primordial_os/hir/equations.py and primordial_os/hir/config.py.This layer maps common pathophysiological failure modes as structured degradation pathways using the OAM (Organismal Autonomy Model) as the degradation engine and HIR (Honesty, Integrity, Respect) as the evidence-governance boundary. Each condition is represented as a causal chain: pressure source → system strain → degradation pathway → feedback failure → measurable sign → downstream effect → uncertainty boundary.
This is a biological architecture planning study. It is not a clinical tool, a diagnostic system, a risk-scoring instrument, a treatment protocol, or a medical opinion. It maps degradation mechanisms as they appear in the biomedical literature; it does not prescribe, diagnose, or predict outcomes for any individual.
| In scope | Out of scope |
|---|---|
| Degradation pathway structure for common chronic conditions | Individual risk scores, diagnostic labels, prognosis |
| OAM variable mapping (P, D, Θ, C, Ξ, S, U) onto biological mechanisms | Treatment recommendations, medication guidance |
| HIR evidence boundary classification per pathway | Claims beyond declared evidence limits |
| Measurement/provenance uncertainty per biomarker type | Wearable signals treated as clinical diagnoses |
| Cascade pathways between biological systems (Ξ) | Person-level blame, moral inference, character claims |
| Feedback failure identification (where repair mechanisms break) | Overclaiming mechanistic certainty where mechanisms are contested |
HIR governs what evidence claims are permitted. OAM provides the mathematical structure for modeling degradation dynamics. Together they produce a bounded, auditable pathophysiology mapping engine.
| Layer | Variable / Gate | Pathophysiology Role | What it constrains or models |
|---|---|---|---|
| HIR — H | Honesty | Biomarker/signal fidelity | Label what is directly measured vs. inferred. Declare biomarker limitations, provenance, and unknown mechanisms. Unknown must remain unknown. |
| HIR — I | Integrity | Category coherence | Do not collapse: risk factor ≠ diagnosis; symptom ≠ cause; single reading ≠ condition; population ≠ individual; wearable ≠ clinical. Degradation pathways are not deterministic individual predictions. |
| HIR — R | Respect | Person-level protection | Block person-level blame, shame, capacity, moral, or character claims. No treatment recommendation. Outputs must protect the person from overclaiming. |
| OAM — Degradation Engine (canonical equations: primordial_os/hir/equations.py) | |||
| OAM — P | Pressure FieldP = w_W·W + w_F·F + w_WF·WF | Biological stressor load | W = acute stressor intensity (BP spike, glycemic load, inflammatory trigger). F = chronic background load (sustained HTN, low-grade inflammation, sleep fragmentation). WF = coupling between sustained and acute load. |
| OAM — B | Base FieldB = H+I+R+k(HI+HR+IR) | Biological homeostatic capacity | Integration of signal fidelity (H), structural integrity (I), and regulatory coherence (R) with interaction coupling k. Represents intact homeostatic reserve before pressure is applied. |
| OAM — S | StabilityS = A_audit·B − P | Physiological compensation | Homeostatic capacity minus pressure load. S > 0 = compensated (stable disease). S → 0 = decompensating. S = 0 or negative = decompensated state requiring intervention. |
| OAM — U | Usable AutonomyU = A·B·(1+g_G·G)·F_int | Functional organ capacity | Actual functional capacity available: modulated by grit/reserve (G), intrinsic function (F_int), and homeostatic field. Declines as D accumulates and K (resistance) rises. |
| OAM — C | Carrier DensityC_{t+1} = C + α·E·Ξ·U·(1−C) − δ_C·C | Biological reserve | Reserve capacity of the system: nephron mass, coronary flow reserve, hepatocyte reserve, β-cell mass, alveolar surface area. Decays at rate δ_C; replenishes via E (exposure to healing resources) × Ξ × U. |
