The current sheet, post-audit. Three protocol changes through Aug 1 — everything else is measurement. Adderall is reconciled to its full prescribed 70 mg (Wancata-approved, 7/13). L-citrulline is out, telmisartan holds at 40 (step gated on the 8/1 draw), the cascade is re-paced, and the nocturnal sub-54s are settled as compression artifacts. CGM card →
1 · The cuff. 39 Apple Health readings, Jul 4–8. Fasted 138/68. Postprandial 115–128 / 50–62. Berberine lowers BP ~3–5 mmHg. Your diastolic margin to your own stop rule is five points. Both doses bracket dinner — the one postprandial window with no reading at all — alongside theanine 200, taurine, Magtein, Mg, Holy Basil, on top of L-citrulline, during a telmisartan 40→80 step, at Hgb 8.3 / Hct 25.2, eleven days after syncope.
2 · Pharmacology. Broad-spectrum antimicrobial at SIBO-range dosing (500 mg BID–TID is the SIBO protocol), one day before ProBiota and three before MegaSpore. Its <1% bioavailability exists because it stays luminal; the remodeling is the mechanism. You cannot time-separate from a mechanism.
3 · It has no measurable endpoint. Not glycemic — the instrument is unvalidated. Not lipid — there is no lipid panel anywhere in your record. Berberine is currently running blind, into a hemodynamic risk window, during a five-variable week.
The Adderall/berberine interaction was never binding — and matters even less now. With Adderall back to the full 70 mg (IR at 6:30 AM + 4:00 PM), d-amphetamine covers 6:30 AM → midnight continuously; no waking hour separates it from the 6:15/7:45 PM berberine slots. That never mattered: the CYP2D6 interaction is a hepatic in-vitro finding at concentrations oral berberine never reaches systemically. Berberine stays held on hemodynamics, not this. BP card →
1 · Nutrition. Its primary consumer effect is sweet-taste suppression and appetite reduction. You are 25 days post-Frey, Hgb 8.3, total protein 5.5, globulin 1.5, albumin only just back to 4.0, running HMB specifically for anti-catabolism. An intake-reducing agent is working against your own recovery objective.
2 · Anatomy. Insulinotropic + SGLT1 inhibition, with C-peptide 2.1 (residual beta cells) and no alpha cells. Every glucose-lowering agent carries asymmetric risk in you — that follows from the necrosis, not from a sensor.
3 · Logic. It is dosed 7:45 PM to blunt "the carb load." Your 8 PM dessert is annotated light — Creon 1 cap, milk thistle. An SGLT1 inhibitor before a light dessert is doing nothing.
4 · Your own bar. Small, uncontrolled trials in T2D at A1c 8–9%. It is the weakest-evidenced compound in a stack held to NSF / USP / iTested / ISO-17025. It is also the only live compound with no entry on the gate board.
And under instrument uncertainty this argument gets stronger, not weaker: removing a glucose-active variable increases the interpretability of everything else in the cascade. Removal is free and reversible. Retention is not.
6:30 AM protein bite (Creon + fed Adderall anchor) · Meal 1 at noon · folded Meal 2 at 3 PM · dinner 6:30 · dessert 8 PM.
~Aug 1 is the last gate. Pending a positive Wancata check-in and draw, the 3 PM meal stays where it is and the day becomes canonical 12 PM–8 PM IF. Nothing else moves.
Single-variable rule still holds: each staged addition gets its own clean day. If a day isn't clean — new nausea, cramping, stool change, lightheadedness on standing — nothing new starts.
~7/21 · ProBiota HistaminX — Meal 1. Deferred past the omeprazole stop (7/14), so tolerance reads across the acid rebound, not into it. The one addition standing before 8/1. Single-variable.
~post-8/1 · SPM Pro-Resolve — Dinner, fat-anchored. Slid past the 8/1 draw — the freeze runs only three changes before then.
~8/5 · MegaSporeBiotic — Dinner. After ProBiota tolerance and the 8/1 draw.
~7/14 · Omeprazole ends — rebound hypersecretion peaks over the following two weeks. This will do more to the probiotics than berberine ever would. Read tolerance across the transition, not into it.
~8/1 · Telmisartan → 80 mg (gated, not dated) — steps only if the 8/1 draw clears: Hgb ≥10, Na workup + UACR back and clean, postprandial margin intact. Dose it in the evening then. Draw not clean → keep holding.
— · R-ALA (OptimALA) — un-dated. Gated on ferritin + iron saturation. ALA chelates iron; you are mid-erythropoiesis at Hgb 8.3. It is also a fasted 6 AM dose into a duodenum that bled twelve days ago, during acid rebound. Nothing is lost by waiting — NAC already carries the glutathione axis.
~7/19 · Lion's Mane / Erinamax · ~8/8 · Turkey Tail · ~8/19 · Cordyceps — mushroom track, unchanged. Protocol →
~8/1 · IF gate + draw — Wancata check-in. Bilberry and Panax GS15-4 both move behind this. Both are glucose-active; neither can get a clean CGM window while telmisartan-80, acid rebound, and probiotic establishment are all running.
~mid-Aug · Truvaga Plus — vagal stimulation lowers HR and BP. Correctly deferred. Morning fasted, never postprandial.
The CGM is not currently a competent gate. Four glucose-active reintroductions — R-ALA, Bilberry, Panax, Cordyceps — were each queued behind "its own CGM window." That instrument is unvalidated. Run the 5-day rehabilitation protocol first — stop calibrating, discard day 1 and day 10, ten paired fingersticks, establish the sign of the bias. CGM card → · NAC ramp: 1,200/day → +500 per clean 7-day step → 4,800; overnight bolus lands last; every addition stays ≥72 h from a step, and the eventual telmisartan step counts as an addition.