Phase 0 — Source Control and Redox Foundation

Non-negotiable. Every subsequent phase depends on this one. The autophagic machinery, collagen synthesis enzymes, TET demethylation system, and mast cell stabilization interventions all operate in a redox environment that must be functional first.

Why Phase 0 Must Come First

The core deadlock: [[4-HNE]] impairs the very machinery that would repair the damage it causes.

4-HNE on Complex I/II → mitochondrial dysfunction → reduced alpha-ketoglutarate → [[TET Enzymes]] can't demethylate aberrant methylation
Oxidative DNA damage → PARP hyperactivation → NAD⁺ depletion → sirtuins can't deacetylate pro-inflammatory chromatin marks
Glutathione depletion → GPx non-functional → more lipid peroxidation → more 4-HNE

Restoring the redox environment is not one intervention among many. It is the prerequisite that makes every other intervention possible.

Interventions — Weeks 1–4

Fat Source Control (Immediate)

Switch cooking fat to: beef tallow, lard, or clarified butter (ghee).

These are predominantly saturated and monounsaturated. They do not generate the linoleic acid oxidation cascade that produces 4-HNE and OXLAMs at frying temperatures. This single change eliminates the primary ongoing MERTK/AXL impairment signal, reduces hepatic glutathione demand, and stops the continuous TLR4 activation from dietary OXLAMs.

Implement [[11-Step Protocol]] for fat maintenance. Begin [[In-Fryer Antioxidants]] immediately.

Eliminate: soybean oil, canola oil, corn oil, sunflower oil, vegetable oil, anything labeled vegetable shortening for regular cooking.

NAC (N-Acetylcysteine) — 600mg twice daily

Provides cysteine, the rate-limiting precursor for glutathione synthesis. Glycine is the second independently limiting precursor (not cysteine alone — both must be present). NAC + glycine together restore glutathione more effectively than either alone.

Clinical use precedent: used in emergency medicine for acetaminophen overdose precisely because it rapidly restores hepatic glutathione.

Glycine — 3–5g daily

The second glutathione precursor. Also: one-third of collagen by residue, GlyR mast cell stabilizer, one-carbon metabolism substrate, NMDA co-agonist (sleep), bile acid conjugation. Tasteless. Dissolves in anything. One of the highest leverage-per-dollar interventions in the entire protocol. → [[Glycine]]

Liposomal Vitamin C — 1g twice daily

Liposomal form achieves significantly higher plasma concentrations than standard oral ascorbic acid (gut absorption is limited by SVCT transporters).

Functions in this context:

[[TET Enzymes]] cofactor — maintains Fe²⁺ (ferrous state) required for TET oxidation of 5mC; without ascorbate, TET runs 1–2 cycles and stops
Prolyl and lysyl hydroxylase cofactor — collagen synthesis
Antioxidant network recycling — regenerates vitamin E
Functionally deficient under chronic oxidative stress even without dietary deficiency

Sulforaphane — Daily from Broccoli Sprouts or Supplement

Why sulforaphane is uniquely valuable:

Irreversible Keap1 modification → 24–48hr sustained Nrf2 activation
All other Nrf2 activators (curcumin, resveratrol, quercetin) form reversible bonds — activity drops when they're cleared
Sulforaphane's covalent modification lasts until Keap1 is replaced by new protein synthesis (~24–48h)
Source specificity: Broccoli sprouts contain 50–100× higher sulforaphane than mature broccoli. 1–2 tablespoons fresh sprouts daily. The myrosinase enzyme required for sulforaphane formation is destroyed by cooking — sprouts must be consumed fresh or the supplement must contain stabilized active sulforaphane.

Astaxanthin — 12mg daily with fat-containing meal

Unique structural properties: spans the full lipid bilayer (hydrophilic ends outside, hydrophobic middle), providing membrane protection that other antioxidants can't access. Specifically protective for mitochondrial membranes and renal tubular cells. → [[Terpenoids]]

The Non-Negotiable Sequence Logic

Starting mast cell stabilization or collagen synthesis supplementation before Phase 0 is established:

Mast cell stabilizers (quercetin) work better in a lower oxidative environment
Collagen synthesis enzymes (prolyl hydroxylase, lysyl oxidase) are impaired by 4-HNE adducts — restoring them requires the redox environment that Phase 0 establishes
TET demethylation needs both ascorbate (Phase 0) and alpha-ketoglutarate (mitochondrial restoration) — neither works without the other

Minimum Phase 0 establishment period: 2–4 weeks before adding Phase 2+ interventions.

Concurrent Bile-Axis Foundation

If upper GI dysbiosis is suspected or confirmed, the [[Bile-Micelle-Antioxidant Axis]] is also relevant in Phase 0:

Glycine 3–5g daily is non-optional — serves as glutathione precursor (this phase), mast cell GlyR stabilizer (Phase 2), and bile acid conjugation substrate (bile axis). One supplement, three purposes.
Continue low-dose wild vinegar (1 tbsp raw ACV in water, 15 min before largest meal) to begin cephalic phase restoration. See [[Wild Vinegars]].
NAC at 1200mg/day (higher than the standard 600mg BID Phase 0 dose) also addresses upper GI biofilm matrix disruption. See [[Upper GI Biofilm Disruption]].
If H. pylori is suspected (chronic gastritis, halitosis, refractory iron deficiency), add mastic gum 1000–2000mg on empty stomach + lactoferrin 200–400mg to the Phase 0 stack.

Phase 0's role in the bile axis is not the full intervention (that comes in the 5-layer [[Upper GI Biofilm Disruption]] protocol), but the foundation interventions overlap meaningfully — Phase 0 isn't replaced, it's augmented.

Connections

[[Supplement Stack]] — complete reference
[[One Carbon Metabolism]] — why B vitamins matter here
[[NAD Pool]] — why sulforaphane helps NAD⁺ (reduces PARP activation)
[[Phase 1 - Gut Barrier]] — concurrent with Phase 0
[[Lipid Oxidation Chemistry]] — what's being reduced
[[Collagen Synthesis Pathway]] — what gets unlocked
[[Bile-Micelle-Antioxidant Axis]] — the upper GI bile dysfunction layer
[[Upper GI Biofilm Disruption]] — the biofilm work that overlaps with this phase
[[Wild Vinegars]] — the daily cephalic phase + maintenance protocol
[[Die-off Management]] — the protocol failure-mode prevention
[[Microbiome Onramp Protocol]] — the rebiosis layer that follows biofilm clearing