Lignan Intake and Risk of Coronary Heart Disease

Abstract

Background: Evidence regarding lignan consumption in relation to coronary heart disease (CHD) risk remains limited and mixed.

Objectives: The aim of this study was to prospectively examine associations between lignan intake and CHD risk in U.S. men and women.

Methods: We prospectively followed 214,108 men and women in 3 cohorts who did not have cardiovascular disease or cancer at baseline. Diet was repeatedly assessed using a validated food frequency questionnaire every 2-4 years since baseline.

Results: During 5,517,225 person-years of follow-up, we documented 10,244 CHD cases, including 6,283 nonfatal myocardial infarction and 3,961 fatal CHD cases. In multivariable-adjusted analyses, comparing extreme quintiles, the pooled hazard ratios of CHD were 0.85 (95% CI: 0.79-0.92) for total lignans, 0.76 (95% CI: 0.71-0.82) for matairesinol, 0.87 (95% CI: 0.81-0.93) for secoisolariciresinol, 0.89 (95% CI: 0.83-0.95) for pinoresinol, and 0.89 (95% CI: 0.83-0.95) for lariciresinol (all P values for trend ≤0.003). Nonlinear relationships were found for total lignan, matairesinol, and secoisolariciresinol: the risk reduction plateaued at intakes above approximately 300 μg/d, 10 μg/d, and 100 μg/d, respectively (P < 0.01 for all nonlinearity). The inverse associations for total lignan intake appeared to be more apparent among participants with higher total fiber intake (P = 0.04 for interaction). In addition, lignan intake was more strongly associated with plasma concentrations of enterolactone when fiber intake was higher.

Conclusions: Increased long-term intake of lignans was associated with a significantly lower risk of total CHD in both men and women. Possible synergistic effects may exist between lignan and fiber intake in relation to CHD risk reduction, possibly through enhancing the production of enterolignans.

Keywords: coronary heart disease; lignan; prospective cohorts.

Central Illustration.. Dose-response relationships between lignan intake and CHD risk.

Data were truncated between 1^st −99^th percentile value. The axis for hazard ratio is in natural log-scale. Models were age- (months) and calendar-time stratified and adjusted for ethnicity (white, African American, Asian, others), smoking status (never smoked, past smoker, currently smoke 1–14 cigarettes per day, 15–24 cigarettes per day, or ≥25 cigarettes per day), time-varying BMI (<21.0, 21.0–22.9, 23.0–24.9, 25.0–26.9, 27.0–29.9, 30.0–32.9, 33.0–34.9, or ≥35.0 kg/m²), alcohol intake (0, 0.1–4.9, 5.0–9.9, 10.0–14.9, 15.0–29.9, and ≥30.0 g/d), multivitamin use (yes, no), physical activity (quintiles), healthy plant-based diet index (quintiles), and family history of myocardial infarction. Panel A: P value for non-linearity: 0.003.Panel B: P value for non-linearity: <0.001.Panel C: P value for non-linearity: <0.001.Panel D: P value for non-linearity: 0.17. Panel E: P value for non-linearity: 0.11.