I dont think you'll find it will freeze at any temp. It's well known that even a small amount of dilution will throw the freeze point out to something completely unrelated to the dilution ratio.
Just picked up some g which I believed to be 1,4-B. Slight bitterness to it not a terrible taste, no smell off 20ml. Chucked it in the fridge for close to 24 hours and it hasn't froze.
Is this most likely not 1,4-B anyone?
This is bullshit. I'd explain but there's lots to consider/write and I can't do that right now. Chemical equilibrium is the fundamental reasoning here.
γ-Hydroxybutyric acid (GHB), also known as 4-hydroxybutanoic acid and sodium oxybate (INN), is a naturally occurring substance found in the human central nervous system, as well as in wine, beef, small citrus fruits, and almost all animals in small amounts.[1] It is also categorized as an illegal drug in many countries.[2] It is currently regulated in Australia and New Zealand, Canada, most of Europe and in the US. GHB as the sodium salt, known as sodium oxybate, is sold by Jazz Pharmaceuticals under the name Xyrem[3] to treat cataplexy[4] and excessive daytime sleepiness in patients with narcolepsy.
GHB has been used in a medical setting as a general anesthetic, to treat conditions such as insomnia, clinical depression, narcolepsy, and alcoholism, and to improve athletic performance.[5] It is also used as an intoxicant (illegally in many jurisdictions) or as a date rape drug.[6] GHB is naturally produced in the human body's cells and is structurally related to the ketone body beta-hydroxybutyrate. As a supplement/drug, it is used most commonly in the form of a salt, for example sodium gamma-hydroxybutyrate (Na.GHB, sodium oxybate, or under the brand name Xyrem.) or potassium gamma-hydroxybutyrate (K.GHB, potassium oxybate). GHB is also produced as a result of fermentation, and so is found in small quantities in some beers and wines. Succinic semialdehyde dehydrogenase deficiency is a disease that causes GHB to accumulate in the blood.
GHB is a CNS depressant used as an intoxicant.[10] It has many street names, including "Georgia Home Boy", "Juice", "Liquid Ecstasy", "Mils", "G", "Liquid X", and "Liquid G", as well as "Fantasy" and the reordered initialism GBH (abbreviation of grievous bodily harm in English law). Its effects have been described anecdotally as comparable with alcohol and ecstasy use, such as euphoria, disinhibition, enhanced sensuality and empathogenesis. At higher doses, GHB may induce nausea, dizziness, drowsiness, agitation, visual disturbances, depressed breathing, amnesia, unconsciousness, and death. The effects of GHB can last from 1.5 to 3 hours, or even longer if large doses have been consumed.[11] Consuming GHB with alcohol is dangerous as it can lead to vomiting in combination with unrouseable sleep, a potentially lethal combination.[12]
In general, the doses used recreationally are between 500 mg and 3,000 mg. When used as a recreational drug, GHB may be found as the sodium or potassium salt, which is a white crystalline powder, or as GHB salt dissolved in water to form a clear solution. The sodium salt of GHB has a salty taste.[11] Other salt forms such as calcium GHB and magnesium GHB have also been reported, but the sodium salt is by far the most common.
Some chemicals convert to GHB in the stomach and blood stream. GBL, or gamma-butyrolactone, is one such prodrug. Other prodrugs include 1,4-butanediol. There may be additional toxicity concerns with these precursors. 1,4-B and GBL are normally found as pure liquids, although they may be mixed with other more harmful solvents when intended for industrial use, e.g., as paint stripper or varnish thinner.
GHB can be easily manufactured at home with very little knowledge of chemistry, as it only involves the mixing of its two precursors, GBL and an alkali hydroxide (such as sodium hydroxide) to form the resulting GHB salt. Due to the ease of manufacture and the availability of its precursors, its production is not done in relatively few illicit laboratories like most other synthetic drugs, but in private homes by low level producers instead. While available as a prescription for rare and severe forms of sleep disorders such as narcolepsy in some other countries, notably most of Europe, GHB was banned (in the U.S.) by the FDA in 1990. However, on 17 July 2002, GHB was approved for treatment of cataplexy, often associated with narcolepsy. GHB is "colourless and odorless".[13]
GHB is often taken because users find that it enhances their experiences of being in a club, party, or rave; small doses of GHB can act as a stimulant and aphrodisiac. GHB is sometimes referred to as G, liquid ecstasy, liquid X, or liquid E due to its tendency to produce euphoria and sociability and its use in the dance party scene.[14] Despite this nickname, GHB has entirely separate chemical and pharmacological modes of action compared to ecstasy.
One report has suggested that Xyrem (pharmaceutical GHB, or "Sodium Oxybate") overdose may be fatal, based on deaths of three patients who had been prescribed the drug.[27] However, for two of the three cases, post-mortem GHB concentrations were 141 and 110 mg/L, which is within the expected range of concentrations for GHB after death, and the third case was a patient with a history of intentional drug overdose.[28]
One publication has investigated 226 deaths attributed to GHB.[29] Of 226 deaths included, 213 suffered cardiorespiratory arrest and 13 suffered fatal accidents. Seventy-one deaths (34%) had no co-intoxicants. Postmortem blood GHB was 18–4400 mg/L (median=347) in deaths negative for co-intoxicants.
GHB is produced in the body in very small amounts, and blood levels may climb after death to levels in the range of 30–50 mg/L.[30] Levels higher than this are found in GHB deaths. Levels lower than this may be due to GHB or to postmortem endogenous elevations.
