GHB risks, social and health risks.
GHB – Gamma OH: risks and danger
- Excessive hits could lead to sickness, stiff muscles, fits and even
collapse, Coma and seizures.
- If incorrectly produced, can badly burn the mouth.
- It is very dangerous and can be fatal when mixed with other depressants
such as alcohol or tranquilisers.
- The long-term effects are not yet fully known.
- GHB combined with methamphetamine appears to increase risk of seizure.
- Combining use with other drugs such as alcohol can result in nausea
and difficulty breathing.
Always keep your glass with you on nights out!
- Produces sedative-hypnotic effects including muscle relaxation and
- People may unknowingly be given the drug which, when mixed with alcohol,
can incapacitate victims and prevent them from resisting sexual assault.
As with pure alcohol, the dose-response curve of GHB is very steep, and proper dosing of illegal GHB can be difficult since it often comes as a salt dissolved in water, and the actual amount of GHB and/or other additives per “capful” can vary. Legal GHB comes in standardized doses and is free from contaminants, so it is much safer (cf. legal alcohol vs. bathtub gin). Also, like pure alcohol, small doses of GHB are considered safe, but high doses can cause unconsciousness, convulsions, vomiting, suppression of the gag reflex and respiratory depression. These effects vary between persons and are dose dependent. Synergy of its sedative effects are seen when combined with other CNS depressants such as alcohol, benzodiazepines (e.g. diazepam), barbiturates, and others.
Another complication is the difference in pharmacokinetics between GHB and its two prodrugs, 1,4-B and GBL. 1,4-butanediol is converted into GHB in the body by two enzymes alcohol dehydrogenase and aldehyde dehydrogenase, which gives it a delayed onset of effects and a longer duration of action. GHB is then further metabolised, again by alcohol dehydrogenase and aldehyde dehydrogenase, into the inactive succinate.
If alcohol has also been consumed this can saturate the dehydrogenase enzymes and so delays the conversion of 1,4-B into GHB, meaning that 1,4-B takes much longer to take effect and people may re-dose thinking it hasn’t done anything, leading to an accidental overdose later on once it finally takes effect. 1,4-B itself can also contribute to the enzyme saturation, so when alcohol and 1,4-B are consumed together it produces a complex and somewhat unpredictable interaction between the varying levels of alcohol, 1,4-B and GHB present in the body. Alcohol also makes the GHB last longer in the body by competing for dehydrogenase enzymes and hence delaying the conversion of GHB into succinate.
The other precursor gamma-butyrolactone (GBL) is rapidly converted into GHB by lactamase enzymes found in the blood. GBL is more lipophilic (fat soluble) than GHB and so is absorbed faster and has higher bioavailability; paradoxically this can mean that GBL has a faster onset of effects than GHB itself even though it is a prodrug. The levels of lactamase enzyme can vary between individuals and GBL is not active in its own right, so people who have never tried GBL before may have delayed or less effects than expected; however once someone has taken GBL a few times the production of lactamase enzymes is increased and they will feel the effects like normal.
Because of these pharmacokinetic differences, 1,4-B tends to be slightly less potent, slower to take effect but longer acting than GHB, while GBL tends to be more potent and faster acting than GHB, and lasts around the same duration. The growth hormone releasing effects of GHB which have led to its use by bodybuilders are mediated by the metabolite succinate. Some bodybuilders believe that these beneficial effects can be achieved by taking succinate instead of GHB which avoids the potential dangers, abuse potential and illegal status of GHB itself.
Alcohol worsens both CNS depression and vomiting, so combining alcohol with GHB or its precursors can be particularly dangerous. Another factor to be considered is that people who drink alcohol regularly tend to induce expression of their dehydrogenase enzymes and thus have higher levels of these enzymes than people who do not drink alcohol regularly; this means that regular alcohol drinkers will both convert 1,4-B into GHB more rapidly, and also break down GHB into succinate faster than people who don’t drink alcohol. This multitude of different factors can make the interactions between 1,4-B, GHB and alcohol very complicated and highly variable between different individuals.
Death while using GHB is most likely when it is combined with alcohol or other depressant drugs, however as with all substances, an overdose of GHB alone may be lethal. A review of the details of 194 deaths attributed to or related to GHB over a ten year period found that most were from respiratory depression caused by interaction with alcohol or other drugs; several were from choking on vomit and asphyxiating; remaining causes of death included motor vehicle and other accidents. The review included 70 cases where high levels of GHB were found post-mortem without concomitant ingestion of other drugs or alcohol.
Determining conclusively whether someone’s death was caused by GHB is very difficult because a lab test will always detect the presence of some GHB in the human body, and levels of GHB can vary in the same individual depending on what part of the body is tested. GHB is a naturally occurring substance that is always present in everyone, but little research has been done on what levels are normal in what parts of the body at what times.
There have been no systematic studies into the effects of GHB if taken chronically in humans, and hence whether prolonged use of GHB causes any bodily harm remains unknown. 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.