Alpha-Linolenic Acid Intake and 10-Year Incidence of Coronary Heart Disease and Stroke in 20,000 Middle Aged Men and Women in The Netherlands

Whether intake of alpha-linolenic acid (ALA), the plant-derived n3 polyunsaturated fatty acid (PUFA), could prevent cardiovascular diseases is not yet clear. We examined the associations of ALA intake with 10 year incidence of coronary heart disease (CHD) and stroke in the Netherlands. Data were collected from a general population of 20,069 generally healthy men and women, aged 20 to 65 years. Habitual diet was assessed at baseline (1993 to 1997) with a validated 178 item food frequency questionnaire. Incidences of CHD and stroke were assessed through linkage with mortality and morbidity registers. Hazard ratios (HR) were calculated with multivariable Cox proportional hazards models, adjusted for age, gender, lifestyle, and dietary factors. During 8 to 13 years of follow-up, we observed 280 incident CHD events (19% fatal) and 221 strokes (4% fatal). Intakes of energy-adjusted ALA in quintiles ranged from less than 1.0 g/d in the bottom quintile (Q1) to more than 1.9 g/d in the top quintile (Q5). ALA intake was not associated with incident CHD, with HRs varying between 0.89 and 1.01 (all p < 0.05) in Q2 to Q5 compared with the bottom quintile of ALA intake. For incident stroke, however, participants in Q2 to Q5 had a 35 to 50% lower risk compared with the reference group. HRs were 0.65 (0.43 to 0.97), 0.49 (0.31 to 0.76), 0.53 (0.34 to 0.83), and 0.65 (0.41 to 1.04) for Q2 to Q5 respectively. In this general Dutch population, ALA intake was not associated with incident CHD. The data suggested that a low intake of ALA may be a risk factor for incident stroke. These results warrant confirmation in other population based studies and in trials. (Authors abstract)
In Western countries, the intake of ALA is 5�10 times higher than n3 PUFA from fish. In this study, the 10 year incidence of CHD and stroke in relation to ALA intake in a population-based cohort of over 20,000 adults in the Netherlands was examined. No association between ALA intake and incident CHD was found. However, ALA intakes of greater than 1.1 g/d were associated with a 35 to 50% lower risk of incident stroke, mainly ischemic stroke, compared with ALA intakes of less than 1.1 g/d. This study has several strengths, including almost complete mortality follow up and detailed information on potential confounders. There were also limitations. Misclassification of participants for ALA intake may have occurred.  Despite the small range of intake in the study, an inverse association of ALA intake with incident stroke was found which was most pronounced for ALA from salad dressings. It is not likely that ALA from different food sources would act differently.  A proposed mechanism for a protective effect of ALA on incident ischemic stroke is that ALA would be neuroprotective after induced ischemia, by beneficially affecting the brain blood flow. In conclusion, in this study ALA intake was not associated with incident CHD. However, the data suggested that a low intake of ALA may be a risk factor for incident stroke (Editors comments)