GHB: Much More Than You Wanted to Know
This article was written in 2020.
GHB, or gamma-Hydroxybutryic-acid, is pretty darn similar to alcohol. It causes relaxation and euphoria, mostly by acting on GABA in the brain. High doses cause loss of conscious and depressed breathing. Higher doses kill you. Both substances decrease inhibition and produce a similar buzz (body high). GHB sometimes causes nausea and vomiting, though less consistently than alcohol does. In high doses, it always worsens motor skills / general bodily control, though to a lesser degree than alcohol. Consistent use of GHB can lead to tolerance and physical dependence. Withdrawal is terrible and can cause seizures and actual death.
Notably, GHB does not cause a hangover (thought it does have a peculiar rebound effect – more on that later). A medium dose is about 2.5 grams, takes effect in 15 minutes, and lasts about 2.5 hours. It has a steep dose-response curve; 1.5g threshold, 5g pass-out, 10g death are reasonable estimates for most people. (See Appendix for more info on dosage). It usually is kept and consumed as a solution (dissolved in water). Its effects increase superlinearly with alcohol – three drinks on a normal GHB dose probably lead to vomiting or passing out. GHB is notorious for being (allegedly) a common date-rape drug.
Ready for the twist? GHB is a prescription drug in the US! It’s prescribed to patients with narcolepsy; apparently GHB both helps induce sleep and increases the quality of sleep. And, other than the addiction and overdose potential, it is a remarkably safe drug – no long-term heart/liver/brain damage, as far as anyone can tell. Prescription GHB calls itself ‘sodium oxybate’ for some reason, and is only available under the brand ‘Xyrem’.
Effects
(Epistemic status: I’m relying heavily on my own experience here. I take GHB about twice a week when I have it – I’ve probably used it 100 times in my life. I’ve taken and talked about it with all my friends who care to try it. They say that drugs affect everybody differently; your experience may not align with my descriptions.)
As I mentioned earlier, alcohol is indeed a good comparison to GHB, and I’ll be comparing them a lot. It’s worth noting that alcohol is not the absolute closest drug, effects-wise. Phenibut feels even more similar, and then there’s GBL and 1,4-BDO which are metabolized into GHB. In any case, I’ll stick to comparing GHB with alcohol — both because we’re all familiar with alcohol and also because it can play a similar role to alcohol in daily life. Anyways: if GHB is so similar to alcohol, why do people actually take it? The short answer is that it’s more euphoric, less impairing, and doesn’t leave you with a hangover. The long answer is — well, this essay.
Let’s start with the physical euphoria. Most of GHB’s euphoria comes from its really strong body high. On GHB, you feel a constant energetic pulsing throughout your body. Sometimes this feeling is general and hard to pinpoint; other times you feel it located in a particular area, like your feet or groin. This body high can rival MDMA’s in terms of intensity, which is probably what inspired the epithet “liquid ecstasy”. Despite this intensity, the body high feels qualitatively more like like an alcohol buzz than an MDMA buzz (in my experience). Some describe the feeling of GHB as being between alcohol and MDMA; I think this is mostly right, although it’s about 9 parts alcohol to 1 part MDMA. This MDMA comparison is further apt because GHB’s bodily euphoria comes with a heightened pleasure in tactile sensations. This effect is smaller here than with psychedelics or MDMA, but it is noticeable, and it stands in stark contrast to alcohol and other GABA drugs which tend to numb the body. This is also responsible for some of GHB’s appeal as a sex drug, which we’ll discuss in a bit.
Then there’s the nonphysical (or “cognitive”) euphoria. Even when sober, this feeling is nebulous and it’s hard to describe what it actually feels like, at least for me. To a first approximation, nonphysical euphoria feels like being in a good mood. This description fails to evocate because A: it’s abstract and B: there are many different types of good moods. There’s the good mood associated with being content; with having been productive; with resting after exercise; with having won a game; with feeling clever; with feeling confident and sexy (“I’m feeling myself tonight!”). In the case of GHB, the nonphysical euphoria is most clearly attributable to confidence and lack-of-anxiety. Sounds like alcohol, right? Yes, but not really. Yes on the neurological level; GABA drugs decrease anxiety through their GABA action. Not really on the psychological level; I think GHB reduces anxiety mostly through a different mechanism than alcohol does. Allow me to elaborate.