| OAM — Θ | Repair TractionΘ = σ(Θ_base + θ_C·C + θ_E·E − θ_K·K) | Biological repair capacity | Repair sigmoid: rises with C (reserve) and E (healing resources), falls with K (resistance to repair — fibrosis, calcification, β-cell depletion). Θ_base = −1.0 (repair starts hard, requires overcoming basal friction). |
| OAM — K | Resistance (config: K=0.3) | Biological resistance to repair | Structural resistance: arterial calcification, fibrosis, scar tissue, β-cell depletion, epigenetic changes in immune cells. Represents the biological friction that opposes normalization. Rises as degradation accumulates. |
| OAM — E | Exposure (config: E=0.6) | Biological exposure surface | Endothelial surface exposed to dyslipidemia; nephrons exposed to pressure; hepatocytes exposed to fat; alveolar surface exposed to hypoxia. Also: exposure to repair resources (exercise, sleep, nutrition). |
| OAM — Ξ | PropagationΞ = Ξ_base + (σ·Ξ_unit·Act_{t−τ})·Λ | Cascade between systems | How one degrading system drives degradation in another: HTN → CKD → cardiovascular → metabolic cascade; inflammation → insulin resistance → MASLD. Trusted carriers = functional organ systems maintaining cascade propagation. Lambda (Λ) = cascade coupling strength. |
| OAM — ΔD | Degradation ReductionΔD = β·U·C·L_life·R_s·E·Θ | Biological repair rate | Rate at which biological repair reduces accumulated damage. High when U (function), C (reserve), L_life (life-supporting conditions), R_s (risk reduction), E (healing resources), and Θ (repair traction) are all elevated. Falls when any factor is depleted. |
| OAM — D | Cumulative DegradationD_{t+1} = D_t + growth − ΔD | Cumulative biological damage | Accumulated tissue damage: atherosclerotic plaque burden, fibrosis extent, nephron loss, β-cell depletion, hepatic fat accumulation. Grows at rate `growth_per_cycle` (0.05 default), reduced by ΔD. Floored at 0 (cannot be negative). |
The OAM degradation cycle, as defined in the canonical runtime, maps onto biological pathophysiology as a sustained pressure-versus-repair dynamic. The key relationship: chronic disease occurs when P (biological pressure) persistently exceeds repair capacity (Θ × C) over time, causing D (cumulative damage) to accumulate faster than ΔD (repair) can reduce it.
Each condition is mapped as an OAM degradation pathway. The chain reads: pressure source → system strain → degradation pathway → feedback failure → measurable sign → downstream effect. Uncertainty boundaries are stated for each. These pathways describe population-level biological mechanisms, not individual predictions.
| ID | Condition | Domain | Key OAM pressure | Key degradation | Measurable sign | Key HIR block |
|---|---|---|---|---|---|---|
| PP-09 | Endothelial Dysfunction | BD-01 | Oxidative stress · low NO bioavailability · inflammatory cytokines · hyperglycemia; F-dominant pressure | Reduced flow-mediated dilation; impaired vasodilation → downstream perfusion↓; permissive for PP-02 | FMD (research tool) · biomarkers (non-specific) | No direct wearable signal for endothelial function. FMD is a research measure, not clinical standard |
| PP-10 | Sleep Apnea-Related Strain | BD-05/06 | Intermittent hypoxia (W: acute) + chronic sleep fragmentation (F) + SNS surges; intrathoracic pressure swings | Endothelial dysfunction; atrial remodeling (PP-15 risk); nocturnal HTN; sympathetic hyperactivation; metabolic dysregulation | AHI · SpO2 nadir · time below 88% · BP nocturnal dipping loss | Home sleep test ≠ full PSG in many cases. AHI alone ≠ clinical severity. Wearable SpO2 not equivalent to polysomnographic oximetry. |
| PP-11 | Chronic Stress / Autonomic Load | BD-05 | Sustained HPA activation (cortisol F) + SNS surge W; psychosocial stressors → glucocorticoid + catecholamine excess | HRV↓ · HTN contribution · visceral fat accumulation · immune dysregulation · sleep architecture disruption | HRV metrics · cortisol (AM) · BP · subjective stress measures | HRV is a cardiac metric, not a direct brain measurement (from BF Layer). Cortisol is context-sensitive; single measurement insufficient. |
