posted February 08, 2000 02:13 PM            

A sad story, no matter where one stands on prohibition. In September of 1996, this innocent and well-reputed 17 year-old went to a dance club in her hometown of La Porte, TX, where she spent the night with friends, drinking Sprite. That night, she suddenly and inexplicably died. Analysis found no drugs or alcohol showing up in her blood [61].

Then, someone thought to check for the sinister new date rape drug, GHB. There it was, 27mg/kg [42] - far more than natural concentrations, but reachable with a dose of less than 2g. Open and shut. In her death, all GHB's sins remembered: The secret administration, the sudden death, the low, reasonable dose that yet can kill.

If you've been paying attention so far, at least one siren should be sounding.

GHB's effects do not develop over many hours; any conceivable toxicity, normal or abnormal, should have appeared within fifteen minutes. Hillory drove herself home and said goodnight to her grandmother; a theoretical dose huge enough to kill her would have made both of these activities impossible.

If not the drug, then, what killed Hillory Farias? In their seminal book on GHB [151], Dean et al. claim that the coroner eventually determined that she suffered from a congenital heart disease, and was in fact killed by a cardiac thrombosis - a blood clot.

This convenient resolution, though, ignores the GHB that was present in her body. Did Hillory simply have the unbelievable misfortune to be chemically assaulted and suffer heart failure in one hellish night?

It seemed that we were forced to this improbable conclusion, until Fieler, et al. turned up a surprising new piece of this puzzle[140]. In a test of their GHB assay technique, they were able to detect GHB levels of up to 168mg/L in the blood of cadavers that had not ingested any! Barring the possibility of a desperately confused necrophiliac at the coroner's office, it seems that the body may produce huge quantities of endogenous* GHB when near death. Considering various findings that GHB protects the brain [141] and organs [30] from low-oxygen conditions, and the body's own use of GHB to reduce oxygen consumption [45], it seems reasonable to theorize that a death due to loss of circulation would naturally lead to the production of high levels of GHB during (or after) the final moments. Note that this is, as of now, by no means a supported or peer-reviewed conclusion, but I hope to soon have it critiqued by minds armed with medical training.

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GHB myths:

GHB has no dose-response curve!!!!

In other words, there is no reliable relationship between the amount of GHB you take and what happens to you. A dose that gets you high tonight might land you in the emergency room tomorrow, or in Tahiti two days from now. GHB isn't a biological agent, it's the devil in a teaspoon*!

Perfectly untrue. Granted, the borderline between doses that will make an individual euphoric* vs. dormant is thin, but the areas enclosed are reasonably wide (That is, most people have a good margin between an effective dose and a soporific* one, but there may not be much warning that a dose is close to pushing them over). All other things (e.g., mental state, physical fatigue, presence of food in the stomach) being equal, GHB's effects vary no more than other drugs'. Even opponents of GHB admit, in more sober moments, that the dose-response curve does exist [34].

GHB will stop your lungs!!!!
GHB does slow one's breathing, and this tends to make medical professionals very jumpy. Not knowing why their patient has such depressed respiration, they intubate*, and when the GHB wears off in its natural handful of hours, credit themselves with a daring raid into the very keep of death to steal back the precious soul under their care. What they do not know is that GHB's other physiological effects cause those sparse breaths to take in more air, and may also induce changes in oxygen use and metabolism that leave actual oxygen/carbon dioxide levels unchanged [45].

Please know that I'm not talking about GHB mixed with alcohol, heroin, marijuana, Valium or other benzodiazepides, SSRIs like Prozac, MAO inhibitors, or anything else. Alcohol and other depressants, at least, have been shown to truly make GHB as dangerous as you may have heard.

Note: The above may appear belittling of physicians, nurses, EMTs, and others who labor for our health. I in fact have great respect for those who seek to understand the body and all its wonderful mechanisms, and who use them for the good of others. In the absence of other useful knowledge, their reaction to GHB-induced coma is not even unreasonable. In terms of treating the condition, however, it is wildly inappropriate. Thus, it is up to the user to stay out of their hands!

GHB is paint thinner and lye!!!!
Forget GHB! Did you know there's a drug regularly used by well over 50% of the population that's made out of an EXPLOSIVE metal and a POISON gas? And it can cause heart attacks! Paint thinner don't look so bad anymore, eh?

The chemically-educated probably recognize the substance in the above rant as NaCL, table salt. The situation with GHB is similar: Gamma-butyrolactone, which is a chemical in industrial solvents, and sodium hydroxide*, the active ingredient in lye*, undergo a chemical change on the molecular level which makes them into something quite user-friendly. It is for the purpose of ensuring that whatever you consume is, in fact, real GHB without any of the above adulterants that I recommend you make your own.