of aspiration pneumonia and positional asphyxia can be reduced by placing the patient in a supine position, face down. Vomiting in victims of poisoning most often occurs when they are unconscious and when they wake up. It is important to keep the patient/friend awake and mobile, and not to allow victims to be left alone, as the risk of death due to vomiting is very high. The good mood of the patient does not mean the absence of risk. An overdose of GHB is a medical emergency and immediate admission to the emergency room. Convulsions while taking GHB can be controlled with or with lorazepam. Although these drugs are also CNS depressants, they are GABA agonists, while GHB is primarily a GABA agonist. Due to the faster and more complete absorption of (gamma-butyrolactone) relative to GHB, its dose-response curve is steeper and overdose is generally more dangerous and problematic than that associated with GHB or 1,4-B. An overdose of GHB / requires urgent medical attention. A newer synthetic drug, SCH-50911, which acts as a selective GABA antagonist, rapidly reverses GHB overdose in mice. However, this treatment has not yet been tested in humans, and it is unlikely that it will be tested for this purpose in humans due to the illegal nature of GHB clinical trials.
Usage detection
GHB can be quantitatively measured in blood or plasma to confirm the diagnosis of poisoning in hospitalized patients, to testify to impaired driving while intoxicated, or to assist in a forensic examination in the event of death. GHB concentrations in blood or plasma tend to be in the range of 50-250 mg/l in people treated therapeutically (under general anesthesia), 30-100 mg/l in people arrested for drunk driving, 50-500 mg / l in patients with a high degree of intoxication and 100-1000 mg / l in fatal overdose victims. A urine sample is often used to monitor abuse. Gamma-butyrolactone () and 1,4-butanediol are converted in the body into GHB.
Neurotoxicity
Numerous studies have found that GHB causes deterioration in spatial memory, working memory, and decreases learning and memory scores with long-term use in rats. These effects are associated with a decrease in the expression of NMDA receptors in the cerebral cortex and possibly in other areas. Pedraza et al. (2009) found that repeated administration of GHB to rats for 15 days drastically reduced the number of neurons and non-neuronal cells in the CA1 region of the hippocampus and in the prefrontal cortex. Interestingly, GHB has a biphasic effect on neuronal loss, with lower doses (10mg/kg) being associated with more neurotoxicity than higher doses (100mg/kg). Pretreatment with NCS-382, a GHB receptor antagonist, prevents learning/memory deficits and neuronal loss in GHB-treated animals. It is assumed that the neurotoxic effects of GHB are mediated by the activation of the GHB receptor. In addition, neurotoxicity can be caused by oxidative stress.
addictive
Although deaths have been reported with discontinuation of GHB, these findings are not conclusive and further research is needed to substantiate them. Habituation develops when repeated substance use disrupts the normal balance of brain circuits that control reward, memory, and cognition mechanisms, ultimately leading to compulsive substance use. Rats forced to consume high doses of GHB periodically prefer GHB solution to water, however, after testing on rats, it was noted that "none of the rats showed any signs of withdrawal symptoms when GHB administration was finally terminated at the end of the 20-week period" or in periods of voluntary abstinence.
Discontinuation
The withdrawal syndrome upon discontinuation of GHB is associated with symptoms of insomnia, anxiety, and tremors, usually observed within 3-21 days. Withdrawal symptoms can be quite severe and cause symptoms of acute delirium. The patient may require hospitalization and intensive care. The main form of treatment for severe withdrawal is supportive care and benzodiazepines. Sometimes larger doses are required (eg > 100 mg/day). has been proposed as an alternative or adjunct to benzodiazepines based on anecdotal evidence and some animal data. However, there are few data on use when GHB is discontinued. was first proposed as a supplement because benzodiazepines do not act on GABA receptors, and thus do not have cross tolerance with GHB, while they act on GABA receptors, and have cross tolerance with GHB, and may be more effective in the fight against withdrawal symptoms during the withdrawal of GHB.
