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for educational and safety purposes
sci-wiki~$open stack stimulant-recovery
twelve items for the months after heavy stimulant use, ranked honestly: one has a real human trial, most have none
12 items; 10 structures drawn from pubchem, 2 drawn generically because pubchem has no record of the name.
The problem this aims at is real and well measured. Dopamine D2 receptor availability is genuinely lower in methamphetamine users, and it tracks with reduced frontal metabolism; the flatness, the anhedonia and the months of low drive after heavy stimulant use are a described clinical picture rather than folklore.
What this roster does not have is a body of evidence matching the confidence of the mechanistic story usually told about it. Every claim behind these twelve items was checked against the primary literature, and the results were lopsided: citicoline has a randomised, double-blind, placebo-controlled trial in exactly this population with a structural imaging endpoint, and almost nothing else here has been given to a stimulant user in any study at all. Several of the mechanisms cited most confidently are contradicted by the papers they come from.
So the ordering above is by evidence rather than by theory, which is the opposite of how the brief was written. Citicoline first because it earned it. The precursor and receptor-upregulation arms are marked for what they are. Six items carry an optional flag, and that is not politeness; it is the list of things to drop first if this gets expensive.
The items that plausibly combine are the membrane and mitochondrial layers, and they are also the cheap half. Citicoline supplies cytidine and choline for phosphatidylcholine synthesis, uridine feeds the same pathway from the other end, and the fish oil most people already run supplies the fatty acid; that trio is the one part of this stack whose biochemistry is uncontroversial even where the clinical benefit is unproven.
Acetyl-L-carnitine, PQQ and astaxanthin are the oxidative-stress layer. They overlap heavily with each other, which is why two of the three are marked optional; running all three is unlikely to add much over running one.
Agmatine and inositol are the only night-time items and they are deliberately kept away from the morning stack. Agmatine's rodent anxiolytic work runs through imidazoline receptors rather than the NMDA modulation it is usually credited with, which matters if it is being taken for sleep rather than for the dopamine story.
⚠️ TTFD and any other thiamine derivative are the same intervention. Do not stack them.
The honest description is that recovery from heavy stimulant use is slow and mostly not pharmacological, and people who expect a stack to compress it are usually disappointed in the first month. What gets reported from something like this is a gradual return of ordinary motivation rather than anything acute.
The two items with a same-day character are TTFD and tyrosine. Both are stimulant-adjacent in feel, and both are the items most likely to be mistaken for the recovery itself.
⚠️ THE FRAMING THIS ROSTER CAME WITH IS WRONG ABOUT D3, AND THE ERROR POINTS THE DANGEROUS WAY. D2 availability is reduced in stimulant users; D3 is ELEVATED, by roughly 46% in the substantia nigra on human PET and one- to threefold in post-mortem cocaine cases, and that elevation is linked to drug-wanting. Any protocol aiming to raise D3 in recovery would be worsening the thing it is trying to fix. ⚠️ 9-me-BC HAS NO HUMAN EXPOSURE DATA OF ANY KIND, and beta-carbolines are a family with a neurotoxin reputation; 9-methyl-beta-carbolines are photosensitising DNA-damaging agents in vitro. It is the most speculative item here by a wide margin. NSI-189 missed its primary endpoint in a phase 2 depression trial, and the hippocampal-volume result it is usually cited for was not significant in the trial that measured it. Cortexin's evidence base is essentially absent from indexed literature. Neither is an approved medicine. Tyrosine, TTFD and any residual stimulant use are a bad combination; the point of this list is the period AFTER stopping, and pushing catecholamine synthesis while still using is not recovery. Stimulant withdrawal carries real depression and real suicide risk, and it is the one part of this that a supplement stack does not address. If the low mood is severe or lasting, that is a doctor's problem and not a shelf's.
nothing flaggedcurated roster
every pair here reads as compatible on the mechanisms the site holds. that is the absence of a known conflict, not a clearance.
9 of 12 in one basketAmazon
9 of 12 priced
3 of these carry no listed price, so there is no honest total to print; the lines above are what can actually be costed.
5 overlapssame lever, twice
interested in protocols? join the discord; that is where dosing, timing and the practical side get discussed.
the sci-wiki publishes this as a description of what these compounds do together, not as a recommendation to take them. Nothing here is medical advice.