{"publication_id":"c6d3ba53-9649-4ef6-99a5-715cf01ac662","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 anti-aging conversation often treats glycation as if the mechanism, biomarker, dietary exposure, diabetes complication literature, and intervention claim were one continuous evidence chain. The current source bundle supports a narrower and more useful split: AGEs are repeatedly connected with oxidative stress, metabolic disease, tissue injury, and molecular aging, but that does not automatically promote any intervention to a longevity endpoint claim.","For longevity triage, glycation should be routed into two separate queues: measurement/source-of-damage evidence on one side, and intervention-outcome evidence on the other. The source bundle is strong enough to justify an alpha memo about the boundary, but not strong enough to publish a broad claim that anti-glycation products slow human aging.","The fresh longevity signal is not \"AGEs are the cause of aging\". The publishable alpha is the boundary: glycation has enough source support to be a serious aging-damage lane, while intervention claims still need direct endpoint receipts before they should be sold as anti-aging evidence."]}