| PP-12 | Obesity-Related Strain | BD-02 BD-01 BD-08 | Mechanical (joint, spinal loading) + metabolic (visceral adipose, adipokines) + respiratory (upper airway narrowing) pressure — multi-domain simultaneous P | Osteoarthritis acceleration · sleep apnea (PP-10) · insulin resistance (PP-06) · cardiovascular risk · MASLD (PP-13) | BMI · waist circumference · adiposity measures | BMI is a population-level statistical measure; poor individual predictor of metabolic health or risk. No weight-related shame claim permitted. |
| PP-13 | Fatty Liver Pathway (MASLD) | BD-07 | Caloric excess → hepatic lipid overflow (W); insulin resistance → FFA excess delivery to liver (F); fructose overload; gut-derived LPS (endotoxemia) | Hepatic steatosis → MASH (inflammation) → fibrosis → cirrhosis risk; hepatic insulin resistance amplifies systemic IR | Liver enzymes (ALT/AST, non-specific) · hepatic steatosis index · FIB-4 · elastography | Elevated ALT ≠ MASLD without imaging. Liver enzymes are non-specific to etiology. REVIEW_REQUIRED for non-invasive fibrosis staging thresholds |
| PP-14 | Respiratory / Oxygenation Impairment | BD-06 | Airway obstruction (structural or inflammatory) · alveolar damage · pulmonary vascular resistance · ventilation-perfusion mismatch | Hypoxemia → multi-organ demand; hypercapnia → acidosis; pulmonary hypertension → RV strain; impaired exercise capacity | SpO2 (resting + exertional) · spirometry · ABG · 6MWD · DLCO | Wearable SpO2 at rest is not equivalent to exertional SpO2. Spirometry requires technique validation. Single SpO2 reading ≠ chronic impairment. |
| PP-15 | Arrhythmia Risk Pathways | BD-01 BD-05 | Atrial remodeling (PP-10, HTN, CAD) · electrolyte disturbance · autonomic dysregulation · ischemia → re-entry substrate · genetic channelopathy | Atrial fibrosis → AFib substrate; QT prolongation → VF risk; ischemia → re-entry circuits; autonomic → triggered activity | ECG · Holter · cardiac event monitor · electrolytes · echocardiography · BNP | Wearable ECG single-lead ≠ 12-lead clinical ECG. Wearable AFib detection: sensitivity/specificity depends on device and algorithm — not equivalent to Holter. |
| PP-16 | Heart Failure Progression | BD-01 | Advanced CAD (PP-03) + HTN (PP-01) + DM + arrhythmia → progressive LV dysfunction; P = volume/pressure overload | Neurohormonal activation (RAAS, SNS) → maladaptive remodeling; cardiomyocyte loss; fibrosis ↑; HFrEF or HFpEF phenotype | LVEF · BNP/NT-proBNP · 6MWD · functional class · diuretic requirement | LVEF is a single-modality measure with significant inter-observer and modality variation. BNP elevated in obesity, AF, CKD independently. REVIEW_REQUIRED for HFpEF diagnostic criteria evolution |
| PP-17 | Chronic Pain / Injury Feedback Loops | BD-08 BD-05 | Tissue injury → peripheral sensitization → central sensitization → allodynia/hyperalgesia → pain behavior → reduced activity → deconditioning → increased vulnerability | Nociceptive pathway sensitization; HPA activation; sleep disruption amplifying pain; social/psychological comorbidity; medication effects | Pain scales (subjective) · functional capacity measures · sleep quality · psychological measures | Pain is subjective — pain scale ≠ objective nociception. "Pain behavior" must not be used to question legitimacy of experience. No character inference from pain report. |
| Measurement Type | What it directly produces | Key limitations | Default uncertainty |
|---|---|---|---|
| Clinical BP (office) | Auscultatory or oscillometric arterial pressure at a moment in time | White coat effect; masked HTN; position/arm; single reading insufficient; requires ≥2 separate occasions | PB-01 PB-02 |
| Wearable BP / cuffless | Oscillometric or pulse transit time estimate of blood pressure | Not validated as clinical standard in most devices; accuracy varies by device, individual, arm position, arrhythmia; cannot diagnose HTN | PB-04 PB-01 |
| Fasting lipid panel | Serum concentrations of TC, LDL-C, HDL-C, TG at blood draw time | LDL-C is calculated in most labs (Friedewald equation, inaccurate at high TG); acute illness, diet, medication alter values; non-fasting affects TG | PB-03 PB-06 |
