coronary 2.0.0: 2026 evidence rebuild of the Generation I expert module (O. Borysova). Adds every independent genome-wide-significant lead of the largest 2021-2026 GWAS for the trait plus functional variants, with evidence tiers (S-D); errors in the original rows corrected with recorded reasons (provenance in logs/authoring.log); gnomAD v4.1 frequencies; closed. Built with just-dna-compiler main a05cd54.

data/coronary/v2.0.0/README.md

@@ -0,0 +1,141 @@
+# Coronary Artery Disease (coronary) — version 2.0.0
+
+This module reports DNA spots linked to coronary artery disease (CAD): narrowing of the heart's own arteries,
+which can cause chest pain (angina) or a heart attack. Each result says whether your version of a spot is
+linked to a slightly higher, slightly lower or typical chance, compared with people who carry the most
+common version. Almost every spot has a small effect on its own. Blood pressure, cholesterol, smoking,
+diabetes and family history matter far more than any single spot, and nothing here is a diagnosis.
+
+## What changed in 2.0.0 (2026 evidence rebuild)
+
+Version 1.x carried 27 hand-curated variants (Olga Borysova). Large GWAS now report hundreds of CAD loci,
+so this version adds every independent genome-wide-significant lead variant from the largest 2022 CAD
+meta-analyses, plus a few rare functional variants with large effects. The 27 original rows are kept unchanged.
+
+| Tier | What | Variants | Genotype rows | Source |
+|---|---|---|---|---|
+| A | GWAS lead variants, Aragam et al. 2022 (anchor) | 257 | 771 | PMID 36474045, Suppl. Tables 3 and 17 |
+| A | Distinct novel loci, Tcheandjieu et al. 2022 | 56 | 168 | PMID 35915156, Suppl. Tables 2 and 3 |
+| B | Rare functional variants (APOB R3527Q, APOC3 R19X) | 2 | 6 | PMID 9603795, PMID 24941081 |
+| C | Legacy expert-curated rows (O. Borysova) | 27 | 81 | v1.1.0 |
+| | **Total** | **342** | **1,026** | 63 papers, 437 study rows |
+
+### Response to co-author comment C68 ("too few meaningful SNPs")
+
+The comment was right for v1.x: 27 variants were a literature-triage selection, not a systematic one.
+v2.0.0 applies a stated, reproducible inclusion rule. Every conditionally independent genome-wide-significant
+signal of the largest CAD GWAS (Aragam 2022: 241 signals at 198 loci in 1.17 million people, plus 38
+cross-ancestry loci with Biobank Japan) is included. So is every novel multi-ancestry locus from the Million
+Veteran Program study (Tcheandjieu 2022) that lies outside those regions, including the first X-chromosome
+CAD loci. Rare high-impact variants come from primary literature. Of 374 anchor candidates, 340 passed the
+locus-distinctness rule. 24 of those were then dropped because their effect allele could not be established
+safely (strand-ambiguous SNPs, multi-allelic indels, an allele mismatch), and 3 were already legacy rows.
+The module now covers 342 variants near 283 genes. Every dropped candidate and its reason is listed in
+`REBUILD_REPORT.md`.
+
+## Inclusion rule (exact)
+
+1. **Tier A — anchor.** Aragam KG et al., *Nat Genet* 2022 (PMID 36474045): all 241 conditionally independent
+   associations (GCTA-COJO, p<5e-8) of Supplementary Table 3, and all 38 loci of Supplementary Table 17
+   (p<5e-8 after meta-analysis with Biobank Japan).
+2. **Tier A — merge.** Tcheandjieu C et al., *Nat Med* 2022 (PMID 35915156): novel lead SNPs from Supplementary
+   Table 2 (Whites, 33) and Table 3 (multi-population, 62) with fixed-effect (METAL) p<5e-8, kept only if they lie more
+   than 500 kb (GRCh37) from every Aragam lead and from each other. Result: 61 distinct leads; 3 MR-MEGA-only loci
+   were excluded (no single per-allele effect).
+3. **Allele checks.** Strand-ambiguous A/T or C/G SNPs are kept only if the study effect-allele frequency is
+   ≤0.40 or ≥0.60 **and** the study's minor allele equals the 1000 Genomes minor allele (Ensembl). Indels are kept
+   only if the study's two alleles map uniquely to the GRCh38 resolved ref/alt pair by length. rsIDs merged in
+   dbSNP are authored under the current ID (rs2457480 → rs527052).
