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Gout Action Guide — what to do, by situation

This is the "I have gout, what do I do?" entry surface for Open Enzyme. The research wiki has the depth — mechanisms, evidence levels, study citations, contradictions. This page surfaces what those findings imply for action: what to start today, what to build out over a month, what to plan for over a year.

Not medical advice. Open Enzyme is Phase 0 (Research & Design). None of the engineered-strain interventions on this page are FDA-approved or clinically available. Everything in the "today / this month / this year" sections is over-the-counter or dietary; even so, work with a physician on anything that interacts with your medications or comorbidities. The point of this page is to translate research findings into actionable starting points, not to replace clinical care.

Step 1 — Identify your situation

Pick the closest match. Each row links to a tailored section below.

If you are… Start here
Male, mid-life, no genotype info, mostly diet-managed gout Default path
Androgen-elevated (high endogenous T, on TRT, on Clomid/enclomiphene) Androgen-elevated path
Q141K-positive ABCG2 (from 23andMe / genome sequencing) Q141K-positive path
In an active flare right now Active flare
Already on allopurinol or febuxostat, looking for adjuncts On a urate-lowering drug
No flare yet, family history or borderline UA Prevention path

Default path

Most readers. No genotype info, mostly diet-managed gout, want a sensible mechanism-grounded stack.

Calibration note (updated 2026-05-08 with comp-019 flux-model results): the engineered-strain mechanism (gut-lumen uricase via koji) is predicted to work in non-Q141K males at the SAME or LARGER effect size than in Q141K-positive readers — not smaller. comp-019 (flux-model Monte Carlo, n=5000, 2026-05-08) found the gut-lumen uricase mechanism is substrate-limited rather than ABCG2-capacity-limited: WT/WT non-Q141K males get the LARGEST predicted ΔSUA (−0.83 mg/dL at 25 mg/day) because they have more urate flowing through the gut compartment for the engineered uricase to degrade. Q141K-het predicted −0.67 mg/dL; Q141K-hom −0.50 mg/dL. The platform's primary-demographic positioning is supported by the in-silico flux model. Caveat: this is in-silico, not human RCT. Clinical effect size remains unproven; the eventual Phase 2b RCT (typical-gout cohort, Q141K + Q126* as stratification rather than enrichment, single 25 mg/day dose, pre-stratified by CKD stage) is what would actually settle this. Practical implication: the Default path's dietary + over-the-counter entries are genuinely broadly applicable today; the engineered-strain Future entries are predicted to apply broadly too, pending Phase 2b confirmation. Genotyping yourself still matters — but for adjacent clinical reasons (HLA-B*58:01 carriers have high allopurinol-allergy / SCAR risk; SLC2A9 / URAT1 variants affect baseline UA handling; family-history risk stratification) rather than gut-lumen-sink-mechanism conditionality. See personal-genome-protocol. If you do test Q141K-positive, the Q141K-positive path still has tailored stack guidance for adjuvant interventions (sulforaphane, lactoferrin, EGCG) regardless of the engineered-strain mechanism's predicted effectiveness.

Today (start in the next 24 hours)

  • Cut high-fructose corn syrup — fructose drives PRPS-mediated purine biosynthesis upstream of XO (the enzyme allopurinol blocks). This is a single dietary change with real mechanistic backing. See PRPS chokepoint, fructose connection.
  • Hydrate aggressively — >3L/day. Dilutes urate, supports renal excretion.
  • Cut the obvious dietary triggers — organ meats, beer, sardines, anchovies. Moderate red meat. (Standard advice; documented in primary clinical literature.)
  • Tart cherry concentrate — 8–12 oz/day OR 500–1500 mg/day dried-extract capsule. Lowers UA modestly + reduces flare frequency in observational data. Cheap, broadly tolerated. Catalog →

This month (build out)