| HbA1c | % of glycated hemoglobin reflecting ~3-month average glucose exposure | Altered by hemoglobin variants (HbS, HbC), hemolysis, iron deficiency, CKD, transfusion; not equivalent across all populations; reflects average, not variability | PB-08 PB-07 |
| hsCRP | Serum C-reactive protein concentration (high-sensitivity assay) | Non-specific acute phase reactant; elevated in infection, trauma, autoimmune, obesity, smoking; cannot identify source; single value limited | PB-03 PB-01 |
| eGFR (calculated) | Estimated glomerular filtration rate from serum creatinine (+/- cystatin C) + demographic inputs | Equation-dependent; muscle mass confounds creatinine; CKD staging requires ≥3 months confirmed; cystatin C more accurate in certain populations | PB-01 PB-08 |
| Wearable heart rate | Inter-beat interval from PPG or optical sensor at wrist/finger | Not equivalent to ECG; motion artifact; poor accuracy in arrhythmia (AFib); pigmentation affects optical accuracy; no waveform morphology | PB-04 PB-09 |
| Wearable SpO2 | Estimated oxygen saturation from pulse oximetry at peripheral site | Not calibrated for clinical use in most consumer devices; skin pigmentation affects accuracy; nail polish, cold extremities, motion artifact; not equivalent to arterial blood gas | PB-04 |
| Wearable ECG (single lead) | Single-lead rhythm strip; can detect rate and some rhythm | Not equivalent to 12-lead; cannot evaluate ST segments, axis, QRS morphology, or most ischemia patterns; AFib detection sensitivity/specificity device-dependent | PB-04 |
| Wearable sleep staging | Accelerometer/PPG-derived estimate of sleep stages | Not equivalent to polysomnography; significantly less accurate for N1/N2 discrimination; REM detection variable; cannot detect sleep apnea events | PB-04 PB-05 |
| Liver enzymes (ALT/AST) | Serum transaminase concentrations reflecting hepatocellular injury | Non-specific — elevated in alcohol, MASLD, medications, muscle injury, celiac, thyroid; normal values do not exclude liver disease; significant inter-lab variation | PB-03 PB-07 |
| Self-report scales | Subjective ratings by the person (pain, fatigue, stress, mood) | Subjective by design; affected by recall bias, social desirability, scale interpretation; not convertible to objective biological measures without validation in that context | PB-05 |
| Class ID | Class | Cat. | Effect | May suspend? | May raise confidence? |
|---|---|---|---|---|---|
| PA-01 | mechanism_incompletely_characterized | PA | Biological mechanism producing observed degradation is not fully established; known associations do not equal confirmed mechanism | No | Never |
| PA-02 | individual_pathway_variation_high | PA | Group-level degradation pathway does not apply uniformly; individual variation in progression rate, threshold, and target-organ response is substantial | No | Never |
| PA-03 | compensation_state_unknown | PA | Whether system is compensated (stable with elevated D) or decompensating cannot be determined from single-time-point data; requires longitudinal context | Conditional | Never |
| PA-04 | multi_domain_cascade_active | PA | Degradation propagating across multiple biological domains simultaneously; attribution to single condition inappropriate; Ξ coupling complicates isolation | No | Never |
| PA-05 | progression_rate_individual_unknown | PA | Rate of D accumulation for this individual is unknown; population-level trajectories do not determine individual timeline | No | Never |
| PA-06 | threshold_effect_unresolved | PA | The pressure or degradation threshold beyond which decompensation occurs is individual-specific and not predictable from current data | No | Never |
| PA-07 | interaction_effects_complex | PA | Interaction between co-morbid conditions (PP-07, metabolic syndrome) is non-linear and bidirectional; single-condition framing is incomplete | No | Never |
| CATEGORY PB — MEASUREMENT / PROVENANCE | |||||