(Epistemic status: armchair theory.)
Alcohol really lowers inhibition. When you’re sufficiently disinhibited, you don’t think before acting. That means no worrying about what to do, no imagining scary situations in which bad things follow from a hypothetical action, no thinking about things that could’ve happened. These mental actions are all anxiety-inducing, especially when you’re in a situation where you’re self-conscious and thinking a lot about your actions (say, a party for many of us?). Similarly, alcohol gives you confidence by making you not think about the things that make you insecure. GHB lowers inhibitions, but not nearly as much. Instead, GHB consistently gives you a confidence boost. You not only feel good, you feel like you are good; and you feel like this even though you’re still thinking about the ways in which you’re bad.
My claim here is that GHB increases confidence directly, whereas alcohol’s confidence-boost is downstream from its lowering of inhibitions. This may seem like a trivial framing difference or even downright untrue, but I think this point both explains why the drugs have different effects and elucidates how they subjectively feel different. I just said that alcohol gives you confidence, but for most of us it only sometimes does this and often causes the opposite: hating yourself, feeling self-conscious and stupid, “wallowing in self-pity”. In the wrong context — such as when you’re alone in your room and thinking uninhibitedly rather than acting uninhibitedly — lower inhibitions can actually decrease confidence.
(With all this said, I still think that alcohol’s peak and average effect is stronger in the anxiety department whereas GHB’s is more consistent and less intrusive.)
There are a few other contributors to euphoria worth mentioning. First is a broader sense of relaxation (separate from not being anxious) – pretty much identical to alcohol. Second is a general feeling of love (for yourself or your friends) – similar, but again the context matters much more with alcohol, as it can sometimes heighten anger and hatred rather than love. Third, there’s a silliness or sense that things are simply more fun — alcohol wins in this category. And then there’s the rest of the euphoria, the euphoria that is not explained by any of these things but is very real and very ineffable. Overall, in the category of nonphysical euphoria, GHB wins in consistency and in mean effect-size as well (for most people, although some find alcohol to be a better time.)
Now, let’s talk about impairment. GHB is less impairing than alcohol (not like that’s a high bar!). On a low-medium dose of GHB (think 3 drinks), there’s almost no noticeable impairment. Your thinking feels (and hopefully is) completely normal, and while I’m not going to tell you it’s okay to drive… Ahem. In medium-high or higher doses, you are undoubtable impaired. I find that my balance and motor skills are pretty good, but I get double vision and have trouble with visual focus (no heavy machinery!). And while I feel clear-minded, I have trouble planning my sentences out and finding the right words; statistics indicate that I’m significantly worse at word games. I’ve observed that I particularly struggle with giving explanations on a high dose of GHB.
Decision-making suffers surprisingly little, even at high doses. Partially this is because you remain somewhat inhibited. Partially it’s because you still can (and do) think about things + remember and respect your sober self’s preferences. It also doesn’t lead to emotional amplification in the way alcohol can, which is a real catalyst for regrettable actions.
I cannot in good conscience end this section without talking about GHB and sex. If anything deserves to be called a sex drug, it’s this one; and it gets this reputation in the gay community, where it’s used casually or for more hardcore ‘chem-sex’ sessions. It increases libido and makes touching feel really good. GHB does not cause performance problems in males, and in fact leads to greater performance control. Fun fact: among the GABA drugs, only GHB and phenibut are generally renowned for having positive sexual effects.