endogenous production
Cells produce GHB by reducing succinite semialdehyde through the enzyme succinite semialdehyde reductase. This enzyme is caused by cAMP, so substances that increase cAMP levels, such as forskolin and vinpocetine, can increase the synthesis and release of GHB. People with a disorder known as succinate semialdehyde dehydrogenase deficiency, also known as gamma-hydroxybutyric aciduria, have elevated levels of GHB in their urine, blood plasma, and cerebrospinal fluid. The exact function of GHB in the human body is not known. It is known, however, that the brain expresses a large number of receptors that are activated by GHB. These receptors are excitatory and are not responsible for the sedative effects of GHB. These receptors have been shown to increase levels of the main excitatory neurotransmitter, glutamate. The benzamide antipsychotics amisulpride and sulpiride bind to this receptor in vivo. Other antipsychotics that have been tested have no affinity for this receptor. The substance is a precursor of glutamate in certain areas of the brain. GHB has neuroprotective properties and protects cells from hypoxia.
Natural by-product of fermentation
GHB is also produced by fermentation and is found in small amounts in some beers and wines, particularly fruit wines. The amount of GHB in wine is pharmacologically negligible and not sufficient to produce psychoactive effects.
Pharmacology
GHB has at least two distinct binding sites in the central nervous system. GHB is an agonist at the GHB receptor, which is an excitatory receptor, and a weak agonist at the inhibitory GABA receptor. GHB is a natural substance that similarly acts on several neurotransmitters in the mammalian brain. GHB is probably synthesized in GABAergic neurons, and is released when the neurons fire. When taken orally, it itself inefficiently crosses the blood-brain barrier. GHB causes accumulation of a tryptophan derivative or tryptophan itself in the extracellular space, possibly by increasing the transport of tryptophan across the blood-brain barrier. With peripheral administration of GHB, the content of some neutral amino acids in the blood, including tryptophan, also increases. GHB-induced stimulation of serotonin turnover in tissues may be associated with an increase in tryptophan transport to the brain and its uptake by serotonergic cells. Since the serotonergic system may be involved in the regulation of sleep, mood, and anxiety, stimulation of this system by high doses of GHB may be associated with certain neuropharmacological effects. However, at therapeutic doses, GHB reaches higher concentrations in the brain and activates GABA receptors, which are primarily responsible for its sedative effects. The sedative effects of GHB are blocked by GABA antagonists. The role of GHB receptors in GHB-induced behavioral effects is more complex. GHB receptors are actively expressed in the body, including the brain and hippocampus, and GHB displays the highest affinity for these receptors. Research on GHB receptors is rather limited; however, there is evidence that activation of the GHB receptor in some areas of the brain leads to the release of glutamate, the main excitatory neurotransmitter. Drugs that selectively activate GHB receptors, such as GHB and GABA (B) agonists, cause absence seizures at high doses. Simultaneous activation of GHB and GABA receptors (B) is responsible for the development of addiction when taking GHB. GHB has a biphasic effect on dopamine release. Low concentrations stimulate the release of dopamine through the GHB receptor. Higher concentrations inhibit dopamine release via GABA(B) receptors, as do other GABA(B) agonists such as and. After the initial phase of inhibition, dopamine release is increased via the GHB receptor. The inhibition and increase of dopamine by GHB is inhibited by opioid antagonists such as naloxone and naltrexone. Dynorphin may play a role in inhibiting dopamine release via kappa-opioid receptors. This explains the paradox of GHB's sedative and stimulant effects, as well as the so-called "rebound" effect experienced by GHB hypnotic patients who suddenly wake up after several hours of GHB-induced deep sleep. That is, over time, the concentrations of GHB in the system fall below the threshold for significant activation of GABA receptors and activate predominantly the GHB receptor, which leads to wakefulness. Recently, analogues of GHB such as 4-hydroxy-4-methylpentanoic acid have been synthesized and tested in animals. GHB analogs such as 3-methyl-GHB, 4-methyl-GHB, and 4-phenyl-GHB have been shown to produce GHB-like effects in some animal studies, but these compounds are even less studied than GHB itself. Of these analogs, only 4-methyl-GHB (γ-hydroxyvaleric acid) and its prodrug form, gamma-valerolactone (HVL), have been reported as addictive in humans and are reported to be less potent but more toxic. than GHB, tending to cause nausea and vomiting. Other GHB prodrugs, including 1,4-diacetoxybutane, methyl 4-acetoxybunatoate, and ethyl 4-acetoxybutanoate, also occasionally fall into the hands of law enforcement, but little is known about them. The intermediate 4-hydroxybutaldehyde is also a prodrug of GHB; however, like all aliphatic aldehydes, this compound is alkaline and has a strong odor and unpleasant taste; topical application of this compound as an intoxicant can be unpleasant and can cause severe nausea and vomiting. Also note that both pathways of GHB metabolic degradation can act in either direction, depending on the concentrations of the substances involved in the reaction, so the body can synthesize GHB either from or from semialdehyde succinate. Under normal physiological conditions, the concentration of GHB in the body is quite low. However, when GHB is consumed for recreational or medical purposes, its concentration in the body is much higher than normal, due to which the enzyme kinetics change so that the body begins to absorb GHB and stops producing it.