| PB-01 | single_measurement_insufficient | PB | Single reading (BP, glucose, biomarker) insufficient to establish a persistent pattern; repeated confirmed measurements required per clinical standards | Yes | Never |
| PB-02 | situational_or_white_coat_effect | PB | Reading may reflect situational state (white coat HTN, anxiety-driven glucose spike, post-exercise) rather than persistent condition; ambulatory/home monitoring needed | Yes | Never |
| PB-03 | biomarker_nonspecific | PB | Biomarker elevation has multiple possible causes; elevated value cannot be attributed to specific condition without clinical context and differential | Conditional | Never |
| PB-04 | wearable_not_clinically_validated | PB | Consumer wearable signal (HR, SpO2, ECG, BP, sleep) does not meet clinical standard; accuracy claims depend on device, population, and validation study context | Yes — may not support clinical interpretation | Never |
| PB-05 | missing_clinical_context | PB | No clinical referral question, examination findings, medication list, or differential diagnosis provided; interpretation without clinical context cannot be validated | Yes | Never |
| PB-06 | medication_effects_undocumented | PB | Medications that alter biomarker values (statins → LDL, beta-blockers → HR, diuretics → electrolytes) not documented; biomarker interpretation unreliable | Yes | Never |
| PB-07 | comorbidity_confound | PB | Comorbid condition (CKD, anemia, obesity, liver disease) alters biomarker expected values or interpretation; standard reference ranges may not apply | Conditional | Never |
| PB-08 | population_reference_mismatch | PB | Reference ranges or diagnostic thresholds derived from different population; ethnicity, age, sex, or body composition of index population differs from guideline source | Conditional | Never |
| PB-09 | provenance_or_chain_unverified | PB | Source, collection conditions, lab accreditation, or chain of custody cannot be confirmed; results unreliable | Yes — hard override | Never |
| PB-10 | technical_error_suspected | PB | Result implausible given clinical context; possible hemolysis, lipemia, calibration failure, sample mix-up; requires repeat before interpretation | Yes — hard override | Never |
// Pathophysiology degradation pathway record — Primordial Pathophysiology Layer v0.1 { // --- Identity --- "record_id": "string // unique record ID", "condition_id": "enum // PP-01 through PP-17", "condition_name": "string", "biological_domain": "enum[] // BD-01 through BD-08", "created_at": "ISO8601", "schema_version": "string", // --- OAM Pathway Variables --- "oam_pressure_source": "string // W (acute stressor) and F (chronic load) components described", "oam_system_strain": "string // how P manifests as tissue/organ strain", "oam_degradation_pathway": "string // mechanism by which D accumulates", "oam_feedback_failure": "string // where repair (Θ) breaks down or K rises", "oam_cascade_targets": "enum[] // PP IDs that receive Ξ propagation from this condition", "oam_P_estimate": "enum // low | moderate | high | very_high | unknown", "oam_D_estimate": "enum // none | mild | moderate | severe | unknown", "oam_Theta_estimate": "enum // high | moderate | low | depleted | unknown", "oam_C_estimate": "enum // preserved | reduced | significantly_reduced | unknown", "oam_K_estimate": "enum // low | moderate | high | unknown // resistance to repair", "oam_compensation_state": "enum // compensated | decompensating | decompensated | unknown", // --- Measurable Signs --- "measurable_signs": [ { "sign_id": "string", "measurement_type": "enum // clinical_bp | lab_biomarker | wearable | imaging | exam | functional_test | self_report", "measurement_label": "string // e.g. hsCRP, eGFR, LVEF, SpO2", "what_it_directly_measures": "string // NOT what it is claimed to represent", "uncertainty_classes": "enum[] // PB-01 through PB-10 active for this sign", "single_value_sufficient": "bool // false = PB-01 applies; repeat required", "wearable_not_clinical_std": "bool // true = PB-04 applies" } ], // --- Downstream Effects --- "downstream_effects": "string[] // described