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Dopamine Ratios + Tubulin Stability: a simple, testable map of psychiatric states21.8.2025Epistemic status: exploratory but falsifiable; proposing a compact model to be pressure‑tested.TL;DR: Many psychiatric phenotypes can be sketched by two axes: (A) relative dopamine level and (B) structural stability of neuronal microtubules. Rough cut: ADHD ≈ 0.5× dopa, HPPD ≈ 1.5×, schizophrenia ≈ 2×; de/stabilization depends on tau/tubulin/BDNF/inflammation. If microtubules collapse, control reroutes through the amygdala → boundary‑pushing compulsions. Model yields concrete lab/clinical predictions below.ClaimsA1: Phenotype ≈ f(dopamine setpoint, microtubule stability).A2: “Amygdala‑override loop” occurs when frontal inhibition is offlined by microtubule collapse → intrusive thought → compulsory act.A3: Some existing psych meds (e.g., lithium/valproate via GSK‑3β→tau) are indirect tubulin stabilizers; future CNS‑safe microtubule stabilizers should restore frontal coherence.Operational predictions (falsifiable)1. Salivary/CSF markers: cohorts labeled ADHD/HPPD/schizophrenia show mean dopamine/precursor ratios near ~0.5× / ~1.5× / ~2× baselines (with variance explained by a tubulin‑stability index).2. Inflammation link: higher CRP/cytokines ↔ lower tubulin stability ↔ more amygdala‑override behaviors.3. Perturbation test: micro‑dose lithium (where clinically appropriate) improves a composite “frontal coherence” score more in low‑stability subjects than in matched controls.4. Behavioral signature: boundary‑pushing, hierarchy‑insensitive acts cluster with a biomarker panel (tau/tubulin/BDNF) more than with classic “impulsivity” scales.How to test quicklyCross‑sectional: saliva (dopamine/tyrosine), bloods (CRP, BDNF), digital phenotyping (compulsion episodes).Interventional: n=1 and small cohorts with lithium/valproate; pre/post changes in stop‑signal RT, error monitoring, and compulsion frequency.Differential fit: compare this 2‑axis model vs DSM labels on variance explained.Cruxes / what would change my mindIf dopamine ratios don’t separate groups at all after adjusting for stability.If tubulin‑stability proxies don’t predict the “amygdala‑override” behavior cluster.If indirect stabilizers (lithium/valproate) show no coherence gains where theory predicts.Why post here: LW is good at ripping apart map‑making. I want the strongest counter‑examples and better proxies for “stability” you’d actually trust.

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