+4. **Tier B.** Rare functional variants with a published carrier odds ratio: APOB R3527Q (R3500Q, familial
+   defective apoB-100; ClinVar Pathogenic/Likely pathogenic, 2 stars; OR 7.0 for ischaemic heart disease, PMID 9603795) and
+   APOC3 R19X (loss-of-function; carrier OR 0.60 pooled across four APOC3 LoF variants, PMID 24941081). LPA
+   rs10455872, PCSK9 R46L, ANGPTL4 E40K, APOE ε2/ε4, the LDLR splice variant rs72658867 and the 9p21 signals are
+   already Tier A anchor leads. LPA rs3798220 and PCSK9 R46L also stay as legacy rows.
+5. **Tier C.** All 27 legacy variants kept unchanged. Where a legacy rsID is itself an anchor lead (rs11591147,
+   rs515135, rs964184), the legacy rows are kept and only the anchor study was added to `studies.csv`.
+
+## Weights (two scales — read before summing)
+
+* **New rows** (`method` = `gwas-lead-tierA` or `functional-tierB`): weight = −ln(OR) per copy of the row's
+  `effect_allele`, additive. The other homozygote is 0.0 (`neutral`), the heterozygote is −ln(OR) and the
+  effect-allele homozygote is −2·ln(OR), rounded to 3 dp. Positive = protective, negative = risk. The effect allele is the allele with
+  frequency <0.5 in the anchor data, so the most common genotype is the neutral baseline. The OR is the anchor's
+  per-allele OR re-expressed for that allele. Tier A magnitudes are 0.02–1.03 (median 0.06 per non-neutral
+  row). Tier B uses the published carrier OR, capped to [−3, 3] (the APOB R3527Q homozygote is capped at −3).
+* **Legacy rows** (`method` empty → default `expert-curated`, curator `just-dna-seq`): Olga Borysova's
+  hand-set scale (about −1.7 to +1.2). It is not log-odds and is not comparable with the new rows.
+* Several legacy rows sit in the same region as a Tier A lead (9p21, SORT1/CELSR2, LPA, PCSK9, LDLR, SMAD3,
+  MIA3, CXCL12, GUCY1A1 and others), so a simple sum double-counts those signals. The module is a set of
+  per-variant annotations, not a polygenic score. For a validated score, use a published PGS (e.g. from the
+  PGS Catalog) instead of summing this column.
+
+## Populations and limits
+
+Effect sizes come mostly from people of European ancestry; the Tcheandjieu and Aragam Table 17 loci add
+African American, Hispanic and East Asian data. Effects may differ in other ancestries. Eight leads are on the X
+chromosome (Tcheandjieu). Genotypes are written as two-copy (female) calls; a man's single X copy usually appears
+as a homozygous call, and how the study scaled male dosage is not stated.
+GWAS leads mark regions; the nearest gene named in each row is not necessarily the causal gene. Gene labels
+use current HGNC symbols where the source used an old one (e.g. GUCY1A3 → GUCY1A1, PPAP2B → PLPP3). The label
+is blank where the source named only an unnamed transcript.
+
+## Sources
+
+* Aragam KG et al. Discovery and systematic characterization of risk variants and genes for coronary artery
+  disease in over a million participants. *Nat Genet* 2022. PMID 36474045. Supplementary Tables 3 and 17
+  (file 41588_2022_1233_MOESM4_ESM.xlsx).
+* Tcheandjieu C et al. Large-scale genome-wide association study of coronary artery disease in genetically
+  diverse populations. *Nat Med* 2022. PMID 35915156. Supplementary Tables 2 and 3 (41591_2022_1891_MOESM3_ESM.xlsx).
+* Clarke R et al. Genetic variants associated with Lp(a) lipoprotein level and coronary disease. *NEJM* 2009. PMID 20032323.
+* Tybjærg-Hansen A et al. Association of mutations in the apolipoprotein B gene with hypercholesterolemia and the
+  risk of ischemic heart disease. *NEJM* 1998. PMID 9603795.
+* TG and HDL Working Group of the Exome Sequencing Project. Loss-of-function mutations in APOC3, triglycerides,
+  and coronary disease. *NEJM* 2014. PMID 24941081.
+* Legacy citations (59 papers) are in `studies.csv`, rows 1–118.
+
+Effect sizes were transcribed from the supplementary workbooks; per-row `provenance_quote` cells are left empty,
+and the source table of each row is named in `studies.csv` → `statistical_test`.
+
+## Authorship and review
+
+Original expert curator: Olga Borysova (v1.x, all `expert-curated` rows). The 2026 rebuild (new rows, studies,
+README, weighting) was AI-assisted (recorded in `authorship:` as `kind: [ai, agent]`). No human has reviewed
+the new rows yet. The independent lay-reader and scientific reviews described in module-voice have not been run.