  • Omega-3 (high EPA + DHA) — 3–4 g/day. NLRP3-pathway resolution via specialized pro-resolving mediators (SPMs). DHA-derived MSU-gout animal evidence is strongest. Catalog →
  • NAC (N-acetylcysteine) — 600–1,200 mg/day split AM + evening. Glutathione/ROS axis suppresses NLRP3 priming. ~$15/month. Catalog →
  • Lactoferrin (bovine) — 100–300 mg/day commercial oral. Anti-inflammatory + Mechanistic Extrapolation toward ABCG2 derepression via TNFα suppression. Catalog →
  • Whole-fermentate Cordyceps + GLPP (speculative — wet-lab gate pending) — emerging two-organism stack from the medicinal-mushroom-complement track. Targets ADA (adenosine deaminase) upstream of XO. Currently mechanism-grounded, not yet wet-lab confirmed at human dose. Reality check: typical fruiting-body extracts deliver only ~3–4 mg cordycepin per serving (sub-therapeutic by ~25–150×); a pure-cordycepin nutraceutical at 100–500 mg/day OR home Cordyceps fermentation is the only way to deliver a dose where the URAT1-inhibition mechanism is plausible. See medicinal-mushroom-complement-track.

This year (advanced)

  • Run the closed-loop n=1 pharmacogenomics workflow — genotype → variant-informed compound selection → home/community-biolab production → Tier 2 batch QC → calibrated dose → biomarker tracking. The canonical user-facing entry point is genotype-informed-supplement-workflow.md — walks the five-step pipeline end-to-end with a Q141K worked example. The two prerequisite steps below feed into it.
  • Get genotyped via clinical-grade testing — order ABCG2 Q141K (rs2231142), SLC2A9, URAT1 variants through a clinical-grade lab (e.g., via your rheumatologist or a direct-to-consumer clinical service that returns CLIA-grade results). Changes the stack design substantially. Consumer panels (23andMe, AncestryDNA, etc.) are not recommended for any gout-stack-design decision — see the canonical Consumer SNP data-quality caveat for the full reasoning. See personal-genome-protocol for ordering paths. The unified variant index at gout-genetic-variants.md is the canonical reference for which variants matter and what they do.
  • Self-experiment with rigor — log SUA monthly, track flares, A/B test compounds. See self-experiment-protocol. Acute-flare-abort comparator table — choosing between prednisone / anakinra / canakinumab for an active flare. Per-flare and cumulative-over-years framing for someone with recurrent gout:
Option Mechanism Dosing for acute flare Acute side effects Cumulative burden (recurrent flares × decades) Cost per flare Access
Prednisone taper Glucocorticoid receptor — system-wide 30–40 mg/day × 5 days then taper over 7–10 days Glucose spike, BP rise, sleep disruption, mood changes, immunosuppression Real, dose-dependent: bone loss / osteoporosis, cataracts, adrenal suppression, glucose intolerance, weight gain ~$10–30 (generic) Any prescriber
Anakinra (Kineret) SC IL-1R1 competitive antagonist (recombinant endogenous IL-1Ra) 100 mg SC daily × 3 days, self-administered in thigh/abdomen. ~85–94% achieve good response across real-world series; meaningful pain reduction often within 24 h, full resolution by day 3–5 (Ottaviani 2013 PMC3978950, Jeria-Navarro 2023 PMC9877612, Saag 2021 anaGO RCT) Injection-site reactions in <2% of gout 3-day-protocol cohorts (the 70% ISR rate widely quoted is from chronic-RA daily dosing where ISRs develop over first 4 weeks); immediate stinging at injection mostly resolves within seconds; modest infection-risk signal at 3-day acute use (~0.9% in flare arm vs 31.8% in long-term-anakinra populations — bracket the distinction sharply) Minimal known burden — anakinra is recombinant version of body's endogenous IL-1Ra; no bone / glucose / adrenal effects; long-term concern is only infection masking under chronic use (not relevant for 3-day acute use × few flares/yr) ~$300/dose × 3 = ~$900 Rheumatologist (off-label for gout)
Canakinumab (Ilaris) SC Anti-IL-1β monoclonal 150 mg single SC Same injection-site profile; longer half-life (~26 days) so chronic exposure window per dose Same as anakinra's mechanism (no steroid burden); ADAs possible with chronic use but rare ~$3,000/dose (FDA-approved for gout but cost barrier) Rheumatologist; insurance variable
Colchicine + NSAID (mild flares) Microtubule inhibition + COX 1.2 mg colchicine + NSAID at flare onset GI (colchicine), GI bleed risk (NSAID), renal (NSAID) NSAID: real renal burden over years; colchicine: minimal at acute-use dose ~$20–50 OTC or any prescriber
Inhaled mRNA-IL-1RA (future, 5–10 yr horizon) Same as anakinra — pulmonary mRNA expression of IL-1Ra Per comp-036: BID × 4–14 days reaches median 50–56% of flare window above 80% receptor occupancy (best regimen tested); doesn't match anakinra Cmax but partial-suppression may be clinically meaningful vs prednisone burden Pulmonary irritation; possible LNP innate immune activation; anti-PEG buildup over many lifetime exposures TBD; in principle cleaner than steroid burden; chronic-LNP-exposure question is open $25–200/flare projected Doesn't exist yet (partner-tier development)