as risks or associated pathways, not predictions", "cascade_pathway_ids": "enum[] // PP IDs downstream via Ξ", // --- Pathophysiological Uncertainty (Category PA) --- "path_unknown_class": "enum[] // PA-01 through PA-07 | none", "mechanism_status": "enum // well_characterized | partially_characterized | contested | unknown", // --- Measurement / Provenance Uncertainty (Category PB) --- "measurement_unknown_class": "enum[] // PB-01 through PB-10 | none", "provenance_class": "enum // verified | partially_documented | unverified", "hard_override_triggered": "bool // true = PB failure sufficient to invalidate interpretation", // --- HIR Claims Governance --- "hir_inference_allowed": "bool // DEFAULT false. true only if PA none + PB none + provenance verified + repeated measures confirmed", "claims_permitted": "string[] // what may be stated, bounded to evidence", "claims_blocked": "string[] // explicit list of overclaims blocked for this record", "person_level_claim_blocked": "bool // ALWAYS true — R gate active unconditionally", "treatment_recommendation": "bool // ALWAYS false — never produced by this system", "diagnosis_label": "bool // ALWAYS false — never produced without validated clinical context", // --- Interpretation Status --- "interpretation_status": "enum // valid | caution | suspended | invalidated", "notes": "string[]", "source_needed": "string[] // any items requiring SOURCE_NEEDED or REVIEW_REQUIRED" }
// Sample record — confirmed sustained HTN pathway { "condition_id": "PP-01", "biological_domain": ["BD-01"], "oam_pressure_source": "W: acute SNS surges, exertion spikes; F: sustained elevated MAP, RAAS activation, sodium retention", "oam_system_strain": "Endothelial shear stress; LV afterload increase; renal glomerular pressure; arteriolar remodeling", "oam_degradation_pathway": "Endothelial dysfunction → vascular hypertrophy → LV mass ↑ → glomerulosclerosis → microalbuminuria", "oam_feedback_failure": "Baroreceptor resetting at elevated setpoint; endothelial NO↓ → impaired vasodilation → worsened HTN; RAAS perpetuation", "oam_P_estimate": "high", "oam_D_estimate": "mild_to_moderate", "oam_Theta_estimate": "moderate — depressed by chronic oxidative stress", "oam_K_estimate": "moderate — baroreceptor resetting, arterial stiffening resist normalization", "oam_compensation_state": "compensated — LV hypertrophy maintaining output; state unknown without echo", "oam_cascade_targets": ["PP-03", "PP-04", "PP-05", "PP-15", "PP-16"], "measurable_signs": [ { "sign": "BP readings", "uncertainty": ["PB-01", "PB-02"], "single_value_sufficient": false }, { "sign": "Wearable BP", "uncertainty": ["PB-04"], "wearable_not_clinical_std": true } ], "path_unknown_class": ["PA-01", "PA-02"], "mechanism_status": "partially_characterized — primary HTN mechanism unknown in ~90% of cases", "claims_permitted": ["BP readings above thresholds noted", "sustained elevation requires confirmation", "downstream organ strain is plausible if sustained"], "claims_blocked": ["Single wearable reading = hypertension diagnosis", "Confirmed organ damage without measurement", "Treatment recommendation of any kind"], "person_level_claim_blocked": true, "treatment_recommendation": false, "diagnosis_label": false, "interpretation_status": "caution — sustained elevation requires confirmed repeated measurements + clinical evaluation" }
{
"condition_id": "PP-02", "biological_domain": ["BD-01", "BD-03"],
"oam_pressure_source": "W: oxidized LDL load, inflammatory triggers; F: chronic dyslipidemia, endothelial shear at bifurcations, sustained hyperglycemia",
"oam_degradation_pathway": "LDL oxidation → endothelial activation → monocyte recruitment → foam cell → fatty streak → fibrous plaque → potential calcification",
"oam_feedback_failure": "Endothelial NO↓ → impaired vasodilation; plaque-driven inflammation amplifies endothelial dysfunction; HDL dysfunction impairs reverse cholesterol transport",
"oam_K_estimate": "high when calcified plaques present — calcification resists modification",