A UK parliamentary committee commissioned report found the use of GHB to be less dangerous than tobacco and alcohol in social harms, physical harm and addiction.[31]
Overdose of GHB can be difficult to treat because of its multiple effects on the body.[5][32][33] GHB tends to cause rapid unconsciousness at doses above 3500 mg, with single doses over 7000 mg often causing life-threatening respiratory depression, and higher doses still inducing bradycardia and cardiac arrest. Other side-effects include convulsions (especially when combined with stimulants), and nausea/vomiting (especially when combined with alcohol).[10]
The greatest life threat due to GHB overdose (with or without other substances) is respiratory arrest.[2][10] Other relatively common causes of death due to GHB ingestion include aspiration of vomitus, positional asphyxia, and trauma sustained while intoxicated (e.g., motor vehicle accidents while driving under the influence of GHB).[citation needed] The risk of aspiration pneumonia and positional asphyxia risk can be reduced by laying the patient down in the recovery position. People are most likely to vomit as they become unconscious, and as they wake up. It is important to keep the patient/friend awake and moving, plus do not allow them to be alone as death through vomiting can easily happen. Frequently they will be in a good mood but this does not mean they are not in danger. GHB overdose is a medical emergency and immediate assessment in an emergency department is needed.
Convulsions from GHB can be treated with diazepam or lorazepam,[10] even though these are also CNS depressants they are GABAA agonists, whereas GHB is primarily a GABAB agonist, so the benzodiazepines do not worsen CNS depression as much as might be expected.[citation needed]
Because of the faster and more complete absorption of GBL relative to GHB, its dose-response curve is steeper, and overdoses of GBL tend to be more dangerous and problematic than overdoses involving only GHB or 1,4-B. Any GHB/GBL overdose is a medical emergency and should be cared for by appropriately trained personnel.
A newer synthetic drug SCH-50911, which acts as a selective GABAB antagonist, quickly reverses GHB overdose in mice.[34] However, this treatment has yet to be tried in humans, and it is unlikely that it will be researched for this purpose in humans due to the illegal nature of clinical trials of GHB, and the lack of medical indemnity coverage inherent in using an untested treatment for a life-threatening overdose.[original research?]
Although there have been reported fatalities due to GHB withdrawal, reports are inconclusive and further research is needed.[44] Addiction occurs when repeated drug use disrupts the normal balance of brain circuits that control rewards, memory and cognition, ultimately leading to compulsive drug taking.[45][46]
GHB has also been associated with a withdrawal syndrome of insomnia, anxiety, and tremor that usually resolves within three to twenty-one days.[10][44][49] The withdrawal syndrome can be severe producing acute delirium and may require hospitalization in an intensive care unit for management.[10] The mainstay of treatment for severe withdrawal is supportive care and benzodiazepines for control of acute delirium, but larger doses are often required compared to acute delirium of other causes (e.g. > 100 mg/d of diazepam). Baclofen has been suggested as an alternative or adjunct to benzodiazepines based on anecdotal evidence and some animal data.[50] However, there is less experience with the use of baclofen for GHB withdrawal, and additional research in humans is needed. Baclofen was first suggested as an adjunct because benzodiazepines do not affect GABAB receptors and thus have no cross-tolerance with GHB while baclofen, which works via GABAB receptors, is cross-tolerant with GHB and may be more effective in alleviating withdrawal effects of GHB.[51]
GHB withdrawal is not widely discussed in text books and some psychiatrists, general practitioners, and even hospital emergency physicians may not be familiar with this withdrawal syndrome.[52]
GHB is also produced as a result of fermentation and so is found in small quantities in some beers and wines, in particular fruit wines. However, the amount of GHB found in wine is insignificant and not sufficient to produce any effects.[60]
GHB has at least two distinct binding sites[61] in the central nervous system. GHB is an agonist at the newly characterized GHB receptor, which is excitatory,[62][63] and it is a weak agonist at the GABAB receptor, which is inhibitory.[63] GHB is a naturally occurring substance that acts in a similar fashion to some neurotransmitters in the mammalian brain.[64] GHB is probably synthesized from GABA in GABAergic neurons, and released when the neurons fire.[63]
If taken orally, GABA itself does not effectively cross the blood-brain-barrier.[65]
GHB induces the accumulation of either a derivative of tryptophan or tryptophan itself in the extracellular space, possibly by increasing tryptophan transport across the blood–brain barrier. The blood content of certain neutral amino-acids, including tryptophan, is also increased by peripheral GHB administration. GHB-induced stimulation of tissue serotonin turnover may be due to an increase in tryptophan transport to the brain and in its uptake by serotonergic cells. As the serotonergic system may be involved in the regulation of sleep, mood, and anxiety, the stimulation of this system by high doses of GHB may be involved in certain neuropharmacological events induced by GHB administration.
However, at therapeutic doses, GHB reaches much higher concentrations in the brain and activates GABAB receptors, which are primarily responsible for its sedative effects.[66] GHB's sedative effects are blocked by GABAB antagonists.
The role of the GHB receptor in the behavioural effects induced by GHB is more complex. GHB receptors are densely expressed in many areas of the brain, including the cortex and hippocampus, and these are the receptors that GHB displays the highest affinity for. There has been somewhat limited research into the GHB receptor; however, there is evidence that activation of the GHB receptor in some brain areas results in the release of glutamate, the principal excitatory neurotransmitter.[56] Drugs that selectively activate the GHB receptor cause absence seizures in high doses, as do GHB and GABA(B) agonists.[67]