r/Medicinal_GHB_Info

They were right after all about GHB being liquid gold đŸ€·â€â™‚ïž
â–Č 13 r/Medicinal_GHB_Info+2 crossposts

They were right after all about GHB being liquid gold đŸ€·â€â™‚ïž

A cheap compound for 100k?

“GHB is a remarkable molecule because it can suppress depressive ideation and anxiety, sometimes within less than 30 minutes. It also seems to be immediately active on the most severe and treatment-resistant forms of depression. Because of such remarkable properties I jokingly used to call GHB "Or Potable", which means "drinkable gold" in French! Indeed a molecule which can block your depression and suicidal ideas, anxiety, etc, in such an efficient way is as precious as gold because it can save your life. GHB saved my own life many times when all other antidepressants failed.”

Claude Rifat

u/yshcrp — 5 days ago
â–Č 11 r/Medicinal_GHB_Info+1 crossposts

Interesting article about GHB


The Great GHB Debate

Behind the media reports is an intense GHB debate comprised of two very vocal opposing factions — on the one side is the FDA, DEA, and families whose loved ones reportedly died of GHB overdose. This is the group that has conducted a public awareness campaign and is responsible for getting GHB made into a Schedule I drug.

On the other side of the debate is a much smaller group of doctors, researchers, and GHB users, including narcoleptics, who are sometimes prescribed GHB to treat their debilitating daytime sleeping disorder. This group claims GHB is an exceedingly safe and useful substance that has been banned for the benefit of pharmaceutical companies, who they say are intrinsically intertwined with the FDA. They point out that the mainstream press often refers to GHB as a ‘designer drug’, but it is a natural substance found in meat and vegetables and every cell of the human body.

Central to the debate is the case of Hillory Farias, a seventeen-year-old La Porte, Texas, girl whose 1996 death was attributed to GHB overdose. Before the Farias case, no death had been attributed exclusively to GHB ingestion alone.

Dr. Ward Dean, co-author of ‘GHB: The Natural Mood Enhancer’, describes GHB as “one of the most useful substances known to man.” He is so confident in GHB and its precursor chemicals’ safety that he gives it to his kids to help them sleep.

After studying the autopsy report, Dean and his team say GHB had nothing to do Farias’ death. First, the amount of GHB found in Farias’ body isn’t even enough to get someone high.

In clinical studies, rats are regularly given many times that amount of GHB without dying. Narcoleptics use much higher doses of GHB daily without any reported side effects and three grams of GHB is typically prescribed to induce sleep. They also point out that Farias died in her sleep many hours after getting home.

Since GHB is a fast acting molecule, any effects from unusual toxicity would have showed up within an hour, they say. GHB overdose causes deep sleep within minutes, but Farias was able to say goodbye to her friends, get out of the car, get inside her house and climb into bed on her own.

Also GHB is naturally found in the blood post-mortem, says Dean. Up to 168 milligrams have been found in the blood of cadavers that had not ingested any GHB. Dean believes that that body can produce huge amounts of GHB at the time of death as a way to try and protect the brain and organs from low oxygen levels, thus essentially any death can be attributed to GHB ingestion if that’s what investigators are seeking.

Dean and his team say the coroner eventually determined that Farias suffered from a congenital heart disease, and died as the result of a blood clot. Nevertheless, the title of the bill that President Bill Clinton signed is officially called the Hillory J. Farias and Samantha Reid Date-Rape Drug Prohibition Act (although neither of the girls were sexually assaulted).

In Samantha Reid’s case, she died the day after GHB ingestion. The death was blamed on GHB, although the drug leaves the body within a matter of hours. Reid’s parents were conspicuously absent from the list of people who testified in support of the bill named after their daughter.

Full article: https://andewanderer.com/?portfolio=ghb-death-of-a-party-drug

u/yshcrp — 8 days ago
â–Č 2 r/Medicinal_GHB_Info+1 crossposts

Grok: Which is worse for the liver, alcohol or 1,4 BD?

Alcohol (ethanol) is generally much worse for the liver than 1,4-butanediol (1,4-BD), especially with chronic or heavy use. pubmed.ncbi.nlm.nih.gov

Alcohol (Ethanol) and Liver Damage

Ethanol is a well-established hepatotoxin. Chronic heavy consumption leads to:

‱ Alcoholic fatty liver (steatosis), alcoholic hepatitis, fibrosis, and cirrhosis.
‱ It causes oxidative stress, inflammation, fat accumulation, and cell death in the liver via metabolism (primarily by alcohol dehydrogenase and aldehyde dehydrogenase, producing acetaldehyde and reactive oxygen species).
‱ Epidemiology: Alcohol-associated liver disease (ALD) affects millions globally (prevalence around 4-5% in general populations, much higher in heavy drinkers). It accounts for a large share of liver disease deaths, cirrhosis cases, and transplants. Mortality rates have risen significantly in recent years. pubmed.ncbi.nlm.nih.gov
This is dose- and duration-dependent, with risks escalating over years of regular heavy drinking. Many people develop irreversible damage.

1,4-Butanediol (1,4-BD) and Liver Effects

1,4-BD is an industrial solvent and GHB precursor. It is metabolized in the liver primarily by alcohol dehydrogenase (ADH) to gamma-hydroxybutyraldehyde, then to GHB (via aldehyde dehydrogenase). This shares metabolic pathways with ethanol, leading to competitive inhibition when both are present. pmc.ncbi.nlm.nih.gov

Evidence on hepatotoxicity:

‱ Animal studies (e.g., rats) show mild-to-moderate liver inflammation or minor changes at high doses (e.g., 500 mg/kg), but not severe or statistically strong organ-specific toxicity in subchronic studies. No strong carcinogenic signal. ntp.niehs.nih.gov
‱ In human recreational/chronic misuse (often high/frequent doses), reports mention toxic hepatitis as a complication, along with other organ effects (kidneys, heart, etc.). This occurs in the context of heavy polydrug or compulsive use. pmc.ncbi.nlm.nih.gov
‱ Acute overdoses can cause severe effects (respiratory depression, coma, death), sometimes mimicking toxic alcohol poisoning, but liver damage is not the primary acute feature. Co-ingestion with ethanol can worsen outcomes, including increased mortality and tissue damage in animal models (due to competition for ADH, leading to higher levels of the parent compound or altered kinetics). pubmed.ncbi.nlm.nih.gov

1,4-BD lacks the extensive long-term population data of alcohol; use is less common and often episodic or addictive in specific contexts rather than a daily societal norm.

Key Comparison and Caveats

‱ Chronic exposure: Ethanol has far stronger, dose-dependent evidence for progressive liver scarring and failure. 1,4-BD can contribute to toxic hepatitis in heavy users but appears less potent per se for long-term fibrotic/cirrhotic disease.
‱ Acute/high-dose: Both are risky; 1,4-BD has a narrower therapeutic window for CNS/respiratory depression (via GHB), and mixing with alcohol is particularly hazardous. nejm.org
‱ Individual factors: Genetics (e.g., ADH/ALDH variants), dose, frequency, nutrition, and co-exposures matter for both. Neither is “safe.”
‱ Neither is recommended: 1,4-BD is not for human consumption and carries risks of addiction, overdose, and multi-organ toxicity.

Bottom line: Alcohol poses a substantially greater overall risk to the liver due to its prevalence, well-documented chronic effects, and public health burden. 1,4-BD is toxic (especially acutely or in combination), but not a comparable driver of widespread liver disease.

reddit.com
u/yshcrp — 14 days ago