500 patients66,097 observations150 daysLIVE

Human Model · HM(t) at day 148

State-timeSynthetic demo data⟨ I, St, H0:t, Et, Θt, T, Ut ⟩ — belief, not fact; uncertainty shown, not hiddenSteering view
1
Localization — where is this individual biologically now?
Belief state b_t per dimension: value ± sd from within-person noise plus the observation model's semantic distance. Trajectory features (velocity, autocorrelation, recovery time) are state variables.
Dimensionb_tdS/dtautocorrrecoveryobservation model
Therapy response62 ± 9-0.63/d0.7916 dImaging + tumour markers, interpolated · proxy · last read ≤ 14 d
Gastrointestinal function19 ± 6.3-0.6/d0.86Daily GI check-in · direct · today
Treatment toxicity19 ± 7.3+0.14/d0.445 dLabs, interpolated between draws · proxy · last draw ≤ 7 d
Inflammatory activity29 ± 10.9-0.18/d0.541 dCRP/ferritin + immune signature · inferred · weeks
Immune / metabolic59 ± 11.3-0.2/d0.037 dMetabolic panel + wearable · inferred · weeks
Nutritional sufficiency66 ± 7.9+0.35/d0.461 dWeight, albumin, food log · proxy · days
Adherence91 ± 4.8-0.12/d0.737 dDose + to-do completion · direct · today
Function / quality of life66 ± 5.7-0.1/d0.391 dPRO items · direct · today

High autocorrelation and slow recovery are early-warning signatures of a critical transition (Scheffer et al.), independent of the level.

2
Provenance — how did they arrive here?
The path H_0:t: baseline constraints, divergence, perturbations, actions and responses in order.
  1. day 0baselineBaseline S15: MR phenotype; Normal metabolizer; butyrate 75
  2. day 87perturbationDaily walks resumed (3.3)
  3. day 122perturbationDietary drift (-2.6)

Now: in the restoration basin, heading towards failing.

3
Mechanism — which theories best explain the trajectory?
Versioned competing theories with supporting (E+), contradicting (E−) and missing-but-discriminative (E?) evidence. The contradiction engine lists what should NOT happen under each theory and whether it did.
T1 v2leading
confidence 86%

Mucosal barrier loss: drug-induced epithelial injury amplified by a FUT2-dependent glycan deficit; histamine and inflammatory load add on top.

E+
  • FUT2 non-secretor genotype (barrier glycan deficit)
  • Histamine load → GI +3.6 next day
E−
E? · would discriminate
  • Faecal calprotectin (would separate barrier from motility)
  • Serum DAO / histamine
  • Zonulin
Forbidden under this theory
✓ holdsGI should not improve while histamine intake stays high (GI velocity -0.31/day)
✓ holdsLow-residue meals should reduce GI within a week (not tested)
v1 baseline: genotype + phenotype → v3 dietary attribution from 60-day log
T2 v2falsified
confidence 5%

Bile-acid diarrhoea on a low-butyrate ecology: reduced SCFA production leaves bile acids unconjugated after fat-rich meals; GI burden tracks fat intake with a one-day lag.

E+
E−
  • Butyrate producers intact
  • No fat-load signal in the log
E? · would discriminate
  • Faecal bile acids
  • 7α-hydroxy-4-cholesten-3-one (C4)
  • Rechallenge: 3 high-fat days under observation
Forbidden under this theory
✗ violatedGI should not rise on low-fat days (fat effect -1.2 over 44 low-fat days)
v1 baseline: microbiome → v2 dietary attribution
T3 v1falsified
confidence 5%

Drug-exposure toxicity: pharmacokinetic over-exposure drives GI and systemic toxicity together; dietary and microbial factors are secondary.

E+
  • GI autocorrelation 0.83 (slow recovery)
E−
  • Normal metabolizer
  • Toxicity within range
E? · would discriminate
  • Trough drug level
  • Dose-timing rechallenge (evening vs morning)
Forbidden under this theory
✗ violatedGI should not move with diet if exposure is the driver (2 dietary detractors with ≥ 80% confidence)
v1 baseline: pharmacogenomics
T4 v1competing
confidence 5%

Behavioural spiral: symptomatic days cut adherence and sleep, which raise GI and stress, which cut adherence further; the biology is a follower, not the driver.