The decision frame: if you flare 3–6× per year over decades, cumulative prednisone burden is the load-bearing concern (bone / glucose / mood / cataract effects compound). Anakinra SC is the cleanest acute-flare-abort option clinically available today — same chokepoint as canakinumab and inhaled mRNA, just SC route. Canakinumab has the longest half-life (one shot covers months) but cost is prohibitive without insurance. Colchicine + NSAID is the right tool for mild flares; inadequate for severe. The inhaled mRNA-IL-1RA route is on a 5–10 year development horizon (per comp-033 + comp-036) and is what would change the economics if it lands — same mechanism as anakinra, much lower per-dose cost, different delivery format. Head-to-head RCT evidence (added 2026-05-19, source: logs/anakinra-3day-gout-patient-experience-2026-05-19.md): Saag 2021 (anaGO, n=165) found anakinra and a single IM triamcinolone shot produce essentially identical pain reduction at 24–72 h (−41.2 vs −39.4 on 0–100 VAS, p=0.688); Janssen 2019 (n=88) found anakinra non-inferior to free-choice standard care with more patients achieving ≥50% pain reduction by day 3 (OR 2.56, 95% CI 1.03–6.37, p=0.04). The case for anakinra over prednisone for a single flare is mostly about cumulative-steroid-burden avoidance over years, not single-flare pain control where the two are comparable.

Relapse without a ULT/prophylaxis bridge (added 2026-05-19, load-bearing for recurrent-flare patients). Real-world series consistently show that the 3-day anakinra course aborts the index flare but ~26% of patients relapse within ~2 weeks if no flare-prevention bridge therapy (allopurinol/febuxostat + low-dose colchicine prophylaxis) is in place — Ottaviani 2013 PMC3978950 reports relapse 70% in patients without prevention vs 20% with prevention (p=0.006). Anakinra is an acute-abort tool, not a prophylactic. Pair with ULT initiation or continuation. The combined-route flare protocols below assume this ULT bridge is being put in place at the same time the flare is being aborted.

