title: Fish intake may limit the increase in risk of coronary heart disease morbidity and mortality among heavy smokers. The Honolulu Heart Program.
abstract: BACKGROUND
  Research has shown that fish consumption limits damage to the lungs caused by cigarette smoking, possibly by the effects of fish on arachidonic acid metabolism. We explored this fish-smoking interaction using coronary heart disease (CHD) incidence and mortality as the outcome.
  
  
  RESULTS
  The Honolulu Heart Program began in 1965 to follow a cohort of 8006 Japanese-American men aged 45 to 65 years who lived on Oahu, Hawaii, in 1965. Fish intake was measured at baseline by use of a questionnaire. For current smokers at baseline (n = 3310) who reported low fish intake (< 2 times/wk), age-adjusted 23-year CHD mortality rates increased with the number of cigarettes smoked per day (2.3, 3.1, and 6.9 per 1000 person-years for men who smoked < 20, 20 to 30, and > 30 cigarettes/d, respectively; trend test P < .0001). Among current smokers whose fish intake was high (> or = 2 times/wk), CHD mortality rates showed no relation with cigarettes/d (3.7, 3.2, and 3.7 per 1000 person-years for the corresponding levels of smoking). A Cox proportional hazards model based on current smokers, adjusted for age, years in Japan, calories/d, alcohol intake, physical activity index, years smoked, hypertension, and serum cholesterol, blood glucose, and uric acid levels, was examined. In the high-smoking group, the risk factor-adjusted relative risk (RR) for CHD mortality among those with high fish intake was half that of those with low fish consumption (RR = 0.5, 95% confidence interval = 0.28 to 0.91). A Cox model that adjusted for similar risk factors confirmed a significant interaction of cigarettes/d and fish intake (P < .01) on CHD mortality. Analyses for CHD incidence showed similar results.
  
  
  CONCLUSIONS
  Despite the findings of this investigation, the public health message for smokers continues to be to stop smoking. However, an interaction between fish intake and cigarette smoking is biologically plausible and deserves further investigation. The study of this phenomenon may shed light on the biological mechanisms by which cigarette smoking leads to CHD.
authors.affiliation: John A. Burns School of Medicine, University of Hawaii at Manoa, Hawaii, USA. beatriz@hhs.cba.hawaii.edu
authors.forename: B L
authors.initials: BL
authors.lastname: Rodriguez
authors.forename: D S
authors.initials: DS
authors.lastname: Sharp
authors.forename: R D
authors.initials: RD
authors.lastname: Abbott
authors.forename: C M
authors.initials: CM
authors.lastname: Burchfiel
authors.forename: K
authors.initials: K
authors.lastname: Masaki
authors.forename: P H
authors.initials: PH
authors.lastname: Chyou
authors.forename: B
authors.initials: B
authors.lastname: Huang
authors.forename: K
authors.initials: K
authors.lastname: Yano
authors.forename: J D
authors.initials: JD
authors.lastname: Curb
mesh_terms: D000368:Aged; D000818:Animals; D003327:Coronary Disease / Q000401:mortality* / Q000517:prevention & control; D005395:Fish Oils / Q000008:administration & dosage; D005399:Fishes; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects*
chemical_list: D005395:Fish Oils