Story
The chemical synthesis of GHB was first reported by Alexander Zaitsev in 1874, however the first major study of its use in humans was carried out in the early 1960s by Dr. Henri Laborie, who used the substance to study the neurotransmitter. The substance quickly found a wide range of uses, due to its minimal side effects and short duration of action. The only drawback was the narrow therapeutic dose range and the risks associated with its combination with alcohol and other nervous system depressants. GHB has been widely used in France, Italy and other European countries for several decades as a sedative and pain reliever for childbirth, but the risks associated with its potential for abuse, as well as the development of new drugs, have led to a decrease in legitimate medical use in recent times. GHB. Previously, in the Netherlands, GHB could also be purchased as a sedative, however, after several incidents, the substance was included in the list of substances regulated by law. In medical practice, GHB is currently used only for the treatment of narcolepsy, and less often for alcoholism. Typically, GHB is synthesized from γ-butyrolactone () by adding sodium hydroxide to ethanol or water. In early November 2007, the popular children's toy Bindeez (also known as Aqua Dots in the United States) from the Melbourne company Moose was banned in Australia. It was found that during the manufacturing process, the non-toxic plasticizer 1,5-pentanediol was replaced by 1,4-butanediol (1,4-B), which is metabolized into GHB. Three young children were hospitalized after swallowing large amounts of toy balloons.
Legal status
GHB is sold in Italy for therapeutic use. In the United States, the substance was placed on Schedule I of controlled substances in March 2000. However, when sold as sodium oxybate, the substance is a Schedule III substance with penalties similar to those for Schedule I substances. On March 20, 2001, the Commission on Narcotic Drugs placed GHB in Schedule IV of the 1971 Convention on Psychotropic Substances. In the UK, since June 2003, the substance has been included in class C drugs. In October 2013, the ACMD recommended moving GHB from Schedule IV to Schedule II, in line with UN recommendations. In Hong Kong, GHB is regulated under Schedule 1 of Chapter 134 of the Hong Kong Hazardous Substances Ordinance. GHB can only be used legally by healthcare professionals and universities for research purposes. The substance can be dispensed from pharmacies with a prescription. When dispensing GHB without a prescription, the pharmacist will face a large fine. For trade or production of GHB, a criminal will face a fine and life imprisonment. Possession of a substance for consumption without a license from the Department of Health is illegal, and carries a fine or 5 years in prison. In New Zealand and Australia, GHB, 1,4-B and are class B illegal substances, along with any possible derivatives of esters, esters and aldehydes. Itself is also on the list of illegal substances, despite the fact that the substance cannot cross the blood-brain barrier. Attempts to get around GHB's illegal status have led to the sale of derivatives such as 4-methyl-GHB (gamma-hydroxyvaleric acid, HVA) and its prodrug form, gamma-valerolactone (GVL), but these substances also fall under this jurisdiction, being "substantially similar to » GHB or; due to which the import, sale, possession and use of these compounds is also considered illegal. In Chile, GHB is a controlled drug under the Law on Psychotropic Substances and Narcotics. In Norway and Switzerland, GHB is considered a narcotic and is only available by prescription under the brand name Xyrem. Sodium oxybate is also used therapeutically in Italy under the brand name Alcover for the treatment of alcohol withdrawal and addiction.
