But "microdosing" per se isn't the issue.

I once stumbled upon a psychiatry case report about a man with a psychotic illness, who found out by experimentation that taking significantly less of his antipsychotics than prescribed, along with up-titration when he began to notice the prodromal signs of relapse, helped him avoid relapse while also avoiding most of the unpleasant side effects. He did this on his own, only later confided in his psychiatrist he was doing it. Some psychiatrists would have reacted rather negatively, but his (being somewhat influenced by R. D. Laing & friends) actually thought it was smart, and wrote it up.

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.

I added the “pretending to be an adult” part because I knew someone was going to be a pedant about it.