{"id":"782eb169-40bb-500b-8c6e-4e389689d5bd","stable_key":"a9dd23c6-978a-5755-8bd8-f29bd1fe0cda:nia-clin-2py-risk","predicate":"associated_with","statement":"Higher serum 2PY was associated with three-year major adverse cardiovascular events in both validation cohorts.","claim_class":"observational","status":"source_derived_draft","evidence_grade":"ungraded","direction":"positive","is_public":true,"mechanism_event_id":"57d84cc7-1ec1-560b-9dda-d4347bfaba0b","mechanism_event_label":"A breakdown-product measurement tracked risk; that does not identify dietary niacin as the cause.","subject":{"id":"d462430c-2f74-56ad-abf6-d1872c4f83a1","slug":"n1-methyl-2-pyridone-5-carboxamide","display_name":"N1-methyl-2-pyridone-5-carboxamide (2PY)","entity_type_key":"small_molecule"},"object":{"id":"8f08bd23-f5e8-5787-b7b5-d6e1e26ed99c","slug":"major-cardiovascular-event-incidence","display_name":"Major cardiovascular event incidence","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"57d84cc7-1ec1-560b-9dda-d4347bfaba0b","stable_key":"a9dd23c6-978a-5755-8bd8-f29bd1fe0cda:nia-clin-2py-risk-event","event_type":"observed_intervention","label":"A breakdown-product measurement tracked risk; that does not identify dietary niacin as the cause.","description":"Higher serum 2PY was associated with three-year major adverse cardiovascular events in both validation cohorts.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"d462430c-2f74-56ad-abf6-d1872c4f83a1","slug":"n1-methyl-2-pyridone-5-carboxamide","display_name":"N1-methyl-2-pyridone-5-carboxamide (2PY)","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"8f08bd23-f5e8-5787-b7b5-d6e1e26ed99c","slug":"major-cardiovascular-event-incidence","display_name":"Major cardiovascular event incidence","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"availability_state","value_text":"biomarker_context","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null},{"dimension":"cross_nutrient","value_text":"Niacin precursor form and the measured endpoint are separate graph entities.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"evidence_span","value_text":"{\"source_cache\": \"artifacts/niacin-clinical-sources/ferrell2024.abstract.txt\", \"locator\": \"Indexed primary abstract\", \"file_sha256\": \"09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19\", \"start_char\": 0, \"end_char\": 2066, \"text_sha256\": \"09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Prospective stable cardiac patient cohorts with three-year event follow-up","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Discovery cohort 1,162; US validation 2,331 and European validation 832; three-year cardiovascular follow-up; physiological-level mouse metabolite exposure","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Human metabolite associations are not randomized effects of niacin intake. Renal handling and other determinants of levels matter. Mouse exposure results do not prove dietary niacin or supplements caused human events.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Niacin research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"niacin","display_name":"Niacin (vitamin B3)","entity_type_key":"nutrient_element"}},{"dimension":"organism","value_text":"Homo sapiens","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"A breakdown-product measurement tracked risk; that does not identify dietary niacin as the cause.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[nia-clin-ferrell2024] A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. (2024). https://pubmed.ncbi.nlm.nih.gov/38374343/ DOI: 10.1038/s41591-023-02793-8","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Serum metabolites and clinical cardiovascular outcomes","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"biomarker_context","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"ac52e4f3-bcc9-5241-b971-fee498960ebe","evidence_kind":"source_excerpt","locator":"Lines 1557-1569","start_line":1557,"end_line":1569,"excerpt":"### nia-clin-2py-risk\nHigher serum 2PY was associated with three-year major adverse cardiovascular events in both validation cohorts.\nCondition category: biomarker_context\nnutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: A breakdown-product measurement tracked risk; that does not identify dietary niacin as the cause.\norganism: Homo sapiens\ntissue_or_cell_type: Serum metabolites and clinical cardiovascular outcomes\nexperimental_model: Prospective stable cardiac patient cohorts with three-year event follow-up\nlimitations: Human metabolite associations are not randomized effects of niacin intake. Renal handling and other determinants of levels matter. Mouse exposure results do not prove dietary niacin or supplements caused human events.\nexposure: Discovery cohort 1,162; US validation 2,331 and European validation 832; three-year cardiovascular follow-up; physiological-level mouse metabolite exposure\ncross_nutrient: Niacin precursor form and the measured endpoint are separate graph entities.\nevidence_span: {\"source_cache\": \"artifacts/niacin-clinical-sources/ferrell2024.abstract.txt\", \"locator\": \"Indexed primary abstract\", \"file_sha256\": \"09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19\", \"start_char\": 0, \"end_char\": 2066, \"text_sha256\": \"09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19\"}\n[nia-clin-ferrell2024] A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. 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