Working model — evidence table
Dense matrix for clinician discussion. Glyphs: + explained · − argues against · · not explained · ? cannot be assessed. Legend is on the same surface as the matrix. Includes H-NULL.
Analysis version v0.4.1 · evidence current through 2026-08-10 · Changelog
analysis v0.4.1 · evidence through 2026-08-10 · as of 2026-08-11 · clinician review: not performed · patient approval: obtained · Research only — not medical advice.
Citation counts are not weights. Supporting and contradicting literature tallies are list lengths only — they are not scores, probabilities, or diagnostic weights.
Matrix covers 18 of 110 published claims that are anchored to at least one hypothesis (explains or does-not-explain). Coverage is incomplete by design — unlinked claims remain on /case/.
| Research preview · Not medical advice · Published with Drift0r’s permission · Permission is not endorsement · Not clinician-reviewed · Licensed clinicians must verify underlying records · Do not start, stop, or change treatment based on this material | ||||||
|---|---|---|---|---|---|---|
| Claim | H-NULL | H1 | H2 | H3 | H4 | H5 |
| CLM-0003 DXA lumbar L3 Z-score −4.3 on 2025-06-16 at Site 1 (BMD 0.631 g/cm²); same-day L3 T-score −4.3 (Z-score preferred for males <50 per ISCD). | · | + | + | · | − | − |
| CLM-0005 Left forearm total Z-score −3.1 and T-score −3.3 on 2026-06-19 Site 1 (BMD 0.516 g/cm²) (Z-score preferred for males <50 per ISCD). | · | · | + | · | · | · |
| CLM-0006 Total hip BMD fell from 0.836 to 0.802 g/cm² (compiled summary states −4.2%; recomputation (0.802−0.836)/0.836 ≈ −4.1%) between 2025-06-16 and 2026-06-19 on the same Site 1 scanner; compiled summary states LSC=0.027 g/cm² and calls the change significant at 95% confidence. | · | · | + | · | · | · |
| CLM-0010 Serum CTX 616 pg/mL on 2026-06-26 (reference 70–780 pg/mL) — upper end of reference interval; fasting/time-of-day not stated in compiled summary. | · | · | · | + | · | · |
| CLM-0011 Bone formation markers (P1NP, bone-specific ALP, osteocalcin) are not documented among ~118 tests in the public ledger. | · | · | · | + | · | · |
| CLM-0013 L5–S1 bilateral pars defects with grade 1 spondylolisthesis and right L5 root impingement are documented on imaging summaries; SCS implanted March 2026. | · | + | · | · | · | · |
| CLM-0015 24-hour urine calcium values 283 → 254 → 333 mg/24h (male; common threshold often 300 mg/day or 4 mg/kg — 2 of 3 collections below 300), with high urine sodium on latest panel (174 mmol/24h) and alkaline urine pH 6.53. Middle value (254 on 2025-09-30) was normal at the performing lab (ref 100–300) and high only against Litholink range 40–250; ranges differ by lab. | · | + | · | + | − | · |
| CLM-0018 Historical total testosterone reported as low as ~34 ng/dL (narrative/clinical-context in summaries); earliest discrete tabulated total T values in endocrine summary begin 2021. | · | − | · | · | − | · |
| CLM-0023 Serum/plasma thiamine 7 nmol/L on 2022-09-29 (reference 8–30) — laboratory-low / deficient by that assay. | · | + | − | − | · | − |
| CLM-0027 IgG subclass 1 persistently low and IgG subclass 4 persistently high across multiple 2025–2026 draws (e.g., IgG1 324 with ref 382–929; IgG4 163.6 with ref 4–86); total IgG remains in range. | · | + | − | − | · | + |
| CLM-0030 Serum tryptase elevated (17.7 µg/L on 2025-10-01; 14.5 mcg/L on 2026-06 panel) above ref <11; urinary mast-cell mediators normal on 2026 panel. | · | − | · | · | · | · |
| CLM-0031 Hereditary alpha-tryptasemia (HαT) reported positive in patient materials. | · | − | · | · | · | · |
| CLM-0034 Hib IgG titer non-protective (0.33 mcg/mL, ref ≥1.00) and many pneumococcal serotype IgG values low on Jun 2026 panel; these are functional titers, not a formal vaccine-challenge study. | · | · | · | · | · | + |
| CLM-0036 Babesia FISH (whole blood) positive on two specialty-lab draws (Jul 2023 and Feb 2024); Babesia PCR (B. microti and B. duncani) and immunoblot IgM/IgG negative on Jul 2023 panel. | · | − | − | · | · | · |
| CLM-0037 Bartonella immunoblot IgM genus/species positive Jul 2023, later indeterminate/negative pattern Feb 2024; Bartonella PCR and FISH negative. | · | · | · | · | + | · |
| CLM-0039 Patient-reported joint pain, night sweats, nightmares, and REM sleep (~15 → ~90 min/night) improved during two courses of atovaquone + clindamycin (± azithromycin); the specialty summaries describe each course as producing sustained (≥6 month) improvement, with joint-pain relapse after the first course and the second (6-week, + azithromycin) course described as larger and more durable. Durability beyond the second course is not documented in the available summaries. This does not by itself prove Babesia, Bartonella, or other infection. | · | · | · | · | − | · |