E+
E−
  • Adherence intact
  • Sleep and stress stable
E? · would discriminate
  • Dose-taking timestamps vs symptom timestamps
  • Sleep-window rechallenge
Forbidden under this theory
✓ holdsGI should not worsen on days with full adherence and good sleep (insufficient paired days)
v1 from tracker trends
4
Forecast — which futures are likely under alternative actions?
30-day rollout of GI burden under the baseline model T and under each safe candidate action (effect ramps over onset). Dashed = prediction, never fact.
No action
GI 1924
8
Intervention as measurement
Each past action as a measurement of this patient's transition dynamics: predicted ΔGI vs observed, prediction error ε_t, and the within-patient evidence patterns → individualized response confidence (observational, kept separate from randomized evidence).

No action started yet.

5
Decision — the Restore controller
Safe set computed first, then A* = argmax E[HealthGain + λ₁·InformationGain + λ₂·ConfidenceGain − λ₃·Risk − λ₄·Burden − λ₅·Cost]. λ₁ = 0.3 (a theory leads), λ₃ = 1 (stable enough). Execution stays with the clinician or the informed patient (EU MDR Class I).
ClassActionHealthInfoConf.RiskBurdenCostUtility
ObserveContinue passive collection, no perturbation
A clean transition can be observed only without a new perturbation.
00.150.0500.0500.03
MeasureFaecal calprotectin (would separate barrier from motility)
Discriminates T1 from its competitors (E?).
00.450.20.020.250.20.01
MaintainHold current regimen and content
Protects nothing while the state deteriorates.
0.050.050.050.050.0500
TestSerum DAO / histamine
Discriminates T1 from its competitors (E?).
00.450.20.020.250.5-0.05
Excluded from the safe set
  • DT-01 Not indicated for the current state.
  • GI-04 Not indicated for the current state.
  • HY-01 Not indicated for the current state.
  • ME-01 Not indicated for the current state.
  • AD-05 Not indicated for the current state.
  • CR-01 Not indicated for the current state.
  • BR-03 Not indicated for the current state.
  • NP-02 Not indicated for the current state.
  • SC-12 Not indicated for the current state.
Evidence weights · w = Authority × Relevance × Persistence
  • Biological identity Normal metabolizer; FUT2, IL6, CYP2D6
    Germline panel, baseline
    0.86 (0.95·0.9·1)
  • High-authority clinical Toxicity 19, response 62
    Labs / imaging, ≤ 14 d
    0.77 (0.9·1·0.85)
  • Intervention response 0 within-patient responses recorded
    ΔS after each action, accumulating
    0.68 (0.75·1·0.9)
  • Deep biological state DeepGene retest day 90: damage 13/100, Shannon 3.42, butyrate 776 CPM, 1 opportunists above, 1 keystone absent
    Synthetic DeepGene metagenomics + host DNA, sample 966746-R (compositional proxy)
    0.43 (0.7·1·0.6100000000000001)
  • Dynamic state GI 19, sleep 8.3 h, HRV 38
    Companion + wearable, today
    0.18 (0.6·1·0.3)
  • Exposure context Keep meals regular; three to four moderate portions spaced through the day; dosing per protocol; adherence 91%
    Food log + dose log, event-level
    0.1 (0.55·0.9·0.2)
LLIFE OS insight · the five questions, in prose
grounded · add an LLM key for prose

P-03091 is on day 148 of ONX-7 (MR, baseline S15): response favorable, tolerance favorable, GI favorable. Over 14 days response moved 0 and GI 0; discontinuation risk is 15%. The state is in the restoration basin, heading towards failing.

Biology sets the gain: FUT2 non-secretor, IL6 high-expression variant; butyrate capacity 75/100, diversity 3.4. Pushing it down: FUT2 non-secretor (-20.9), Clostridioides difficile 0.809% (LPS load) (-18.7), Histamine load (-15.2). Pulling it up: Protein (supports) (+14.8), Butyrate producers intact (+14.7). From the daily log: histamine +3.6 GI next day, protein -3.2 GI next day, lactose +2.4 GI next day.

No action has been tried yet.

No action is indicated now; the trajectory is stable relative to similar patients.