GHB & Sleep
So, what’s up with this GHB-being-prescribed-for-narcolepsy thing? Well, narcolepsy is essentially caused by having naturally terrible sleep quality (at least for some patients). According to Wikipedia, people with narcolepsy have “abnormal REM sleep” and “excessive daytime sleepiness”, and there is a causal relationship here in exactly the way you’d expect. Irrelevant but fascinating is the fact that narcoleptics usually have more REM sleep than normal. Anyways, GHB’s medicinal effect here comes from its benefit on sleep quality; patients report sleeping better on it and sleep studies support this. As expected, this leads to a reduction in daytime sleepiness as well as reduction in a bunch of the other unpleasant narcoleptic symptoms, like cataplexy, “an episodic loss of muscle function, ranging from slight weakness… to a complete body collapse.” (This is the thing where someone with narcolepsy randomly stops moving and appears to be asleep — they’re not asleep, by the way.)
This all is really cool and really question-inspiring: how does GHB benefit sleep, does it work for non-narcoleptics, is it a valid prescription for workaday insomnia? Research says that regardless of one’s narcolepsy status, GHB increases slow-wave sleep and decreases REM sleep. Sleep is complicated, but it apparently can be hierarchically divided into different stages based on ‘depth’. The REM stage is where you dream and is a ‘light’ stage, whereas slow-wave is the deepest stage. You get more rest from deeper stages than from light stages, which is why trading REM for slow-wave counts as an increase in quality. While I find this explanation lacking — why do spend so much time in REM then? — it’s hard to find any deeper theory that is uncontroversial; there really is no scientific consensus on many questions related to sleep. In any case, getting more slow-wave probably is a good thing for most of us, so I conclude that GHB does increase sleep quality in non-narcoleptics.
With this said, we need to think about the effect size here. GHB is genuinely life-changing for some narcoleptics, so I’m going to call its effect size ‘large’ for narcolepsy patients. This is great for them, of course, but it shouldn’t give the rest of us high hopes. First, the relevant baseline for a narcoleptic is really terrible life-deforming sleep quality. There is probably a bigger difference between that kind of sleep and normal sleep than there is between normal sleep and perfect sleep; improving sleep quality simply doesn’t matter that much when your sleep quality is already good. Second, GHB’s REM-reducing effects are probably less important the less REM you naturally get — consider that reducing REM would do nothing if you were already at 0. Anecdotally, people who usually sleep fine don’t report feeling anything special after a night of GHB sleep.
In between the healthy sleeper and the narcoleptic lies a third type of person: the mediocre sleeper. Of course there are many types of mediocre sleepers — examples are left to the reader’s imagination. I haven’t seen any research on what GHB does for sleepers who feel like they toss-and-turn too much. Based on our theory, I think it would be quite helpful for people in this group; tossing-and-turning implies shallow sleep. On the other hand, I don’t think GHB would be much help to people with sleep-apnea or small bladders. Still, I’m surprised that this drug hasn’t really been tried for sleep problems outside of narcolepsy. While lots of drugs make it easier to fall asleep, very few drugs actually increase the quality of sleep — Ambien supposedly does (at least temporarily), but alcohol, Xanax, and Benadryl do not. GHB seems like low-hanging fruit, and I legitimately wonder why it isn’t being investigated more thoroughly by sleep scientists.
Then there’s the fourth and final type of sleeper worth talking about here: the insomniac. Again there are many importantly distinct subtypes here; let’s just consider the sleeper who has significant trouble falling asleep even when sleepy but who sleeps well once asleep. GHB can certainly induce sleep, though it doesn’t consistently knock one out unless the dosage is high. If what I’ve said about this drug is right — that it’s safe, doesn’t cause a hangover, and actually improves sleep quality — then isn’t a high dose of GHB the perfect medication for an insomniac? Unfortunately the answer is no; the culprit is GHB’s rather bizarre “rebound” effect.
