Human Model · HM(t) at day 119

State-timeSynthetic demo data⟨ I, S_t, H_0:t, E_t, Θ_t, T, U_t ⟩ — belief, not fact; uncertainty shown, not hiddenSteering view

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.

Dimension	b_t	dS/dt	autocorr	recovery	observation model
Therapy response	78 ± 7.8	-0.24/d	0.66	7 d	Imaging + tumour markers, interpolated · proxy · last read ≤ 14 d
Gastrointestinal function	20 ± 5.6	+0.5/d	0.71	2 d	Daily GI check-in · direct · today
Treatment toxicity	13 ± 8.4	+0.13/d	0.48	1 d	Labs, interpolated between draws · proxy · last draw ≤ 7 d
Inflammatory activity	23 ± 11.8	+0.47/d	0.39	1 d	CRP/ferritin + immune signature · inferred · weeks
Immune / metabolic	66 ± 11	-0.24/d	-0.11	1 d	Metabolic panel + wearable · inferred · weeks
Nutritional sufficiency	61 ± 7.4	-0.23/d	0.24	1 d	Weight, albumin, food log · proxy · days
Adherence	94 ± 5.4	+0.52/d	0.73	4 d	Dose + to-do completion · direct · today
Function / quality of life	75 ± 4.8	-0.2/d	0.08	1 d	PRO items · direct · today

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

Provenance — how did they arrive here?

The path H_0:t: baseline constraints, divergence, perturbations, actions and responses in order.

day 0baselineBaseline S09: SR phenotype; Intermediate metabolizer; butyrate 50
day 78perturbationAlcohol on dosing days (-1.8)
day 102perturbationDietary drift (-2.6)

Now: in the restoration basin, heading towards restoration.

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 84%

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)
DeepGene: tissue recycling 42
Histamine load → GI +2.3 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 0.50/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 7%

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+

DeepGene: 3 keystone butyrate producers absent
Diversity 2.8

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 -1.3 over 49 low-fat days)

v1 baseline: microbiome → v2 dietary attribution

T3 v1falsified

confidence 6%

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

E+

GI autocorrelation 0.79 (slow recovery)

E−

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 (3 dietary detractors with ≥ 80% confidence)

v1 baseline: pharmacogenomics

T4 v1competing

confidence 3%

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

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 20 → 16

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.

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).

Class	Action	Health	Info	Conf.	Risk	Burden	Cost	Utility
Maintain	Hold current regimen and content Protects a favourable trajectory.	0.35	0.05	0.05	0.05	0.05	0	0.31
Observe	Continue passive collection, no perturbation A clean transition can be observed only without a new perturbation.	0	0.15	0.05	0	0.05	0	0.03
Measure	Faecal calprotectin (would separate barrier from motility) Discriminates T1 from its competitors (E?).	0	0.45	0.2	0.02	0.25	0.2	0.01
Test	Serum DAO / histamine Discriminates T1 from its competitors (E?).	0	0.45	0.2	0.02	0.25	0.5	-0.05

Excluded from the safe set

GI-04 Not indicated for the current state.
DT-01 Not indicated for the current state.
CR-01 Not indicated for the current state.
HY-01 Not indicated for the current state.
BR-03 Not indicated for the current state.
ME-01 Not indicated for the current state.
AD-05 Not indicated for the current state.
SC-12 Not indicated for the current state.
NP-02 Not indicated for the current state.

Evidence weights · w = Authority × Relevance × Persistence

Biological identity Intermediate metabolizer; FUT2, CYP2D6
Germline panel, baseline
0.86 (0.95·0.9·1)
High-authority clinical Toxicity 13, response 78
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 46/100, Shannon 2.56, butyrate 619 CPM, 1 opportunists above, 3 keystone absent
Synthetic DeepGene metagenomics + host DNA, sample 912717-R (compositional proxy)
0.53 (0.7·1·0.755)
Dynamic state GI 20, sleep 7.6 h, HRV 68
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 94%
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-01625 is on day 119 of NBL-101 (SR, baseline S09): response declining, tolerance improving, GI favorable. Over 14 days response moved -6 and GI -2; discontinuation risk is 11%. The state is in the restoration basin, heading towards restoration.

Biology sets the gain: FUT2 non-secretor, Low microbial diversity; butyrate capacity 50/100, diversity 2.8. Pushing it down: 3 keystone species absent (-21.6), FUT2 non-secretor (-17.5), Clostridioides difficile 1.813% (LPS load) (-16.9). Pulling it up: Butyrate producers intact (+12.3). From the daily log: alcohol +2.9 GI next day, histamine +2.3 GI next day, fibre -1.8 GI next day, simple carbs +1.7 GI next day.

No action has been tried yet.

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