{"id":"c10cc7ce-82b9-5c06-8791-e9da0e356d44","stable_key":"182336c6-ed36-5ec6-8a09-25c31096262e:dim-smoking-cessation","predicate":"reduces","statement":"Caffeine clearance fell by 36.1% after cessation; the fitted half-life of CYP1A2 activity decline was 38.6 hours.","claim_class":"observational","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"fce14f99-5165-56ed-bda9-a4acca20bbee","mechanism_event_label":"Stopping an established inducer can raise exposure to its substrates, but these numbers describe smoking.","subject":{"id":"8c5cd7d7-0143-5dec-8b8b-c0383d26302c","slug":"smoking-cessation","display_name":"Cessation of cigarette smoking","entity_type_key":"cellular_process"},"object":{"id":"a7ade0b8-199b-542e-b9be-c8ad2c2b68c1","slug":"caffeine-clearance","display_name":"Caffeine clearance","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"fce14f99-5165-56ed-bda9-a4acca20bbee","stable_key":"182336c6-ed36-5ec6-8a09-25c31096262e:dim-smoking-cessation-event","event_type":"observed_intervention","label":"Stopping an established inducer can raise exposure to its substrates, but these numbers describe smoking.","description":"Caffeine clearance fell by 36.1% after cessation; the fitted half-life of CYP1A2 activity decline was 38.6 hours.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"9b15c13c-a369-5d10-a76a-525e8b19221d","slug":"cyp1a2","display_name":"Human cytochrome P450 1A2","entity_type_key":"protein"},"role":"phenotyped_enzyme","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"8c5cd7d7-0143-5dec-8b8b-c0383d26302c","slug":"smoking-cessation","display_name":"Cessation of cigarette smoking","entity_type_key":"cellular_process"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"a7ade0b8-199b-542e-b9be-c8ad2c2b68c1","slug":"caffeine-clearance","display_name":"Caffeine clearance","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""}]},"contexts":[{"dimension":"evidence_span","value_text":"{\"source_cache\": \"artifacts/dim-research/15289794.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"90eb96e72afdbbb53c322c2be9a34e5aa523c27f2fd0995a8eb224e2ec6e35e2\", \"start_char\": 0, \"end_char\": 1753, \"text_sha256\": \"90eb96e72afdbbb53c322c2be9a34e5aa523c27f2fd0995a8eb224e2ec6e35e2\"}","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Repeated caffeine phenotyping after smoking cessation","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Abrupt cessation after run-in; repeated 148-mg caffeine probe doses","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Smoking-cessation kinetics cannot be assigned to starting or stopping DIM. Clinical dose management requires drug-specific monitoring.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"dim","display_name":"3,3'-Diindolylmethane / DIM","entity_type_key":"small_molecule"}},{"dimension":"organism","value_text":"12 heavy smokers","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"Stopping an established inducer can raise exposure to its substrates, but these numbers describe smoking.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[dim-p15289794] Time response of cytochrome P450 1A2 activity on cessation of heavy smoking. (2004). https://pubmed.ncbi.nlm.nih.gov/15289794/ DOI: 10.1016/j.clpt.2004.04.003","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"CYP1A2 activity and caffeine clearance","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"28185e19-971f-5d2f-94b7-fef0c522d370","evidence_kind":"source_excerpt","locator":"Lines 844-855","start_line":844,"end_line":855,"excerpt":"### dim-smoking-cessation\nCaffeine clearance fell by 36.1% after cessation; the fitted half-life of CYP1A2 activity decline was 38.6 hours.\nCondition category: normal\nnutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Stopping an established inducer can raise exposure to its substrates, but these numbers describe smoking.\norganism: 12 heavy smokers\ntissue_or_cell_type: CYP1A2 activity and caffeine clearance\nexperimental_model: Repeated caffeine phenotyping after smoking cessation\nlimitations: Smoking-cessation kinetics cannot be assigned to starting or stopping DIM. Clinical dose management requires drug-specific monitoring.\nexposure: Abrupt cessation after run-in; repeated 148-mg caffeine probe doses\nevidence_span: {\"source_cache\": \"artifacts/dim-research/15289794.abstract.txt\", \"locator\": \"Primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"90eb96e72afdbbb53c322c2be9a34e5aa523c27f2fd0995a8eb224e2ec6e35e2\", \"start_char\": 0, \"end_char\": 1753, \"text_sha256\": \"90eb96e72afdbbb53c322c2be9a34e5aa523c27f2fd0995a8eb224e2ec6e35e2\"}\n[dim-p15289794] Time response of cytochrome P450 1A2 activity on cessation of heavy smoking. (2004). https://pubmed.ncbi.nlm.nih.gov/15289794/ DOI: 10.1016/j.clpt.2004.04.003","model_system":"Repeated caffeine phenotyping after smoking cessation","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study references: [dim-p15289794] Time response of cytochrome P450 1A2 activity on cessation of heavy smoking. (2004). https://pubmed.ncbi.nlm.nih.gov/15289794/ DOI: 10.1016/j.clpt.2004.04.003","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"b6d70682-97f9-5893-a03c-f9f88836033c","stable_key":"import-182336c6-ed36-5ec6-8a09-25c31096262e","title":"Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17)","document_type":"imported_text","citation_label":"AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text.","file_path":"","sha256":"31e14060de904976d2f5d439f2bc9c8a99a72d34626c562c78429025e050d404","revision_id":"611094c1-a9cf-5b9b-b255-ac70b571696a","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}