The actual logistics of taking GHB for narcolepsy illustrate this rebound — meaning sleep rebound or wakefulness rebound, depending your perspective — quite well. Patients are instructed to take two doses of GHB every night. They take their first dose at, say, 12:00 am. They’re asleep and under the influence of the drug by 12:20. At 4:00, they wake, sans alarm, with a start. They dose again, fall back asleep by 4:20, and wake up (sans alarm, with a start) at 8:00. This happens to most people that take GHB for sleep; about four hours after you take GHB, the rebound occurs and you are suddenly feel (and are) awake. Here’s the kicker: this rebound lasts for about two hours, and you probably can’t fall asleep unless you take another dose.
I called the rebound effect a culprit earlier, which was a presumptuous value judgement. There are some people for whom the rebound is actually positive — so long as you want to sleep 8 hours every night, it’s pretty much just a free energy boost in the morning! But for most of us, the rebound at best annoying and at worse constricting. If you want to sleep for a length of time that isn’t precisely 4, 8, or 12 hours, you’re out of luck. (Of course, these exact numbers will be different for different people.) Okay, I exaggerate; most users could set an alarm to wake up 30 minutes early and be completely fine. 2 hours early? Not so much. Assuming that you actually manage to wake up (it’s hardest to wake up during deep sleep, remember!), you’ll find that you’re intoxicated from the last dose, which means that you’ll feel very sleepy. If you successfully remain awake (and if you have no morning obligations involving operating heavy machinery), you get to be high for an hour, which could be fun.
The rebound can also be a real nuisance if you fail to fall asleep after your dose. Given GHB’s hypnagogic effects, this doesn’t seem like it would ever be a problem. In reality, things happen: you’re really anxious, or having a bout of insomnia, or the baby starts crying, or you’re not actually tired. And since GHB sort of forces its user into an 8-hour a night sleep schedule, those who naturally sleep less will probably find themselves struggling with the latter. Whether or not the rebound effect presents a serious problem, then, depends on the individual. For most people, it’s probably a net mild annoyance. I have what seems to be a 25-hour circadian rhythm, I am afflicted by random bouts of intense insomnia, and I like to sleep 9 hours a night; for me, the rebound effect is deal-breaker.
A few miscellaneous comments before we move on. First, the severity of the rebound effect differs from person to person — I have friends who say they don’t experience it all. Second, many regular users report developing a tolerance to GHB’s hypnagogic effects. Lastly, GHB usually comes as in the form of Na-GHB. GHB is really salty, both in the taste-sense and in the contains-sodium-sense; consuming a couple extra grams of sodium every day guarantees exceeding the daily recommended limit, for what that’s worth.
Pharmacology
Did you know that your brain has literal GHB receptors? It follows that GHB is a neurotransmitter, and your body naturally produces tiny amounts of it. Though having your own receptor indubitably gets you a lot of street-cred if you’re a drug, the GHB receptor appear to be remarkably unimportant in terms of the drug’s primary high. It’s not entirely clear what these receptors do, but the general vibe of them is not a psychoactive one. Wikipedia says the GHB receptors are “riboflavin transporters”; activating them “does not produce a sedative effect, instead causing a stimulant effect followed by convulsions at higher doses, thought to be mediated through increased Na+/K+ current and increased release of dopamine and glutamate.” Well, GHB does produce sedative effects, so this can’t be the whole story. (What about that dopamine and glutamate stuff? We’ll get to that later.)
Most of the story is found in the GABA domain. The fastest way to understand what GABA does is to think about the drugs that affect it — alcohol, Xanax, Ambien, phenibut. These drugs work mostly by increasing your brain’s quantity/release of the neurotransmitter GABA or by directly activating (“agonizing”) GABA receptors. In general these receptors straightforwardly cause relaxation or sedation upon activation though there are various kinds of GABA receptors that do different things.