Scientific experiments and practical observations are being made on the use of GHB in cases of illness, problems, some types, cluster, psychogenic cases of excessive eating. In a number of states, hydroxybutyrate is treated.
In our country, GHB is used as a drug for preserving the respiratory reflex in minor surgery, as a measure to prepare the patient for deeper anesthesia (induction anesthesia). Often used by gynecologists. The drug is useful in cases of need for anesthesia with hypoxia problems in patients. Ophthalmologists, in order to stimulate the metabolic processes of the retina, give Oxybutyrate with an open angle.
Mechanism of narcotic action
The narcotic effect of GHB develops as a result of a competitive effect on the GABAergic neurons of the nervous system by replacing gamma-aminobutyric acid with Butyrate. In addition, the effect of exposure to opioid receptors was noted. It is these influences that lead to the development of euphoria, an increase in mood, and all the main symptomatic manifestations of drug intoxication, or. The final stage of GHB catabolism results in its breakdown into water and carbon monoxide.
Regular intake lowers the body's sensitivity threshold to this substance, which forces the addict to increase the dose.
How GHB manifests its narcotic effect in humans
Despite the restrictive measures and the lack of sale of Oxybutyrate in pharmacies, it can be purchased from illegal distributors.
GHB is taken both orally and by injection.
After entering the body, this narcotic substance manifests itself after 15 minutes. The average duration of action is 1-2 hours. An intravenously injected drug exerts its effects within 4-5 hours. With the alimentary form of taking Butyrate is retained in the body for up to a day.
The duration of its stay depends on the food taken, the physical and mental form of the patient.
Dependence is formed very quickly, it often happens. Therapeutic doses are on average at the level of 0.5 g per day. The narcotic effect develops when 1-3 g of Butyrate enters the body.
Drug addicts often measure doses with beer caps, etc.
Easy degree action develops from small amounts of GHB (0.5 - 1.5 g). The condition resembles a slight alcoholic intoxication, which happens from 50-100 g of vodka.
In this case, patients are noted:
- a pleasant state of complete relaxation;
- excellent mood with complacency;
- desire to communicate with people;
- physical activity.
Average degree (1.5-2.5 g)
Manifestations:
Severe degree (from 2.5 g and above). With this dose, the body ceases to cope and toxic inhibition sets in.
Develop:
- change of hyperactivity by sharp inhibition of the nervous system;
- expressed;
- memory impairment;
- inappropriate behavior and speech;
- sphincter disorders (involuntary excretion of urine and feces).
In this phase, crazy things are done by drug addicts - jumping from a great height, drowning, etc. In the final, a heavy sleep develops, during which the patient often begins. At this point, there is a danger of suffocation, from getting into the respiratory tract of vomit.
Important: in case of an overdose, the patient develops a stupor-like state, later complete. The patient falls into a coma and dies without assistance.
Upon awakening, Butyrate users experience mental retardation, cannot concentrate, their attention is distracted. Among drug addicts, it is believed that physical dependence does not develop with butyratomania. It is this moment, according to many drug addicts, that classifies GHB as a safe substance. But, as practice shows, this is not entirely true.
The formation of butyratomania and the destruction of the body
If a person has been using GHB regularly for several months, then he develops mental addiction .
It is expressed to a weak degree and lasts from three days to one and a half to two weeks. It manifests itself in the development of delusional ideas and statements, a disorder in the thinking process, sleep problems, anxiety, headache and discomfort in the region of the heart.
The initial effects quickly reduce the patient's quantitative control, he again takes increasing doses of Butyrate. Regular use of the drug quickly causes degradation. In behavior, aggressiveness, inappropriate behavior and stupid actions (for example, naked appearance on the street) come first. Patients have an increasing number of memory lapses. The patient is often mistaken with the dosage, which leads to serious consequences and death.
