• GHB has been studied for decades in a wide range of doses, regimens, and populations, so I am confident that if it had some rare or subtle toxicity we would have noticed it. We have basic toxicological information for GBL and 1,4-BD, but not nearly the sheer mass of data.

• GHB is immediately active in the brain, where a naturally-present enzyme metabolizes it into an ordinary sugar and then to carbon dioxide and water. The precursors above have to go through the liver first, where they may compete with other toxins. This would make them even more dangerous than GHB in combination with alcohol, as well as producing interactions which do not pertain to GHB at all. I at least advise against using them with anything that is known to harm the liver, such as the antidepres sant Elavil or acetaminophen (Tylenol or APAP).

• GBL may irritate mucous membranes, which is why most preparations dilute it very heavily.

• There is anecdotal evidence that GBL causes nausea and headaches in some people.

• The extra step required before these chemicals become active creates a sort of "time-release" effect, which makes the experience milder and longer-lasting. This is not necessarily negative, but should be borne in mind by people used to being able to drive within a few hours of taking GHB.

GBL toxicology studies - from the National Institutes of Health
Note that an ordinary GBL user would probably never take more than 100mg/kg in a single dose.

Created and maintained by Michael Cohn - michaelc@medscape.com © 1999