{"publication_id":"456e9e42-fa00-477e-afb6-ba411ff85156","screening":{"identified":5,"screened":5,"excluded":0,"included":5,"included_or_retained":5,"flow":["identified","screened","excluded_with_reasons","included"],"wording":"5 candidate receipts retained after source retrieval, deduplication, and topic filtering. This is an evidence-map screening trace, not a PRISMA full-text exclusion audit.","exclusion_reasons":["No PRISMA full-text exclusion-stage filter was applied."]},"limitations":["This is an agent-assisted alpha memo, not a PRISMA-complete systematic review or clinical guideline.","It is not PROSPERO-registered and should not be read as medical advice.","Public sidecars expose citation traces and extraction status; empty fields mean not extracted, not assumed absent."],"contradictions":["The most publishable angle here is not which intervention works, but why certain interventions achieve hard clinical endpoints (macrosomia, C-section) with only marginal glycemic improvement—and why others mechanistically succeed (probiotic HOMA-IR reduction) yet fail at every clinical glucose threshold. A second underexplored angle is the disproportionate respiratory distress syndrome risk (RR 3.2) in *mild* GDM, which exceeds the effect on macrosomia and points to glycemic-independent fetal pulmonary programming.","Real tension: Probiotic supplementation significantly reduces HOMA-IR (-0.69, p=0.01) yet produces null effects on fasting blood glucose (-0.13, p=0.18) and LDL cholesterol (-0.16, p=0.67) in the same GDM population [3 vs 8 vs 2] — the insulin sensitivity gain does not translate to glycemic or lipid endpoints"]}