  • Anakinra (Kineret) SC for acute flare — bridge while inhaled-mRNA pulse doesn't exist yet. Off-label for acute gout flare, used in rheumatology practice when corticosteroids are contraindicated or undesirable (recurrent flares + steroid burden). Route: subcutaneous injection in thigh or abdomen, 100 mg/day × 3 days — same SC route as insulin, the patient self-administers with a prefilled syringe. NOT intra-articular (no needle into the gout joint itself; that's a totally different procedure used for IA corticosteroid injection or the chassis-pending IA uricase concept at chassis-pending-interventions.md §6). Mechanism: recombinant IL-1 receptor antagonist (IL-1Ra) competitively blocks IL-1β signaling — aborts flare within hours via the same CP5a chokepoint as canakinumab, but daily SC dosing vs canakinumab's monthly SC + ~100× lower cost. Side-effect profile: injection-site reactions (most common), low infection-risk signal at the 3-day acute-use protocol (label cautions about TB / fungal infection are for chronic immunosuppression-tier use). Vs prednisone 30-40 mg/day × 2-week taper: anakinra is faster onset (hours vs days), narrower mechanism (single pathway block vs system-wide glucocorticoid receptor), cleaner cumulative side-effect burden over years of recurrent flares (no bone loss, no glucose intolerance, no adrenal suppression, no mood / sleep / BP effects). Cost: ~$300/dose, ~$900/flare for the 3-day protocol; insurance coverage variable for off-label use. Access: rheumatologist or forward-thinking internist willing to prescribe off-label. Bridge until the inhaled mRNA-IL-1RA modality exists (chassis-pending-interventions.md §4, 5–10 year development horizon per comp-033 partner-tier analysis); anakinra is the same mechanism + same chokepoint, just SC delivery instead of pulmonary mRNA.
  • Compounding-pharmacy access (requires physician partner; not DIY) — a 503A compounding pharmacy can prepare custom formulations along two distinct tracks. (a) Discovery-engine repurposing candidates: drugs not currently used for gout but identified as hitting gout chokepoints. Disulfiram (CP6b GSDMD blockade) is the highest-priority candidate; 503A-eligible via Tier 2 (component of FDA-approved drug); dose modeling completed as comp-027 2026-05-16 → YELLOW-leaning-GREEN: narrow sub-AUD window centered on 100 mg/day (range 75–125 mg/d), where parent DSF Cmax engages GSDMD at 1.3× IC50 while Me-DTC stays at DER hypotension threshold. Two-phase compounding protocol: IR capsule 50→100 mg/d titration over 14 days, then ER lipid-matrix 100 mg QD chronic. Zileuton (CP6a 5-LOX), pentostatin (ADA), and lesinurad (URAT1, FDA-approved 2015, commercially withdrawn 2019 for business reasons — Tier 2 eligibility survives per 21 CFR 216.24) are all 503A-eligible via Tier 2 but have supplier-side bulk-API supply questions. (b) Custom-dose formulations of established gout drugs: allopurinol (pediatric/weight-based doses, liquid suspensions), colchicine (low-dose ER for prophylaxis, fixed-dose combos), probenecid (ER for QD dosing, combinations). These are 503A-eligible via Tier 1 (USP monograph) — no regulatory uncertainty; the question is whether a custom formulation clinically outperforms the commercial product. Full per-compound tier mapping at compounding-pharmacy-track.md. Path requires a rheumatology / functional-medicine prescriber.

Future (Open Enzyme pipeline — none shipping yet, Phase 0)

Androgen-elevated path

If you have high endogenous testosterone, are on TRT, or are taking Clomid/enclomiphene/anastrozole. Androgens upregulate URAT1 (the kidney transporter that reabsorbs urate from urine back into the blood) and may indirectly increase serum UA. The stack should include URAT1 countermeasures.

Important context — the H07 reframe. The Clomid-elevates-UA observation has a recent mechanistic update. The old model said "androgens directly suppress ABCG2 via the androgen receptor." Comp-016 + comp-017 + the H07 hypothesis card argue the actual mechanism is estradiol-pathway antagonism — Clomid blocks an estradiol → PI3K/Akt → ABCG2 induction signal that males largely lack at baseline. Implications for stack design:

  • Aromatase inhibitors (anastrozole, letrozole) and DIM are more unfavorable than the supplement-industry default suggests. They reduce E2 substrate for the same pathway Clomid is already blocking — likely additive to UA elevation.
  • Direct urate-axis modulators (cordycepin, eurycomanone, butyrate, carnosine) are more favorable. They bypass the ER pathway entirely.
  • See H07 clomid intestinal-ER antagonism for the full mechanism.

Today

All Default path → Today entries apply. Plus:

  • Avoid AIs and DIM unless prescribed for other reasons. Estrogen-pathway suppression worsens the gout picture in this group.

