[Main Page][GHB FAQ][Meta-FAQ][Supply FAQ][Therapy FAQ]
[References][Glossary][Link To the Outside World]
[Quick answers from the GHB FAQ Crisis Center]
What about Hillory Farias?
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. Within 24 hours she unexpectedly and inexplicably died, with 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 does not act over the course of a day; any conceivable toxicity, normal or abnormal, should have appeared within the hour.
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.
I recently had the honor of discussing this idea with Dr. Ward Dean of CERI, one of the world's foremost authorities on GHB. He finds it highly intriguing, and is forwarding it to the Farias family lawyer (yes, they find the diagnosis of "death by GHB" that incompetent). With his help, I also hope to get in touch with Fieler, et al. and clear up a few remaining questions about their findings. Look to the CERI newsletter, or this site, for updates.
The Farias case must be seen as integral to the public image of GHB and its current illegalization in more and more states. Even when not explicitly named, it is her death that fuels media reports that GHB is a potentially fatal drug - or even the outlandish claim that it causes heart failure - nevermind that even the most strongly anti-GHB research [52] never mentions such a thing.
Next Segment: Myths about GHB
Table of Contents
[Main Page][GHB FAQ][Meta-FAQ][Supply FAQ][Therapy FAQ]
[References][Glossary][Link To the Outside World]
[Quick answers from the GHB FAQ Crisis Center]
Created and maintained by Michael Cohn - michaelc@medscape.com © 1998