+
+## Evidence tiers
+
+Every variant carries an evidence tier in `flags` (`tier:S` … `tier:D`) and in `priority`
+(S = high, A = medium, B/C/D = low). The tier never changes `weight`. Most variants in this module are
+weak signals, so the top tier is **S**, kept for the few variants that matter on their own. New (2026) rows
+also start their conclusion with the tier's label.
+
+| Tier | Meaning | Variants (of which legacy) |
+|---|---|---|
+| S | Strong evidence: an effect large enough to matter on its own (OR/HR ≥ 1.5 or ≤ 0.67, or ≥ 0.5 SD), robustly supported | 4 (1) |
+| A | Well established, small effect (research grade): genome-wide significant in the anchor GWAS and in ≥ 1 further publication, same direction | 120 (13) |
+| B | Single-study signal, small effect (research grade): genome-wide significant in the anchor GWAS only | 209 (4) |
+| C | Early evidence (research only): not genome-wide significant for this trait | 8 (8) |
+| D | Not supported: contradicted, or null in large GWAS / meta-analysis | 1 (1) |
+
+S is rare here on purpose: almost every CAD GWAS lead raises risk by a few percent per copy (median OR 1.04). Replication was read from the GWAS Catalog (REST v2, retrieved 2026-11-03; cohorts of different
+publications may overlap). `also_in:<module>` marks the 23 variants that also appear in another just-dna
+module. Summing weights across modules counts those twice. The rules are adapted from the Longevity Map v2
+requirements (`docs/longevitymap_v2/`).
+
+## Corrections to the original expert-curated rows
+
+The 2026 audit of the Generation I content (Supplementary Table S14 of the Just-DNA-Lite paper) found errors that were still present in v1.1.0. Version 2.0.0 corrects them, changing only the cell that was wrong. Each change is recorded with its reason in `provenance.json` and `logs/authoring.log`.
+
+| Variant | Genotype | Field | What was wrong |
+|---|---|---|---|
+| rs4977574 | G/G | conclusion | closing sentence said GG 'does not contain the risk' while the row scores GG as risk (-1.54) |
+| rs383830 | T/T | weight | T/T is the non-risk homozygote: the row's own text says the T allele is not associated with CHD in Europeans and the module names A as the risk allele, so the non-zero risk weight (-0.2) contradicted its own conclusion |
+| rs17514846 | A/C | weight | the conclusion says AC carriers have increased CAD risk but every genotype carried weight 0 |
+| rs17514846 | A/A | weight | the conclusion says AA carriers have increased CAD risk but the weight was 0 |
+| rs12413409 | G/G | conclusion | removed two sentences describing a different SNP (rs7692387, GUCY1A3: aspirin trial, PMID 31228190), which this module covers in its own rs7692387 rows |
+| rs12413409 | A/G | conclusion | as G/G: removed the rs7692387 aspirin-trial sentences, which describe a different SNP |
+| rs7250581 | A/G | weight | the row's own cited estimate for AG (OR 1.06, 95% CI 0.79-1.43, PMID 17554300) is not significant, so a risk weight (-0.5) asserted an effect the cited study did not find |
+| rs7250581 | A/G | conclusion | removed a stray file name ('OA-icon.png') pasted into the PMID bracket and stated that the cited estimate is not significant, matching the corrected neutral weight |
+| rs688034 | C/T | weight | the row's own cited estimate for CT (OR 1.11, 95% CI 0.98-1.25, PMID 17554300) is not significant, so the risk weight (-0.4) asserted an effect the cited study did not find |
+| rs17228212 | C/T | weight | the text gives a per-allele OR (1.26, PMID 17634449), so one copy carries half the two-copy weight (-1.10) on the module's own scale |
+| rs11206510 | C/T | weight | heterozygote and homozygote both carried -0.6 |

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data/coronary/v2.0.0/logs/authoring.log

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+2026-11-04T07:36:13Z authored rs4977574 conclusion='G/G: Several GWASs have revealed that the single nucleotide polymorphism (SNP) rs4977574 of ANRIL (CDKN2B-AS1) was associated with increased C...' (judged; no value from PMID 17478681 to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:15Z authored rs383830 weight='T/T: 0.0' (judged; no value from the row's own conclusion and the module's other genotype rows to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:18Z authored rs383830 state='T/T: neutral' (judged; no value from the row's own conclusion and the module's other genotype rows to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:20Z