I am calm. GHB has wreaked havoc in The Netherlands, it is something tweakers consume. Recommending microdosing GHB in my eyes is like recommending microdosing heroin.
> GHB is difficult to dose. The difference between a dose with pleasant effects and the dose at which someone becomes overwhelmed by sleep and becomes unconscious is very small. People quickly take too much GHB. The combination with alcohol enhances the effects of GHB. This means that people can become unconscious even with a small dose of GHB.
To jump in with a nitpick, I would point out that a "microdose", by definition, would be far below "a dose with pleasant effects", and so wouldn't be too hard to dose at all†.
The reason GHB has a narrow tolerance window (which, note, is not exactly the same thing as a therapeutic index, as the upper bound here isn't where the drug becomes toxic; it's just where the drug stops being recreationally "fun" and becomes a potent sleep drug instead) is because you actually require a decently high amount of the drug to get the recreational effect; and then only a little more of it will put you to sleep. But a "microdose" would imply that you're not going anywhere near the dose that gives you the recreational effect in the first place.
The term "microdose" is usually employed in conversations like this to specifically mean "a dose of a normally-conceptualized-as-recreational drug, too small to experience recreational effects" — although it can technically also mean "a dose of a prescription medicine too small to see the regular clinical effect."
People talk about microdoses of e.g. LSD, MDMA, or ketamine, as potential treatments for various mood disorders. In none of these cases is there an expectation that you'd "feel" the drug. It's a microdose, not a dose.
(And a fun tangent, back on the clinical end of things: sometimes microdoses of drugs can have paradoxical or unique effects, due to the particular ligand having higher binding affinity for a postsynaptic autoreceptor than for regular presynaptic receptors, such that microdoses of the ligand will only agonize the autoreceptors, with no accompanying agonism of the regular receptors. Activating the autoreceptor without activating the regular receptors can potentially do all sorts of wacky things — you're essentially giving the receptor's coupled ion channel a "negative stimulus", which for most gated ion channels isn't something they're they know what to do with; it's an "undefined behavior" kind of state. But some of these "undefined behavior" states are very useful! Low-dose naltrexone [LDN] therapy, for example: it has none of the subjective anti-euphoric effects of regular naltrexone therapy; but nor does it have pro-euphoric effects. Instead, it has anti-inflammatory effects, specifically on the tissues of the brain itself [astrocytes + microglia] that express opioid autoreceptors. LDN therapy is thus being investigated as a treatment for ME/CFS.)
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† Presuming that what you have is actually pure GHB. Microdosing GHB's cousin GBL would be a different story, since it is extremely potent, with its active dose (and tolerance window) being measured in micrograms. Don't try to microdose GBL, kids. Not even if you know what solvents dissolve GBL and what serial dilution is.
