Structure note (step 4b) — egg-health case
- H in (step-3): 44
- active (paper-derived survivors, 4a): 39
- merged: 5 (H-13, H-14, H-25, H-32, H-37 — in
hypotheses/merged/) - dropped: 0
- clusters (HC): 15
- 4b-minted structural members: 15 (11 residual
H-49…H-59, 4 constructedH-45…H-48), allactive⇒ 54 active H files total, each in exactly one cluster - generated: 2026-07-23
Cluster inventory (top-level map)
Each HC is one sub-question whose members are its mutually-exclusive answers (ordered ascending-id, residual last — the frozen index for steps 7-8). r = residual (step-4-residual), c = constructed complement (step-4-constructed).
- HC-1 - Overall net effect of moderate habitual egg intake on cardiovascular disease and mortality — What is the net causal effect (sign/shape) of moderate egg intake on CVD/mortality? — H-6 (protective), H-21 (neutral), H-27 (harmful), H-44 (U-shaped), H-49r.
- HC-2 - Regional-population modification of the egg-cardiovascular association — Is the egg-CVD effect genuinely region-modified, or is the Asian inverse an artefact? — H-7 (confounded artefact), H-22 (real modification), H-50r.
- HC-3 - Effect of habitual egg intake on incident type-2 diabetes — Does egg intake causally raise incident T2D, and how uniformly? — H-8 (region-dependent), H-9 (null / Western-pattern confounding), H-51r.
- HC-4 - Cardiometabolic effect of eggs in people with diabetes, prediabetes, or metabolic syndrome — In dysglycemic people, is egg intake net-harmful, safe, or beneficial? — H-4 (RCT-safe), H-19 (glycemically favourable), H-24 (CVD harm), H-33 (harm mechanism), H-52r.
- HC-5 - Operative exposure behind the egg-cardiovascular association — Is the operative agent egg-cholesterol or accompanying fat quality? — H-3 (fat quality dominates), H-26 (dietary cholesterol), H-54r.
- HC-6 - Effect of egg-egg-cholesterol intake on the atherogenic blood-lipid profile — Does egg/egg-cholesterol worsen the atherogenic lipid profile? — H-20 (LDL worse vs carb), H-34 (linear LDL/apoB rise), H-40 (net-neutral/HDL-favourable), H-53r.
- HC-7 - Nature of inter-individual variation in cholesterol response to dietary cholesterol — What is the structure of responder variation, and is it identifiable? — H-1 (discrete hypo/hyper), H-2 (feedback-buffering mechanism), H-35 (continuous trait), H-36 (ApoE non-predictive), H-55r.
- HC-8 - Causal status of elevated TMAO for human atherosclerosis — Is TMAO itself causally atherogenic in humans? — H-15 (animal-model mechanism), H-16 (human causal), H-45c (non-causal marker). [exhaustive]
- HC-9 - Whether habitual egg intake produces a harm-relevant TMAO elevation — Does egg intake raise TMAO enough to matter, and when? — H-28 (form-limited), H-29 (no fasting rise), H-30 (renal-only), H-42 (real postprandial rise), H-43 (rise benign), H-56r.
- HC-10 - Intrinsic versus comparator-background-diet contingency of egg-health (is the verdict well-posed) — Is egg-health intrinsic or comparator/context-contingent (is the verdict well-posed)? — H-17 (intrinsically unhealthy), H-18 (ill-posed/contingent), H-23 (substitution-indexed), H-38 (background-diet-indexed), H-57r.
- HC-11 - Whether early egg introduction causally prevents egg allergy in high-risk infants — Does early egg introduction causally prevent allergy? — H-10 (causal prevention), H-46c (no causal prevention). [exhaustive]
- HC-12 - Intact Grade A shell eggs as the major internally-contaminated vehicle of the Salmonella enteritidis epidemic — Are intact Grade A eggs the major, internally-contaminated SE vehicle? — H-11 (internal route), H-12 (major vehicle), H-58r.
- HC-13 - Whether eggs enhance satiety beyond their protein content — Do eggs boost satiety beyond protein? — H-5 (beyond protein), H-47c (protein-only). [exhaustive]
- HC-14 - Whether dietary choline is an essential nutrient for humans — Is dietary choline essential for humans? — H-39 (essential), H-48c (not essential). [exhaustive]
- HC-15 - Whether nutritional-cohort associations can support causal egg-health claims — Can nutritional cohorts support causal egg-health claims? — H-31 (cannot / reform), H-41 (can / defence), H-59r.
Carving notes
- Two-axis CVD decomposition. Overall sign/shape (HC-1), regional modification (HC-2), and intrinsic-vs-contingent framing (HC-10) are kept as separate orthogonal questions rather than one, with their premise-dependences logged in
depends_on(HC-1↔HC-2, HC-1↔HC-10, HC-2↔HC-10). H-6 (protective) anchors HC-1; its Kadoorie foil H-7 (confounding) anchors HC-2 — the causal-vs-confounding contrast is expressed across the two axes, not duplicated as one partition. - Task-mandated competing pairs kept inside one cluster: H-42 vs H-29 (TMAO postprandial-rise vs fasting-null) → HC-9; H-1 vs H-35 (discrete vs continuous responder distribution) → HC-7; H-17 vs H-18/H-23 (intrinsic vs comparator-contingent) → HC-10.
- Same-source split by endpoint. H-19 (glycemic) → HC-4 and H-20 (LDL) → HC-6, both from the Maki trial: their endpoints co-hold and so cannot be exclusive members of one probability space.
- TMAO split into exposure (HC-9) and causality (HC-8) as genuinely different sub-questions; strong
depends_onbetween them (exposure matters only if TMAO is causal). HC-8 uses an ordinal-rung reading (animal-mechanism / human-causal / marker) to stay exclusive and exhaustive. - Beyond-CVD channels are separate MECE clusters (allergy HC-11, salmonella HC-12, satiety HC-13, choline HC-14) rather than a non-exclusive grab-bag; each single-active-hypothesis channel is paired with a constructed null complement (exhaustive) — except salmonella, whose two facets (route H-11, magnitude H-12) share the thesis and take a residual negation.
- Meta-question (HC-15) cross-cuts every cohort-based cluster but enters downstream via source trust / likelihoods (steps 5, 8), not via other clusters’ priors, so those priors still factorize and its
depends_onis empty. - No H dropped — all 39 active clustered. No numbers/priors/weights written anywhere in the HC layer (descriptive effect sizes/intakes quoted in carving prose only, mirroring the H statements).