authored rs17514846 weight='A/C: -0.061; A/A: -0.122' (judged; no value from PMID 29212778 to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:22Z authored rs17514846 state='A/C: risk; A/A: risk' (judged; no value from the row's own conclusion and the module's other genotype rows to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:24Z authored rs12413409 conclusion='G/G: CNNM2 gene affects the risk of coronary heart disease. G-allele is associated with increased risk of coronary disease.; A/G: CNNM2 gene affects the risk of coronary heart disease. G-allele is associated with increased risk of coronary disease.' (judged; no value from PMID 31228190 to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:27Z authored rs7250581 weight='A/G: 0.0' (judged; no value from PMID 17554300 to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:29Z authored rs7250581 state='A/G: neutral' (judged; no value from the row's own conclusion and the module's other genotype rows to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:31Z authored rs7250581 conclusion='A/G: rs7250581 has been reported in a large study to be associated with heart disease, in particular, coronary artery disease. The risk allele...' (judged; no value from the row's own conclusion and the module's other genotype rows to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:33Z authored rs688034 weight='C/T: 0.0' (judged; no value from PMID 17554300 to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:35Z authored rs688034 state='C/T: neutral' (judged; no value from the row's own conclusion and the module's other genotype rows to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:38Z authored rs17228212 weight='C/T: -0.55' (judged; no value from PMID 17634449 to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false
+2026-11-04T07:36:40Z authored rs11206510 weight='C/T: -0.3' (judged; no value from the row's own conclusion and the module's other genotype rows to disagree with) by=AI agent (just-module-creator), 2026 rebuild human_reviewed=false

data/coronary/v2.0.0/manifest.json

@@ -0,0 +1,683 @@
+{
+  "manifest_version": "1.0",
+  "schema_version": "1.0",
+  "identity": {
+    "namespace": null,
+    "name": "coronary",
+    "version": "2.0.0",
+    "version_coerced_from": null,
+    "canonical_id": null
+  },
+  "display": {
+    "title": "Coronary",
+    "description": "Coronary artery disease risk associations",
+    "report_title": "Coronary Artery Disease",
+    "icon": "heart",
+    "icon_set": "fomantic",
+    "color": "#db2828"
+  },
+  "genome_build": "GRCh38",
+  "curator": "just-dna-seq",
+  "method": "expert-curated",
+  "license": null,
+  "authority_precedence": [],
+  "weighting": {
+    "scale": "Mixed, two scales. (1) Rows with method gwas-lead-tierA or functional-tierB (added 2026): weight = -ln(OR) per copy of the row's effect_allele, additive (heterozygote = -ln OR, effect-allele homozygote = -2 ln OR, other homozygote = 0.0 neutral), rounded to 3 dp; positive = protective, negative = risk. Typical Tier A magnitudes are 0.02-0.3 per copy. Tier B rare-variant weights use the published carrier OR and are capped to [-3, 3]. (2) Rows with method expert-curated (Olga Borysova, v1.x, 27 variants) keep the curator's original hand-set scale (roughly -1.7 to +1.2), which is not log-odds and is not comparable with scale (1).",
+    "method": "Tier A: every conditionally independent genome-wide-significant (p<5e-8) lead variant of the anchor CAD GWAS Aragam et al. 2022 Nat Genet (PMID 36474045; Supplementary Table 3, 241 signals, plus the 38 cross-ancestry loci of Supplementary Table 17), plus the novel lead SNPs of Tcheandjieu et al. 2022 Nat Med (PMID 35915156; Supplementary Tables 2-3, fixed-effect p<5e-8) lying >500 kb (GRCh37) from every Aragam lead. Per-allele OR from the anchor table; the effect allele is the allele with frequency <0.5 in the anchor, so the common homozygote is the neutral baseline. Tier B: rare functional variants with a published carrier OR (APOB R3527Q, PMID 9603795; APOC3 R19X, PMID 24941081). Tier C: legacy rows kept unchanged.",
+    "note": "Do not sum the two scales together, and do not compare these weights with another module's. A sum of the Tier A rows approximates an unweighted-by-LD polygenic log-odds; legacy rows at the same loci (9p21, SORT1, LPA, PCSK9, LDLR, etc.) can double-count a signal already carried by a Tier A lead. Per-variant effects are small; nothing here is a diagnosis."