This month

  • Carnosine — 500–1,000 mg/day oral L-carnosine (split doses preferred). URAT1 + GLUT9 downregulation in animal models; specific countermeasure for androgen-driven UA elevation. Catalog →
  • Tongkat ali (Physta, standardized) — 200 mg/day, standardized to 0.8–1.5% eurycomanone. PRPS-mediated purine-synthesis suppression (eurycomanol, PMID 34785103) + multi-target transporter modulation (URAT1↓, GLUT9↓, ABCG2↑, NPT1↑). 2021 RCT showed SUA ↓7–11% (n=105). The XO-inhibition claim circulating in supplement-industry summaries is a citation-laundering artifact (comp-015 v2) — the actual mechanism is transporter modulation + PRPS suppression. Catalog →
  • Cordycepin (whole-fermentate Cordyceps OR pure-cordycepin nutraceutical at 100–500 mg/day) — URAT1 downregulation. Reality check: standard fruiting-body extracts deliver only ~3–4 mg cordycepin per serving (sub-therapeutic). Use a pure-cordycepin product or commit to home Cordyceps fermentation. See medicinal-mushroom-complement-track.

This year

  • Genotype yourself (ABCG2 Q141K is high-prevalence in this demographic and changes the stack — see Q141K-positive path if you test positive).
  • Self-experiment with rigor — n=1 monthly SUA tracking is genuinely valuable to the field if you're willing to share the data.

Q141K-positive path

If you've genotyped and you're heterozygous or homozygous for ABCG2 Q141K (rs2231142), your gut-lumen secretion pathway is partially compromised at baseline. The stack tilts toward ABCG2-rescue compounds alongside standard intervention.

Why this matters more than for the default path: ABCG2 normally secretes ~30% of daily urate into the gut lumen. Q141K reduces that capacity. Compounds that boost ABCG2 expression or function become especially relevant; compounds that antagonize ABCG2 become especially harmful. See abcg2-modulators for the full ABCG2 axis discussion and intestinal ABCG2 sex dimorphism (comp-017) for the disease-state vs. baseline framing.

Today

All Default path → Today entries.

This month

  • Sulforaphane (broccoli sprouts) — ~50 mg/day supplement, OR 100–150 g/day raw broccoli sprouts (must be raw/freshly chopped to preserve myrosinase). HDAC inhibitor at the food-grade level; partial Q141K rescue mechanism documented in vitro. Catalog →
  • Lactoferrin — direct relevance for Q141K because the lactoferrin → TNFα → ABCG2 derepression mechanism is especially valuable in a group with already-compromised baseline ABCG2.
  • EGCG (standardized green tea extract) — 400–800 mg EGCG/day OR 3–5 cups matcha/day. Wide-spectrum NLRP3 + transporter modulation. Caveat: high-dose EGCG can be a functional ABCG2 inhibitor — start at the low end (400 mg) and watch SUA trajectory. Catalog →

This year

  • Self-experiment with rigor — Q141K-positive responders are who Open Enzyme's gut-lumen-sink thesis depends on most, so good n=1 data here is genuinely valuable.
  • Watch comp-018 — upstream complement modulator sweep (Phase 1 complete 2026-05-08; rosmarinic acid + luteolin + Bupleurum polysaccharides as upstream-CP0 dietary candidates — note: a brief-scrubbed verification re-run as comp-020 flagged that comp-018's headline-promotion of rosmarinic acid was contaminated by user phrasing in the brief; Helicteres benzofuran lignans actually beat rosmarinic acid 4-20× on matched-assay potency — see retrospective at operations/comp-018-vs-comp-020-retrospective.md) and food-grade HDACi screen (comp-007) for new candidate ABCG2-rescue compounds.

Active flare

You are in pain right now. Standard medical care is the priority — colchicine, NSAID, or steroid as your physician directs. The supplements below are adjuncts, not replacements.