"oam_Theta_estimate": "reduced — endothelial progenitor mobilization impaired by chronic oxidative stress",
"oam_cascade_targets": ["PP-03", "PP-04", "PP-09"],
"measurable_signs": [
{ "sign": "LDL-C", "uncertainty": ["PB-03", "PB-06"], "what_it_measures": "serum LDL cholesterol concentration — not plaque burden directly" },
{ "sign": "hsCRP", "uncertainty": ["PB-03"], "what_it_measures": "non-specific acute phase reactant — cannot confirm atherosclerotic inflammation specifically" },
{ "sign": "CAC score", "uncertainty": ["PB-05"], "what_it_measures": "coronary calcium burden — more specific for established atherosclerosis; does not assess non-calcified plaque or stability" }
],
"path_unknown_class": ["PA-03", "PA-06"],
"mechanism_status": "well_characterized at plaque formation level; plaque stability and rupture prediction remains incompletely characterized",
"claims_blocked": ["Elevated LDL = blocked arteries", "hsCRP confirms plaque", "Plaque size = rupture risk", "Any treatment direction"],
"person_level_claim_blocked": true, "interpretation_status": "caution"
}
{
"condition_id": "PP-06", "biological_domain": ["BD-02", "BD-03"],
"oam_pressure_source": "W: glycemic/FFA spikes; F: chronic caloric excess, visceral adipose adipokine secretion, sleep disruption, sedentary pattern",
"oam_degradation_pathway": "GLUT4 signaling impairment → β-cell hypersecretion (compensation) → ectopic fat accumulation → ceramide → β-cell exhaustion → progressive hyperglycemia",
"oam_feedback_failure": "Ectopic fat (hepatic, intramyocellular) blocks insulin signaling; adiponectin ↓; oxidative stress perpetuates IR; K ↑ as ectopic fat accumulates",
"oam_C_estimate": "β-cell secretory reserve: initially preserved (compensatory), declining with progression",
"oam_K_estimate": "rising — ectopic fat, ceramide accumulation resist insulin sensitization",
"oam_Theta_estimate": "moderate — exercise-induced GLUT4 upregulation, GLP-1 signaling partially maintain repair",
"oam_cascade_targets": ["PP-07", "PP-08", "PP-13", "PP-02"],
"measurable_signs": [
{ "sign": "Fasting glucose", "uncertainty": ["PB-01", "PB-02"], "single_value_sufficient": false },
{ "sign": "HbA1c", "uncertainty": ["PB-07", "PB-08"], "what_it_measures": "~3-month average glycated hemoglobin — affected by hemoglobin variants, anemia, CKD" },
{ "sign": "HOMA-IR (calculated)", "uncertainty": ["PB-03"], "what_it_measures": "calculated proxy from fasting glucose × fasting insulin — NOT a direct IR measurement; significant individual variability" }
],
"path_unknown_class": ["PA-02", "PA-05"],
"claims_blocked": ["HOMA-IR = confirmed insulin resistance diagnosis", "Fasting glucose alone = T2DM", "Dietary or medication recommendation", "Lifestyle blame or shame"],
"person_level_claim_blocked": true, "interpretation_status": "caution"
}
{
"condition_id": "PP-10", "biological_domain": ["BD-05", "BD-06", "BD-01"],
"oam_pressure_source": "W: episodic hypoxia + arousal-triggered SNS surges + intrathoracic pressure swings; F: chronic sleep fragmentation, chronic SNS activation",
"oam_system_strain": "Repeated hypoxia-reoxygenation injury; sustained SNS hyperactivation; nocturnal HTN; HPA axis disruption; metabolic dysregulation from sleep fragmentation",
"oam_degradation_pathway": "Endothelial dysfunction → nocturnal HTN → atrial remodeling → pulmonary pressure ↑ (if severe); metabolic syndrome amplification",
"oam_feedback_failure": "Obesity perpetuates airway obstruction → structural K ↑; HIF-1α upregulation; impaired baroreflex; oxidative stress from reoxygenation",
"oam_cascade_targets": ["PP-01", "PP-07", "PP-11", "PP-15"],
"measurable_signs": [
{ "sign": "AHI (apnea-hypopnea index)", "what_it_measures": "events per hour on sleep study — PSG gold standard; home sleep test is limited by no EEG, no leg movements, no RERA detection", "uncertainty": ["PB-01", "PB-05"] },
{ "sign": "Wearable SpO2 / sleep staging", "uncertainty": ["PB-04"], "what_it_measures": "peripheral SpO2 estimate — NOT equivalent to polysomnographic oximetry; cannot detect respiratory events or arousals" }