| CLM-0040 MRI left humerus Feb 2026: mild periosteal edema/enhancement without marrow signal change; reactive-appearing axillary nodes. | · | · | · | · | + | · |
| CLM-0112 The 2021 treatment record includes an aromatase inhibitor alongside the selective estrogen-receptor modulator: the endocrine summary documents the reported regimen during the 2021 titration period as clomiphene 25 mg daily plus anastrozole 1 mg weekly, and its hormone table prints an estradiol of 9.3 pg/mL on 2021-03-15 - measured by sensitive LC/MS/MS against an 8.0-35.0 pg/mL interval per its methodology note (5), while every other estradiol value in the table uses a standard immunoassay the same note says is not directly comparable. In the public video the patient states the aromatase inhibitor was taken "for two years" to lower a clomiphene-induced estradiol rise, and that both medications were then stopped without tapering before the 2021 symptom cascade (the automatic captions render the drug name as "an astrol"). This row records the exposure as history; it asserts nothing about what the exposure did. | · | · | − | · | · | · |
Research preview · Not medical advice · Published with Drift0r’s permission · Permission is not endorsement · Not clinician-reviewed · Licensed clinicians must verify underlying records · Do not start, stop, or change treatment based on this material
Hypothesis summaries
Citation counts are not weights. Confidence uses the five-word vocabulary only (never numeric probability).
H-NULL — Multi-independent axes (null model / no single unifier)
Qualitative null / base-rate baseline — not a competing disease label. Several common or semi-independent processes may coexist without one rare unifying diagnosis. A defensible numeric population prior for this exact multi-system presentation is not available from the sources currently cited; false precision is avoided. This record exists for Bayesian discipline when weighing H1–H5, not as a diagnosis.
confidence: medium · support lit +0 · contradict lit −0 · open: UQ-0017 (counts are not weights)
H1 — Layered skeletal–metabolic–neurologic–immune stack (infection detachable)
Preferred multi-disease research architecture from Round-1 synthesis — a research organizing frame, not a single causal mechanism and not a diagnosis. Infection limb detachable pending adjudication. Does not by itself explain tryptase/HαT (CLM-0030/0031), Babesia FISH×2 (CLM-0036), or historical profound hypogonadism (CLM-0018). Supporting cards are domain or methodological anchors (densitometry reporting, thiamine biomarkers, humoral abnormality), not proof of a layered multi-disease etiology. Models can agree on errors; architecture confidence is medium pending further adjudication.
confidence: medium · support lit +3 · contradict lit −0 · open: UQ-0003, UQ-0013, UQ-0017 (counts are not weights)
H2 — Monogenic / constitutional early-onset osteoporosis spectrum
Best single-primary research alternative (WNT1/LRP5/PLS3/mild OI spectrum; HPP low unless ALP truly low). Gene panel not performed. Related-cohort pathogenic yield is modest; panels can return variants of uncertain significance that complicate interpretation; negative panel does not close unknown genes or multi-hit secondary OP. Contradicting cards are now filed. lit-0340 covers what a bone-fragility gene panel actually finds in people referred for unexplained markedly low BMD for age (partial yield, so a genetic cause cannot be assumed from presentation), and lit-0341 covers male osteoporosis series in which identifiable secondary causes are common and more than one cause is often present at once. Both cut in the same direction as the caveats already named here — modest related-cohort yield and VUS interpretation difficulty — and neither can be read the other way, since a panel has not been done and so no result here argues for a genetic cause either. The 2026-08-10 Fable solo blinded round added two counterweights to this hypothesis's confidence, recorded here without changing its bucket: the record now carries an acquired exposure bearing on bone — an aromatase-inhibitor regimen recorded in the endocrine summary, a sensitive-assay estradiol of 9.3 pg/mL while on it, and about two years of weekly use per the patient's own account (CLM-0112; lit-0134, also filed on the contradicting list, records a year of that drug class lowering spine density in older men, while lit-0308 is carried as its short-horizon comparator — twelve weeks without marker worsening, which clears nothing about longer use) — and the patient's own account of decades of high-impact activity without peripheral fracture, which is an unusual biography for a monogenic fragility disorder of this severity, while also cautioning against reading the areal-BMD numbers as a complete description of bone strength.