GHB is a weak GABA-B agonist, “agonist” meaning that GHB molecules directly activate the GABA-B receptor, “weak” meaning… I don’t know, but that’s what Wikipedia says. GHB is also a precursor to GABA. “Precursor” meaning GHB molecules are used by your body to make GABA; “your body making GABA” meaning more activation of GABA receptors, probably. These neurochemical effects are why GHB is relaxing, euphoric, sedating – in short, a lot like alcohol & friends.
What about that weird GHB rebound, though? Here’s where we need the GHB-receptor! (Epistemic status: Wikipedia doesn’t talk about this.) Activating the GHB-receptor increases release of dopamine and glutamate, remember. These are the two primary excitatory neurotransmitters, which basically means they cause physical and mental stimulation. We’ve found our rebound culprits, eh? Well, I think so, but I actually cannot find any source that tries to connect GHB’s pharmacology to its rebound effect. So, epistemic status: the rest of this section is me theorizing, I have no formal education in pharmacology and frankly no idea if what I’m about to say is plausible, and I would love comments and/or to be corrected on this.
Let’s think about the schedule of effects after taking GHB. You’re sleepy and horny from hours 0-2; from hours 2-4 you might have difficulty falling asleep, but you’ll sleep soundly if you were already asleep; at hour 4 you’re aggressively woken up; and from hours 4-6 you’re very awake. Also, the difference between dopamine and glutamate is relevant here. The oversimplified, ELI5 version of this is that dopamine is euphoric/motivating while glutamate is awake/ready-to-move-your-muscles. (Consider that it’s easy to fall asleep after sex, an activity which presumably increases dopamine.)
With this in mind, here’s what I think this excitatory neurotransmitter release looks like. Hours 0-2 are medium dopamine and no glutamate; hours 2-4 are low dopamine and low glutamate; hours 4-6 are no dopamine and high glutamate. This schedule is consistent with the effects of GHB on sleep. The dopamine action from hours 0-2 explains three of GHB’s unusual properties as a GABA-drug – aphrodisia, euphoria with some distinctly non-GABA tinges, and the feeling of clear-mindedness (relative to its ‘drunken’ effects).
This is a nice theory (a ‘just-so’ theory?). The main problem I see with this theory — well, beside the lack of pharmacological evidence that the GHB receptor actually works this way — is that it requires a rather contrived mechanism of action: dopamine release on a different schedule than glutamate release on a different schedule than GABA action, all from the same drug. Contrived as it may be, at least it’s possible. Here’s what I think is going on in the body:
- Some % of ingested GHB is converted by the body to GABA. This happens continuously for ~2 hours.
- Most of the remaining % agonizes the GHB receptor, where it stays for ~2 hours.
- Activation of GHB receptors causes dopamine release ~immediately.
- Activation of GHB receptors causes glutamate release on a ~3-hour delay.
Is this plausible? No idea. In any case, there is a real puzzle here.
Conclusion
GHB is a good and underappreciated drug. Lots of people would benefit from taking it instead of alcohol. It’s pharmacology is a bit of a puzzle.
Am I overselling it? Or is it genuinely a recreational wonder drug? Is GHB the all-purpose-sleep-medicine of the future? I have no doubt that I live in a bubble of GHB positivity. Still, I feel that this drug has been underappreciated by everyone from scientists to partiers. I worry that I might be overlooking something important here; it seems like I must be biased.
I’d like to hear what everyone else thinks.
Appendix: Dosing & Danger
Earlier I said that ~10g of GHB could cause an overdose/OD. By ‘OD’ I mean a dose that’s lethal if left untreated, assuming the subject is healthy and has no other drugs in their system; also, I’m not talking about death from vomit aspiration, which can happen at lower doses. I got this 10g number from Erowid, though Erowid doesn’t provide a source and I suspect it was made up at some point. This source says “a [GHB] concentration in plasma of ~100 mg/L produces euphoria and disinhibition, whereas 500 mg/L might cause death from cardirespiratory depression.” From this, I would infer that an OD is ~5x a recreational dose, which puts it in the ballpark of 10g. Unfortunately, this 500mg/L number also seems to be ‘made up’ here, and I’m not sure it passes a sanity check; this seems too close to the ‘deep sleep’ dose of 300 mg/L.