],
"path_unknown_class": ["PA-02", "PA-06"],
"mechanism_status": "well_characterized for cardiovascular strain pathway; individual oxygen sensitivity and threshold for harm varies (PA-02)",
"claims_blocked": ["Wearable SpO2 dips = sleep apnea diagnosis", "AHI alone = clinical severity", "CPAP or treatment recommendation", "Home sleep test = PSG equivalence"],
"person_level_claim_blocked": true, "interpretation_status": "caution"
}
{
"condition_id": "PP-08", "biological_domain": ["BD-03", "BD-02", "BD-01"],
"oam_pressure_source": "F-dominant: visceral adipose adipokine secretion (TNF-α, IL-6, leptin), gut dysbiosis, chronic psychosocial stress → HPA/SNS → IL-6; environmental pollutants",
"oam_degradation_pathway": "Sustained cytokine exposure → endothelial activation → NF-κB perpetuation → coagulation activation → plaque destabilization → insulin signaling impairment",
"oam_feedback_failure": "NF-κB perpetuates cytokine production; adipose M1 macrophage polarization persists; SPM (pro-resolving mediator) production impaired → resolution failure",
"oam_Theta_estimate": "reduced — SPM capacity depressed; K rising from M1 epigenetic programming",
"oam_K_estimate": "moderate — M1 macrophage polarization, metabolic endotoxemia resist resolution",
"oam_cascade_targets": ["PP-02", "PP-06", "PP-09", "PP-13"],
"measurable_signs": [
{ "sign": "hsCRP", "what_it_measures": "non-specific acute phase reactant — elevated in infection, trauma, autoimmune, obesity, smoking; source cannot be determined from value", "uncertainty": ["PB-03", "PB-01"] },
{ "sign": "IL-6, fibrinogen, WBC", "what_it_measures": "additional non-specific inflammation markers — directional but not source-specific; require clinical context", "uncertainty": ["PB-03", "PB-05"] }
],
"path_unknown_class": ["PA-01", "PA-07"],
"mechanism_status": "partially_characterized — 'chronic low-grade inflammation' as a unified entity is contested; multiple overlapping mechanisms",
"claims_blocked": ["Elevated hsCRP = confirmed chronic inflammation", "Source of inflammation inferred from hsCRP alone", "Anti-inflammatory diet/supplement recommendation", "Lifestyle attribution or blame"],
"person_level_claim_blocked": true, "interpretation_status": "caution — elevated non-specific markers require clinical differential"
}
Define each biological domain with its OAM reserve (C), primary degradation pattern (D), and repair mechanism (Θ). Schema must be stable before any condition pathway is added.
For each domain, define what W, F, C, K, Θ, and E represent biologically, with example biomarker proxies where available. Distinguish OAM model-level constructs from direct clinical measurements.
Define each condition pathway with its OAM structure. Mechanism status (PA-01), individual variability (PA-02), and compensation state (PA-03) flags set per condition before any measurable sign is added.
Each measurement type is assigned its default PB uncertainty classes before any measurement values are processed. Wearable measurements are categorized as PB-04 by default.
Document which conditions drive which via OAM propagation Ξ. Each cascade edge must cite published epidemiological or mechanistic evidence supporting the association. SOURCE_NEEDED where not well-established.
Sample records must include: a clean single-domain record, a multi-cascade record, a wearable-only suspended record, a provenance-failed invalidated record, and a record where OAM D is high but Θ is also high (not decompensated despite degradation).
Link biofeedback signal modalities (BF-01 through BF-08) to pathophysiology pathway targets where relevant (e.g., HRV biofeedback → PP-10, PP-11; EMG → PP-17; respiratory → PP-14). All biofeedback linkages carry inherited biofeedback layer uncertainty.
Same conditional requirements as Brain Layer Layer 8. Pathophysiology-specific: requires licensed clinician with relevant specialty competence per condition domain. Not activated by default. Cannot produce diagnoses — produces bounded, clinician-reviewed interpretation notes only.