One thing that would actually resolve this rather than argue it: 5-S-cysteinyl-dopamine. It’s the downstream product of the GSH-conjugation branch of dopamine-o-quinone, it’s been measured in human plasma and CSF in PD research, and it is a direct readout of flux down the exact pathway we’re arguing about. Research assay, not clinical, so you’d need a collaborating lab. But it’s the one measurement that converts this from mechanism-arguing into data.
5-S-cysteinyldopa — the L-DOPA conjugate, not the dopamine one — is a real melanoma marker with validated automated plasma and urine assays (ScienceDirect) and clinical availability in Japan and historically Sweden. It is not a proxy for what you care about; it’s driven by melanocyte tyrosinase activity. Don’t let the name similarity tempt you.
Sample handling as a hard gate. Even with a willing lab, this isn’t a mail-in. The validated protocol requires immediate centrifugation and freezing after collection, near-total exclusion of light and oxygen during extraction, and constant sample cooling. (ScienceDirect) Catechol conjugates oxidize on the bench. You’d need a phlebotomy draw next to a centrifuge and dry ice, with the lab shipping you a kit. That’s a collaboration, not a purchase.
Trying Vyvanse again today, a very tiny dose, this makes me feel well already. Will report later how it feels.
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Trying what?
What is the significance of this?
Cathionines have lower VMAT2 activity than AMPH so I suspect they are less neurotoxic
But not all of them
3-MMC, 4-MMC are what some rly like…
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