Outside the lab, we can look for information in the data of death results. What we really want is data showing how much GHB was taken in cases where the victim only had GHB in their system and died from respiratory failure, and unfortunately this data seems not to exist. Here’s what I did find. This UK article mentions 92 deaths from ‘drug poisoning’ in which GHB was the only drug mentioned on the death certificate (I don’t know if deaths from drug-induced-vomit aspiration are classified as ‘drug poisoning’). This US source finds 71 GHB-only deaths and 30 deaths “in victims left ‘sleeping’ or ‘snoring’ by their friends”. This Australia article mentions 74 GHB-related deaths, though “many of the deaths involving inhaling vomit (aspiration) could possibly have been avoided by placing the person in a recovery position” and more than 90% of cases involved other drugs. Among these 74 cases, the median GHB blood concentration was 230mg/L (and the maximum was 1350mg/L). All in all, this doesn’t really tell us anything about the OD dosage.
And then there’s this source, which says the LD50 of GHB is 1.7g/kg in rats and 3.3/kg in dogs — this seems insanely high. It also says that 50-70mg/kg causes “full narcosis, hypnotonia, coma…” in humans and 10mg/kg causes “short-term memory loss, muscle weakness.” (10mg/kg works out to .7g for a 150lb person, which is probably a sub-threshold dose). Either my scientific literacy sucks or this is seriously wrong. My is that I think this source is untrustworthy / I’m not sure what to make of it / I would like to know how the hell they got those numbers and thought they were reasonable.
The strongest evidence that the OD dosage might be > 10g is the fact I can’t actually find any anecdotes about people ODing from <= 10g doses — though note that I haven’t searched very hard. The truth is that I really don’t know what the GHB OD dosage is. 10g might be right, and I would say that it’s probably good for you if in any case if that dosage is with very dangerous to have in your head. If I were forced to put money on it, though, I would bet that the OD dosage for a 150 lb male is at least 1.5x higher. And remember, this is all considering that there no other drugs present; alcohol causes this number to drop a lot. Please be safe.
In practice, people have a lot of trouble with properly dosing GHB. How can you avoid these troubles? First, figure out what dose (in grams!) works for you, and figure this out slowly and over multiple sessions; start with 1.5g and increase the dosage by no more than .2-.4g per session. In reality, this might be difficult (and you may only be able to get an approximate answer) due to the other main dosing problem — knowing how much GHB you’re actually taking. This easy if you have pharmaceutical GHB of course. Illicit GHB sometimes comes in a powder/dry form, so you can weigh your doses. Most of the time, though, it comes as a solution (probably since GHB is hydrophilic and is annoying to keep solid). In these cases, you’ll want to use a mL-metered syringe to measure dosage. The seller might tell you what the concentration is, though of course that isn’t reliable — you could also weigh the solution to figure out its concentration.
When consuming a new source of GHB, start conservative and gradually increase dosage. It helps to know that the max concentration of GHB in water is ~.8g/mL — this also means you won’t kill yourself by starting with 3mL. Well, unless the ‘GHB’ is actually GBL, which isn’t that unusual since GBL is easier to synthesize/procure. Each gram of GBL is converted by the body into ~3 grams of GHB, meaning GBL is 3x stronger by weight (and by volume if undiluted). The best way to identify GBL is by its taste; GBL has an intensely unpleasant and ‘chemical’ taste whereas GHB has a salty (and slightly unpleasant) taste.
[0.9] You can also get (in theory) Ka-GHB. This solves the issue of sodium, and maybe the potassium is even good for you? I’m not sure about this one; potassium bioavailability is kind of complicated.[^099]
[0.99] Sorry about the numbering on the footnotes. I added a footnote spatially prior but temporally posterior to footnotes 1 and 2, so I decided to be clever and save myself some time by 0-indexing. Then I wanted to add another footnote spatially between 0 and 1, and then another between that one and 1, and things just spiraled out of control.