Today (during the flare)

  • Hydrate aggressively — >4 L/day water.
  • Tart cherry concentrate — push to 16–20 oz/day during flare. Strongest acute-flare evidence among supplements.
  • Omega-3 — push to 4–6 g/day during flare.
  • Topical CBD + THC (1:1 ratio, high-mg/oz formulation) applied to the affected joint, plus ice. CB2 receptor activation on synovial macrophages and infiltrating neutrophils suppresses NLRP3 inflammasome assembly and reduces IL-1β release — same downstream chokepoint as colchicine (CP3/CP2), reached via a different receptor. Topical TRPV1 desensitization plus the cooling component (typically menthol / TRPM8 agonist) adds thermoreceptor-mediated pain reduction at the site. Beta-caryophyllene (CB2-selective agonist) and CBG have direct MSU-model evidence for inflammasome suppression — see cannabinoids-terpenes.md §1 + §2 for the full mechanism and sourcing detail. Practical protocol: ice 10–15 min → apply topical 1:1 THC:CBD → ice again 30–60 min later. For more severe presentations or systemic effect, oral or inhaled THC:CBD adds systemic CB1/CB2 activation. In recurrent-flare patients with significant cumulative steroid burden, this protocol may reduce or replace the need for prednisone dose escalation during a step-down rebound. Cannabis is jurisdiction-dependent and requires medical-program access in many places. [In Vitro / Animal Model — direct human gout-flare RCT evidence absent; mechanistic + indirect evidence base in cannabinoids-terpenes.md]
  • Avoid: ketogenic states, intermittent fasting, alcohol, organ meats, high-fructose foods. All transiently raise UA and can extend the flare.
  • Avoid BHB / exogenous ketones during a flare. Ketosis competes with urate for renal MCT/URAT1 reabsorption — transient UA rise of 5–10% is documented and can compound the flare. However, note (2026-05-19): during an untreated active flare, the body's HPA axis is already engaged — 24h UFC rises ~58% above interval baseline, driving cortisol-mediated urate excretion that lowers serum UA via URAT1 downregulation + XOR induction (Zhang 2023, PMC9989260). So serum UA dynamics during an untreated flare are complex: inflammation-driven UA excretion ↓ SUA, ketone competition ↑ SUA, net direction depends on which effect dominates. The conservative recommendation (suspend BHB/ketosis during flare) remains right because the variance is high and adding a known UA-elevating intervention to an unstable system is risky. See cortisol-fasting-glucocorticoid-inflammasome-lit-scan-2026-05-19 for the full evidence map.

Combined-route flare protocols — mechanism-non-redundant stacking (added 2026-05-19)

Two named combined protocols for active flare. Both leverage mechanism-non-redundant convergence on NLRP3 through independent receptor pathways and delivery compartments. [Speculative; mechanism-composition logic, no human gout RCT for either combination as named.]

Protocol A — Colchicine + topical CBD:THC (for users on colchicine). Two independent receptor pathways reaching the same chokepoint: - Oral colchicine (1.2 mg + 0.6 mg at 1 hour per AGREE trial) → β-tubulin binding → CP3 ASC speck blockade + CP2 P2X7 pore inhibition (intracellular, systemic) - Topical 1:1 CBD:THC on affected joint → CB2 GPCR on synovial macrophages → CP2 NLRP3 conformational suppression (plasma-membrane, local) - The two arms hit CP2 via completely different molecular mechanisms (tubulin/P2X7 vs. CB2 Gαi-coupled signaling) and reach the joint via different compartments (oral systemic vs. transdermal local). Mechanism-non-redundant. Not a replacement for either arm alone; a layered acute-flare strategy. See colchicine.md §3.3.1 and cannabinoids-terpenes.md §4a for the per-arm mechanism details.

