GHB - The Sex Drug And A Deadly Killer!!!

Good Day Friends,

Today I want to talk about something that's very very serious. It's a drug called GHB (Gamma Hydroxybutyrate (C4H8O3).

GHB or Gamma Hydroxybutyrate (C4H8O3) is a central nervous system (CNS) depressant that is commonly referred to as a “club drug” or “date rape” drug. GHB is abused by teens and young adults at bars, parties, clubs and “raves” (all night dance parties), and is often placed in alcoholic beverages. Euphoria, increased sex drive, and tranquility are reported positive effects of GHB abuse. Negative effects may include sweating, loss of consciousness (reported by 69 percent of users), nausea, hallucinations, amnesia, and coma, among other adverse effects.

GHB is also a naturally-occurring metabolite of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) found in the brain. The naturally-occurring metabolite GHB is present in much lower concentrations in the brain than those levels found when the drug is abused. As a result of fermentation, natural GHB may also be found in small but insignificant quantities in some beers and wines. Hydroxybutyric acid (GHB), also known as 4-hydroxybutanoic acid, is a naturally occurring neurotransmitter and a psychoactive drug. It is a precursor to GABA, glutamate, and glycine in certain brain areas, and it acts on the GHB receptor and it is a weak agonist at the GABAB receptor.

GHB has been used in a medical setting as a general anesthetic and as a treatment for cataplexy, narcolepsy, and alcoholism.[ It is also used illegally as an intoxicant, to try to increase athletic performance, and as a date rape drug.[4] It is commonly used in the form of a salt, such as sodium γ-hydroxybutyrate (Na.GHB, sodium oxybate, or Xyrem) or potassium γ-hydroxybutyrate (K.GHB, potassium oxybate).

GHB is also produced as a result of fermentation, and is found in small quantities in some beers and wines, beef and small citrus fruits.
Succinic semialdehyde dehydrogenase deficiency is a disease that causes GHB to accumulate in the blood.

Methods of GHB Abuse:
GHB is available as an odorless, colorless drug that may be combined with alcohol and given to unsuspecting victims prior to sexual assaults. It may have a soapy or salty taste. Use for sexual assault has resulted in GHB being known as a “date rape” drug. Victims become incapacitated due to the sedative effects of GHB, and they are unable to resist sexual assault. GHB may also induce amnesia in it’s victim. Common user groups include high school and college students and rave party attendees who use GHB for its intoxicating effects.

GHB has also been postulated to have anabolic effects due to protein synthesis, and has been used by body-builders for muscle building and reducing fat.

GHB is bought on the streets or over the Internet in liquid form or as a white powdered material for illicit use. It is taken orally and is frequently combined with alcohol. Much of the GHB found on the streets or over the Internet is produced in illegal labs. GHB may be adulterated with unknown contaminants that may worsen it’s toxicity. The production of GHB usually involves the use of lye or drain cleaner mixed with GBL, a chemical cousin of GHB and an industrial solvent often used to strip floors.4

In 1990, the Food and Drug Administration (FDA) issued an advisory declaring GHB use unsafe and illegal except under FDA-approved, physician-supervised protocols. In March 2000, GHB was placed in Schedule I of the Controlled Substances Act. The sodium salt of GHB, the brand product Xyrem (sodium oxybate), is a Schedule III drug when prescribed and used legally in a patient restricted-access program. Xyrem is not available at regular retail pharmacies. If Xyrem is trafficked as a recreational drug, it’s status converts to Schedule I and it becomes an illegal drug.

Pharmacology
GHB acts at two receptor sites in the brain, the GABAB and specific GHB receptors. Action at these two receptor sites leads to the CNS depressant, stimulant and psychomotor impairment effects of GHB. Roughly 95 percent of GHB is metabolized in the liver, and it’s half-life ranges from 30 to 60 minutes. Only five percent of the parent drug is excreted via the kidneys. Detection of GHB in the urine may be difficult after 24 hours due to it’s short half-life.1

Health Hazards Due to GHB Use
Euphoria, increased sex drive, and tranquility are reported positive effects of GHB abuse. However, immediate negative effects of GHB use may include sweating and loss of consciousness (reported by 69 percent of users), nausea, auditory and visual hallucinations, headaches, vomiting, exhaustion, sluggishness, amnesia, confusion, and clumsiness.4

GHB can have an addictive potential if used repeatedly. Withdrawal effects may include insomnia, anxiety, tremors, and sweating. Withdrawal can be severe and incapacitating.

Combined use with alcohol, other sedatives or hypnotics (such as barbiturates or benzodiazepines) and other drugs that possess CNS depressant activity may result in nausea, vomiting and aspiration, and dangerous CNS and respiratory depression.

High doses of GHB, even without other illicit substances or alcohol, may result in profound sedation, seizures, coma, severe respiratory depression and death. Emergency department episodes related to the use of club drugs usually involve the use of multiple substances, such as marijuana, cocaine, and other club drugs, such as methamphetamine, Ecstasy, or Rohypnol.

GHB detection methods for emergency room use are not readily available. Emergency room physicians may be unaware that GHB has been abused when a patient presents to the hospital, as well. Due to the short half-life of the drug, detection in the urine may be difficult. Supportive care and keeping airways open are the primary measures used in the emergency overdose situation.

Overdose:
Overdose of GHB can sometimes be difficult to treat because of its multiple effects on the body. 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).

The greatest life threat due to GHB overdose (with or without other substances) is respiratory arrest. 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).] 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 victim awake and moving, who must not be left alone due to the risk of death through vomiting. 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 the benzodiazepines diazepam or lorazepam. Even though these benzodiazepines are also CNS depressants, they are GABAA agonists whereas GHB is primarily a GABAB agonist, and so do not worsen CNS depression as much as might be expected.

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. 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. 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.

Detection of use:
GHB may be quantitated in blood or plasma to confirm a diagnosis of poisoning in hospitalized patients, provide evidence in an impaired driving arrest or to assist in a medicolegal death investigation. Blood or plasma GHB concentrations are usually in a range of 50–250 mg/L in persons receiving the drug therapeutically (during general anesthesia), 30–100 mg/L in those arrested for impaired driving, 50–500 mg/L in acutely intoxicated patients and 100–1000 mg/L in victims of fatal overdosage. Urine is often the preferred specimen for routine drug abuse monitoring purposes. Both γ-butyrolactone (GBL) and 1,4-butanediol are converted to GHB in the body.

In January 2016, it was announced scientists had developed a way to detect GHB, among other things, in saliva.

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