The painful process is exacerbated by the simultaneous use of Oxybutyrate with alcohol, which has a potentiating effect. Other people often suffer from this type of addiction. For example, pedestrians hit by a car driver in a state of butyrate intoxication.
Combinations of GHB with stimulants are especially dangerous.
The use of narcotic doses of GHB very quickly and strongly destroys the personality of a person, his psyche. Among the addicts themselves, the term “vegetable” is used to denote the essence of the state. Severe and irreversible destruction processes take place in the brain. This substance can be called the most "crazy" of all drugs.
Important organs of the patient are also destroyed. The brain, heart, liver, reproductive system suffer.
Treatment of butyratomania
If there is dependence on Butyrate, active and long-term assistance is required in specialized narcological hospitals, with the complete abolition of Butyrate.
In case of an overdose, patients may stay in the toxicological and intensive care units of ordinary hospitals.
Before hospitalization of the patient, people around the addict can provide first aid themselves.
For this you need:
- carry out gastric lavage with water, with a low content of soda, potassium permanganate;
- inside give the patient a few tablets;
- if necessary, put a cleansing enema.
In a hospital setting, people suffering from butyratomania are given:
- active detoxification therapy using intravenous cleaning from sterile vials with a solution of Glucose, Isotonic solution, Rheosorbilact. Reamberin has a powerful poison-neutralizing effect and an action that restores the liver, the heart. In severe and prolonged poisoning, solutions of plasma substitutes help;
- pharmacotherapy for mental disorders . Individual selection of drugs and doses allows you to remove severe forms of mental disorders ( and ). When developing with delusions and hallucinations, doctors prescribe antipsychotics;
- restoration of vitality of all organs . Therapy with vitamins, hepatoprotectors and metabolic agents quickly restores the impaired functions of the affected organs.
- active psychotherapy . As soon as a conscious and critical attitude returns to the patient, active psychotherapeutic methods are added to the treatment process. A specialist in the restoration of mental functions conducts a two-stage motivation of the patient. At the first stage, the psychotherapist convinces the addict that he has an addiction (not everyone considers themselves ill). On the second - the doctor gives an active setting for healing. Without striving for the goals of a future sober life, treatment will not be successful. At the same time, in individual lessons, positive attitudes are reinforced by methods of suggestion. Group types of psychotherapy pursue the goal of persuading recovering patients of the need to lead a normal lifestyle.
- the final stage of treatment - coding . The most effective method for butyratomania is stress therapy according to Dovzhenko . The doctor chooses the most appropriate modification of this method. With the consent of the patient on the appointed day, the patient is encoded for a certain period, during which he will be able to complete the aftercare process.
The most optimal place for rehabilitation is the recovery center. In its conditions, the social readaptation of a recovering person is carried out for several months.
GHB (Gamma Hydroxybutyrate) - a synthetic depressant, similar in action to alcohol.
Chemical Name: 4-hydrobutanoic acid(1,4 butanediol, gamma-butyrolactone)
Chemical formula: C4H8O3 (HOCH2CH2CH2COOH)
Synonyms and slang names for butyrate
English: Blue Verve, G, Gamma-hydroxybutyrate, Gamma-oh, Georgia home boy, Goop, Grievous Bodily Harm, EZLay, Liquid E, Liquid X, SG, Sodium Oxybate,
Russians: Booth, Pinocchio, Water, Lemonade, Oksik, Oksana, Ksenia
Butyrate is a white to yellowish crystalline powder with a slight specific odor. Soluble in water and alcohol. Most often used in the form salt sodium hydroxybutyrate(Na-GHB) and potassium hydroxybutyrate (K-GHB). salt GHB Available in both powder and aqueous solutions. Butyrate used as a sleeping pill, as well as a psychoactive substance - a relaxant, similar in action to alcohol. In the past, it was often used in bodybuilding as a dietary supplement.
In medical practice sodium oxybutyrate It is used to treat neurotic conditions, insomnia, as well as intoxications and traumatic injuries of the central nervous system.