Protocol B — Prednisone + topical CBD:THC + inhaled cannabinoid + ice (four-route layered, n=1 anchor). Brian's actual protocol used during a 2026-05 prodromal rebound after disc-golf overexertion. Mechanism layering: - Prednisone (on existing taper) → systemic glucocorticoid receptor activation → NLRP3, IL-1β, NOS2, ACOD1 transrepression at CP1+CP2 (timing-aligned: per H2 lit scan logs/cortisol-fasting-glucocorticoid-inflammasome-lit-scan-2026-05-19.md, GR works AFTER LPS priming, which is exactly the prodromal / mid-flare window) - Topical CBD:THC → local CB2 → CP2 (transdermal local) - Inhaled cannabis → systemic CB1/CB2 → CP2 (systemic) — different compartment than topical - Ice cycling → TRPM8 nociceptive blunting + tissue temperature drop + cold-induced anti-inflammatory effect (local) - Three layered interventions converging on CP1+CP2 via three distinct cellular compartments + one peripheral nociceptive intervention. See cannabinoids-terpenes.md §4a for the n=1 observation anchor.

Which protocol fits which user: Protocol A is for users already on colchicine with no contraindications (renal function adequate, no statin/macrolide/cyclosporine drug-interaction surface). Protocol B is for users on prednisone (acute or taper) where the colchicine drug-interaction surface is unacceptable or where colchicine isn't part of the regimen. Both are layered onto whatever urate-lowering therapy is in place; both target acute-flare inflammation, not chronic hyperuricemia.

Once the flare resolves (1–2 weeks)

  • Return to maintenance stack from the path that fits your situation.
  • Log the flare (date, suspected trigger, severity, duration). Pattern recognition is the highest-leverage thing you can do for yourself. See self-experiment-protocol.

On a urate-lowering drug

You're already on allopurinol or febuxostat. The drug is doing the XO suppression; the supplement stack should target complementary mechanisms (NLRP3 inflammation, ABCG2 secretion, ROS, gut-lumen sink).

Today

All Default path → Today entries — none antagonize allopurinol/febuxostat.

  • Avoid sustained heavy ketosis if your UA is borderline-controlled — transient UA rise on top of the drug can still trigger a flare.

This month

  • Lactoferrin — TNFα-mediated ABCG2 derepression is mechanistically distinct from XO suppression, so it stacks cleanly.
  • Sulforaphane — ABCG2-axis support (Mechanistic Extrapolation).
  • Omega-3 + NAC — NLRP3 axis. You can have low UA on allopurinol and still flare from residual MSU crystals; these address the inflammatory side independently of UA level.

This year

  • Genotype if you haven't — HLA-B*58:01 carriers have a high allopurinol allergy / SCAR risk. Clinically actionable. See personal-genome-protocol.
  • Self-experiment under physician supervision to test whether the adjunct stack lets you reduce allopurinol dose.

Prevention path

No flare yet. Family history, borderline UA, or just want to avoid the trajectory.

Today

  • Diet baseline (cut HFCS, hydrate, moderate purines).
  • Tart cherry at maintenance dose.

This month

  • Omega-3 at maintenance dose (3–4 g/day).
  • Add NAC if your stack tolerates it.
  • Establish baseline: SUA every 6 months. Track your personal trajectory before something happens.

This year

  • Genotype to know your variant-driven risk.
  • Watch this guide for updates as Open Enzyme's research pipeline matures.

How this page stays fresh

This page is not auto-updated by the wiki sweep daemon. The sweep daemon propagates findings between research wiki pages; promotion to this application surface is currently a manual review pass.

The plan: a fresh-stack.py script (sibling to the existing fresh-synthesis.py) that scans the research wiki for findings that should be reflected here but aren't, surfaces them as a promotion-candidate report, and lets a human review and accept the propagation. Until that script exists, the propagation discipline is: research findings live in their canonical pages; this page is updated by hand whenever a finding crosses the maturity threshold for action recommendations.

If you find a finding in the research wiki that should be reflected here but isn't, that's a propagation gap — open an issue or a PR.

See synthesis/strategic-reflections/ for the platform-architecture reflection on whether the daemon should eventually grow a propagation-to-application-surface pass.

Cross-references