+  },
+  "owner": null,
+  "authors": [],
+  "authorship": [
+    {
+      "who": "Olga Borysova",
+      "role": "created",
+      "kind": [
+        "human_expert"
+      ],
+      "at": null
+    },
+    {
+      "who": "AI agent (just-module-creator tooling), 2026 evidence rebuild",
+      "role": "edited",
+      "kind": [
+        "ai",
+        "agent"
+      ],
+      "at": "2026-11-03"
+    }
+  ],
+  "created_at": null,
+  "published_at": null,
+  "stats": {
+    "variant_count": 342,
+    "weights_rows": 1026,
+    "study_count": 437,
+    "gene_count": 283,
+    "genes": [
+      "ABCG8",
+      "ABHD2",
+      "ABO",
+      "ACER2",
+      "ACVR2A",
+      "ACVRL1",
+      "ADAM19",
+      "ADAMTS7",
+      "AFAP1L2",
+      "AKAP13",
+      "ANGPTL4",
+      "ANKRD13B",
+      "ANKRD55",
+      "APC",
+      "APOB",
+      "APOC3",
+      "APOE",
+      "ARHGAP15",
+      "ARHGAP21",
+      "ARHGAP26",
+      "ARHGAP42",
+      "ARHGEF12",
+      "ARHGEF26",
+      "ARL15",
+      "ARVCF",
+      "ASAP2",
+      "ATP2B1",
+      "ATXN2",
+      "B9D2",
+      "BCAS3",
+      "BDNF",
+      "BLTP3A",
+      "BMP1",
+      "BSND",
+      "C1S",
+      "CABIN1",
+      "CAVIN1",
+      "CCDC30",
+      "CCM2",
+      "CDC123",
+      "CDH13",
+      "CDK12",
+      "CDK8",
+      "CDKN2B-AS1",
+      "CELSR2",
+      "CENPW",
+      "CETP",
+      "CFAP161",
+      "CFDP1",
+      "CFTR",
+      "CMIP",
+      "CNNM2",
+      "CNPY2",
+      "COG5",
+      "COL4A1",
+      "COL4A2",
+      "CPLX4",
+      "CRIPTO3",
+      "CTAGE1",
+      "CXCL12",
+      "CXCR4",
+      "CYSLTR1",
+      "DAB2IP",
+      "DENND1B",
+      "DENND2B",
+      "DHX38",
+      "DMXL1",
+      "DNAH10",
+      "DNASE1L1",
+      "DOCK5",
+      "DOCK8",
+      "DYNLRB2",
+      "EDNRA",
+      "ELL",
+      "ETV1",
+      "EXOC3L2",
+      "FBN2",
+      "FBXL17",
+      "FDX1",
+      "FER",
+      "FES",
+      "FGD5",
+      "FGD6",
+      "FGF1",
+      "FHL3",
+      "FHL5",
+      "FIGN",
+      "FLT1",
+      "FMN2",
+      "FN1",
+      "FNDC3B",
+      "FOXC1",
+      "FOXO6",
+      "FTO",
+      "FURIN",
+      "GABBR1",
+      "GEM",
+      "GIGYF2",
+      "GNPDA2",
+      "GOSR2",
+      "GP2",
+      "GPSM1",
+      "GUCY1A1",
+      "HBS1L",
+      "HDAC9",
+      "HDGFL1",
+      "HHAT",
+      "HHIPL1",
+      "HMGCR",
+      "HNF1A",
+      "HTRA1",
+      "IGF2BP1",
+      "IL38",
+      "IL6R",
+      "INO80",
+      "ITGA1",
+      "ITIH4",
+      "ITPK1",
+      "JCAD",
+      "KAT2A",
+      "KCNK5",
+      "KDF1",
+      "KLF4",
+      "LAMB2",
+      "LDLR",
+      "LINC01016",
+      "LINC01153",
+      "LINC02881",
+      "LIPA",
+      "LIPC",
+      "LIPG",
+      "LNPEP",
+      "LNX1",
+      "LPA",
+      "LPL",
+      "MACC1",
+      "MAD1L1",
+      "MAD2L1",
+      "MAFB",
+      "MAGI3",
+      "MAP1S",
+      "MAP3K1",
+      "MAP7D3",
+      "MAP9",
+      "MC4R",
+      "MCF2L-AS1",
+      "MECOM",
+      "MIA3",
+      "MICA",
+      "MIR124-1HG",
+      "MIR4432",
+      "MIR4693",
+      "MMP13",
+      "MMP24",
+      "MORF4L1",
+      "MRAS",
+      "MSR1",
+      "MTAP",
+      "MTHFD1L",
+      "MYH11",
+      "MYO9B",
+      "N4BP2L2",
+      "NAT2",
+      "NBEAL1",
+      "NCOA6",
+      "NDUFAF6",
+      "NEDD4",
+      "NGF",
+      "NME7",
+      "NOS3",
+      "NPC1",
+      "NREP-AS1",
+      "OPHN1",
+      "OSM",
+      "OTUD7B",
+      "PALLD",
+      "PCSK9",
+      "PDE1A",
+      "PDE1C",
+      "PECAM1",
+      "PHACTR1",
+      "PID1",
+      "PIP4K2B",
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