History of butyrate
First butyrate was synthesized in 1874, although the synthesis method was not published until 1929. A significant role in the distribution of the drug was played by the French researcher Henry Laborit (Dr. Henri Laborit). In the 1960s, he made a series of experiments in which many previously unknown properties of butyrate. In particular, the ability of the drug to stimulate the release of growth hormone (GH), which is necessary for building muscle mass, was established. Which led in the 1980s to its wide distribution as a bioactive nutritional supplement to the diet of bodybuilders.
In recent years butyrate has become quite popular in club culture as a replacement for traditional alcohol. It is increasingly being used as an energy drink, providing an uplifting mood, but without the hangover inherent in alcohol. Some even call it liquid ecstasy due to certain similarities in effects. Also butyrate use, as a rather powerful aphrodisiac that increases the depth of sexual sensations and the duration of sexual intercourse.
The action of butyrate
AT therapeutic doses of butyrate has a pronounced antihypoxic effect: it increases the body's resistance to oxygen deficiency, including in the tissues of the brain, heart muscle and retina. In large doses, it is used as a mild sleeping pill.
Not being an analgesic, however, it has a good anti-shock potential, and also enhances the effects of other painkillers. In medicine butyrate is used for the treatment of narcolepsy and insomnia, as well as for the treatment of alcoholism.
Its non-medical use is mainly associated with effects reminiscent of the effects of alcohol.
The dose of the drug is 0.5-1.5 grams
causes a slight degree of "intoxication", as from about one or two glasses of vodka: a slight euphoria, relaxation, mood lift and increased sociability are characteristic.
The average dose is 1.5-2.5 grams
contributes to increased relaxation, as well as greater disinhibition, instability, incoherence of speech. There is a sharp rise in mood, an increased interest in music and dancing, as well as an increase in sexual desire up to hypersexuality.
Doses over 3 grams
can induce deep sleep lasting 3-4 hours.
Action butyrate begins 10-20 minutes after ingestion, and lasts for one to two hours, sometimes longer. In general, effects and duration - as in the case of alcohol - vary greatly depending on many parameters: for example, dose, body weight, physiological predisposition, and combination with other substances and food.
Post-effects after cessation butyrate expressed in a slight dispersal and lethargy. "Hangover syndrome" is not pronounced, mainly there is some "blurring" of consciousness or, on the contrary, increased vigor and efficiency.
In the body butyrate breaks down into non-toxic components - water and carbon monoxide, however, depending on the individual characteristics of the organism, even relatively small doses of the drug can lead to poisoning.
With regular use, tolerance develops.
Harm and dependence on butyrate
Special danger in non-medical butyrate use presents the possibility of overdose. Any dose starting from 2 grams, depending on individual predisposition, can cause symptoms of poisoning. This is mainly expressed in severe dizziness, disorientation, nausea and vomiting. In more severe cases, the patient may fall into a deep, restless sleep followed by memory lapses, or even into a coma. In this state, a person can easily choke on his own vomit.
In combination with other psychoactive drugs and alcohol, the risk of poisoning is greatly increased. Especially often there are cases of overdose when using butyrate
in the form of a solution of unknown concentration. For example, in the United States over the past few years, about 60 deaths associated with overdose butyrate.
Even in small doses of butyrate significantly increases the risk of injury when driving complex industrial machinery and vehicles.
At the moment, there is not enough data on the possible physical addiction, caused by regular drug use. However, when taking butyrate 3-6 times a week for several months, persistent psychological dependence.
The withdrawal syndrome in this case is pronounced, and is characterized by a constant feeling of anxiety, insomnia, heart failure, dizziness and chest pain. Withdrawal may last for several days after regular use has ended.
The drug is also contraindicated in myasthenia gravis, hypokalemia, as well as during pregnancy and during breastfeeding.
Diagnosis and treatment
At intravenous injection of butyrate completely eliminated from the body within 4-5 hours. When taken orally, the drug can be detected in the blood during the day.
Symptoms of an overdose of butyrate: Difficulty breathing, immobile pupils, immunity to external stimuli, convulsions and vomiting. In this case, first aid should be provided in the form of gastric lavage, as well as the intake of absorbent substances - for example, activated charcoal.