confidence: medium · support lit +5 · contradict lit −3 · open: UQ-0013, UQ-0005, UQ-0020 (counts are not weights)
H3 — Calcium-flux / incomplete bone-turnover phenotyping module
Ongoing calcium-flux research module (serial 24h urine Ca 283→254→333 mg/24h in a male; common male threshold often 300 mg/day or 4 mg/kg — 2 of 3 collections below 300; middle value 254 normal at performing lab ref 100–300 vs Litholink 40–250) plus high urine Na and missing formation markers; module not unifier. CTX alone upper-normal without paired P1NP/BSAP does not prove uncoupling. Cited IH literature (lit-0152/lit-0153) describes mild BMD reduction and rate-of-loss association in stone formers — it does not account for spine T −4.3 magnitude. On stone status the record says two things and both belong here. The CT urogram of 2026-02-27 found no stones, and the urology summary records one lifetime stone, passed spontaneously in his late twenties after about a week of heavy energy-drink and fast-food intake. So this is a stone-forming history at its mildest end, not an absence of one, and the stone-former literature applies weakly rather than not at all. Three contradicting cards are now filed (lit-0337, lit-0338, lit-0339) covering whether urinary calcium tracks bone-density severity at all and whether stone-related fracture excess is site-selective. The last of those counts fractures rather than measuring bone density, so it bears on this module only through a specific step, stated here rather than left to be inferred — the excess it reports is confined to the spine, while the low readings in this record appear at spine, hip and forearm at once, which is more than a stone-and-calcium mechanism has been shown to produce. Magnitude mismatch and incomplete mechanism classification remain the other named counters. Distal renal tubular acidosis — the textbook differential for alkaline urine with high urine calcium and metabolic bone disease, and until now never named anywhere in this record — is registered here as considered and not favoured: the same stone-risk panel shows urine citrate 784 mg/24h against a lower limit of 400 (CLM-0088) where that condition characteristically drives citrate low, and serum total CO2 sits within its reference interval on every documented draw (CLM-0110), where the classic form requires a metabolic acidosis. Neither value excludes an incomplete form with preserved citrate; whether the alkaline-urine picture warrants formal acidification testing is a clinician judgment this record refers rather than closes.
confidence: medium · support lit +4 · contradict lit −3 · open: UQ-0002, UQ-0005 (counts are not weights)
H4 — Bartonella-spectrum residual contributor (specialty LDT contested)
Detachable residual contributor hypothesis for periosteal/nodule signals and contested specialty serology. Specialty IgM contested; PCR/FISH negative. Not commercially confirmed. Support is limited to applicability-limited musculoskeletal/osseous Bartonella case literature, not serology alone. Does not explain magnitude of generalized low BMD, historical hypogonadism, or hypercalciuria. Patient-reported improvement on atovaquone + clindamycin (± azithromycin) (CLM-0039) is a Babesia-directed regimen and is not organism-specific evidence for Bartonella — not listed as explained by H4.
confidence: low · support lit +2 · contradict lit −4 · open: UQ-0017 (counts are not weights)
H5 — Humoral abnormality / possible specific antibody deficiency
IgG1-low / IgG4-high lab pattern is real and polyclonal. Named specific antibody deficiency remains low confidence until same-lab pre/post polysaccharide vaccine challenge and infection history. lit-0206 (Lawrence & Borish 2022) is a diagnostic-pitfalls review cautioning against overcalling SAD from titers alone — filed under contradicting literature, not support. Not classic IgG4-RD — lit-0089 and lit-0096 support that non-classic / elevation-without-RD framing (catalog polarity supports H5's position) rather than contradicting it.
confidence: low · support lit +3 · contradict lit −1 · open: UQ-0007 (counts are not weights)
Research preview · Not medical advice · Published with Drift0r’s permission · Permission is not endorsement · Not clinician-reviewed · Licensed clinicians must verify underlying records · Do not start, stop, or change treatment based on this material