[1] Your brain has an impressive variety of GABA receptors, all which produce some sort of relaxation or sedation upon activation. GABA receptors are either ligand-gated ion channels or G protein-coupled receptors (whatever that means). What matters here is that this is used to divide the receptors into two clean classes, GABA-A and GABA-B — usually, we just talk about these classes. GABA-A seems to produce more sedation than GABA-B.
[2] Dopamine does cause these effects (aphrodisia, euphoria, clear-mindedness), but we are still left to wonder why GHB increases sexual arousal more than many stimulants (which have a greater dopamine effect). Here are two possible explanations: first, because the stimulant’s attention-enhancing effect is causing the user to be intensely focused on something non-sexual; second, because stimulants also increase norepinephrine, which increases stress and vasoconstriction (thus decreasing libido).
[R0] I think most people who take GHB to sleep wake up ~4 hours after the first dose, but this is by no means universal. One long-time, low-dose user with narcolepsy reports that they have to set an alarm to take their second dose and they sometimes sleep through this alarm. Apparently this only started happening after they had kids.
[R1] The problem with using phenibut for sleep is that tolerance builds faster and regular use leads to insane physical dependence. It’s common to develop physical dependence from using phenibut 4x a week and some people report withdrawals from even 2-3x a week. For whatever reason, GHB is on the other extreme of the physical-dependence-relative-to-effects spectrum; 1x daily usage definitely doesn’t lead to dependence and 2x daily seems not to lead to withdrawal for most.[^R2] This may not apply if phenibut is used in low doses (250-500mg). There’s also the question of whether it boosts sleep quality as much as GHB, especially if we’re talking about low dose phenibut; does phenibut work for narcoleptics? My guess is that it is does in high dose but not in low dose, though I haven’t seen any studies on that. [Thanks to AlgiSigmaAlgeba on Reddit for bringing this up.]
[R2] I wonder why this is. For comparison, note that lots of people don’t get physical dependence (and only get a small increase in tolerance) from extended daily medium alcohol consumption, whereas daily Xanax consumption usually leads to physical dependence. Some of this is attributable to duration of action — phenibut lasts 10+ hours — but this is only a partial explanation.
[R3] Here’s something interesting from PolymorphicWetware on Reddit: “Hmm, I just realized, isn’t GHB’s 4-hour rebound effect sort of like what polyphasic sleep is like? Is there a possibility that the GHB receptors in the brain have something to do with polyphasic sleep?”
[R4] Regarding toxicity, there are multiple studies that show that GHB causes impairment in learning and spatial memory… in rats. And then there’s one human study that looks at three groups with 27 subjects each: GHB users who have had >=4 GHB-comas, GHB users who haven’t had a GHB-coma, and non users. It finds that the GHB-coma group has a lower IQ and does worse on a verbal memory test; no significant difference is found between the GHB-NoComa and No-GHB groups. This is just an observational study and there are compelling non-causal explanations for the worse performance of GHB-coma group. (Note that this study uses ‘coma’ to mean ~‘no motor, verbal, or eye response’.) Overall it’s plausible that GHB negatively affects memory, though there’s not much scientific evidence either way. If it does, the effect size is probably <= than that of alcohol on memory, which is pretty damn small in real-world terms (unless we’re talking serious abuse).
[R5] After writing this, I found a detailed paper on GHB pharmacology. Unfortunately, it’s in French. Google translate gives me this snippet from the abstract (which is apparently called the ‘resumé’ in French): “Massive absorption of GHB desensitize GHB receptors and this modification, together with a direct stimulation of GABAB receptors by GHB, induce a perturbation in GABA, dopamine and opiate releases in several region of the brain.” Probably there’s some good stuff in here, though I’m currently content with the untranslated paper simply because of its French beauty.
(fig 1 — French beauty)