In any case, it is necessary to seek qualified medical help.
Legislation
Turnover of butyrate restricted to varying degrees in most countries, including the US, Australia, UK, Japan, Canada, and even the Netherlands.
In Russia sodium hydroxybutyrate and other salts of hydroxybutyric acid are included in Schedule III "Psychotropic substances, the circulation of which in the Russian Federation is limited and for which the exclusion of certain control measures is allowed in accordance with the legislation of the Russian Federation and international treaties of the Russian Federation"
Driver under butyrate crashed into parked car
Video of the consequences of consuming butyrate
Included in medications
ATH:N.06.B.X Other psychostimulants and nootropics
Pharmacodynamics:Pharmacological action - hypnotic, adaptogenic, antihypoxic, tranquilizing, nootropic. It has a GABA-mimetic effect, corrects metabolic disorders of the central nervous system. It increases the resistance of the brain to hypoxia and the effects of toxic substances, stimulates plastic and synthetic processes in neurons and the utilization of glucose and oxygen. Helps normalize sleep, improves memory. It has a tranquilizing effect (without causing muscle relaxation), prevents neurotic disorders and vegetative reactions to stress. Shows a sedative effect with a slight stimulating effect (activating and anti-asthenic action). It has adaptogenic and analgesic properties. Pharmacokinetics:Rapidly absorbed from the gastrointestinal tract, bioavailability is 80%. Easily penetrates the blood-brain barrier due to its lipophilicity. The maximum plasma concentration in the blood is observed 1.5 hours after administration. The plasma half-life is 1.17 hours. Indications: - neurotic and neurosis-like disorders caused by intoxication and trauma, psychogenic influences, sleep disturbances;Chronic alcoholism, withdrawal syndrome with a predominance of asthenodepressive and asthenovegetative symptoms, alcoholic encephalopathy, alcoholic polyneuropathy;
Consequences of traumatic brain injury, residual effects of a stroke, cerebrovascular insufficiency, dyscirculatory encephalopathy.
V.F10-F19.F10.2 Mental and behavioral disorders caused by alcohol use - dependence syndrome
V.F10-F19.F10.3 Mental and behavioral disorders caused by alcohol use - withdrawal state
VI.G40-G47.G47.0 Sleep disturbances and sleep maintenance [insomnia]
VI.G90-G99.G90 Disorders of the autonomic [autonomic] nervous system
Contraindications:- hypersensitivity,Severe disorders of the liver and kidneys,
myasthenia,
Pregnancy, breastfeeding.
Carefully: No data. Pregnancy and lactation:Do not use during pregnancy! Category of action on the fetus according to the FDA - C. Well-controlled studies in humans have not been conducted. In animal experiments, the drug caused teratogenic and embryotoxic effects.Lactation: do not use the drug during lactation or stop breastfeeding for the period of treatment. There is no data on the penetration of the drug into breast milk.
Dosage and administration:inside, before meals, 0.25-0.5 g 3-4 times a day; the maximum single dose is 1 g, the maximum daily dose is 4 g; course of treatment - 4-6 weeks (it is possible to conduct repeated courses).Use in elderly patients
Use in the elderly has not been systematically studied. There is no data on the need to reduce the dosage of the drug in patients of this group, although due to age-related changes in the cardiovascular, respiratory, central nervous and other systems, this may be relevant.
Side effects:Rarely - headache, daytime sleepiness, shortening of night sleep, nausea, dizziness, allergic reactions. Overdose: There were no cases of overdose. The goals of therapy with a possible overdose are the maintenance of vital functions, the rapid appointment of symptomatic therapy. The drug can be excreted from the body by hemodialysis. Interaction: Potentiates the action of barbiturates, analgesics (in particular, morphine) and hypnotics.The action of rocuronium bromide is enhanced by the administration of high doses of gamma hydroxybutyrate.
Special instructions:Use with caution during work for drivers of vehicles and people whose profession is associated with increased concentration of attention.During treatment, ethanol-containing drinks should be excluded.
Instructions