Association between the intake of alpha linolenic acid and the risk of CHD

The intake of the mainly plant derived n 3 PUFA alpha linolenic acid (ALA) has been reported to be associated with a lower risk of CHD. However, the results have been inconsistent. Therefore, the objective of the present study was to examine the association between the intake of ALA and the risk of CHD. Potential effect modification by the intake of long chain n 3 PUFA was also investigated. Data from eight American and European prospective cohort studies including 148 to 675 women and 80 to  368 men were used. The outcome measure was incident CHD (CHD event and death). During 4 to 10 years of follow up, 4493 CHD events and 1751 CHD deaths occurred. Among men, an inverse association (not significant) between the intake of ALA and the risk of CHD events and deaths was observed. For each additional gram of ALA consumed, a 15 per cent  lower risk of CHD events (hazard ratios (HR) 0.85, 95 per cent  CI 0.72,  1.01) and a 23 per cent  lower risk of CHD deaths (HR 0.77, 95 per cent  CI 0.58, 1.01) were observed. No consistent association was observed among women. No effect modification by the intake of n 3 LCPUFA was observed. (Authors abstract)

CHD is the leading cause of morbidity and mortality in the world. CHD arises from genetic and modifiable lifestyle factors including diet. A recent meta analysis of three prospective studies carried out in 2012 has suggested that each 1 g per d of ALA intake is associated with a 20 per cent lower risk of CHD events. In the present study, the association between ALA intake and CHD risk in populations consuming different diets and exhibiting a wide range of ALA intakes was assessed using data from eight American and European prospective cohort studies included in the Pooling Project of Cohort Studies on Diet and Coronary Disease. It was hypothesized that the intake of ALA was inversely associated with the risk of CHD and that the inverse association between the intake of ALA and the risk of CHD was stronger in subjects with a low intake of n 3 LCPUFA than in those with a high intake of n 3 LCPUFA. A non significant inverse association between the dietary intake of ALA and the risk of incident CHD events and CHD deaths among men. The pooling of data from eight large cohort studies is a major strength of the present study and allowed studying the association between the intake of ALA and the risk of CHD among women and men in different populations consuming different diets and exhibiting a wide range of intakes. Variations in intake are essential for detecting potential associations with health. Furthermore, an advantage of using a pooling study design rather than a meta analysis is that this design greatly reduces the risk of publication bias, because results originated both from studies that did not previously publish on the association between ALA intake and CHD risk and from studies that did. ALA levels in human tissue may provide a more accurate measure of habitual ALA intake than dietary records or questionnaires. However, ALA status in tissues may be influenced by metabolic differences between subjects with regard to genetics, sex and background diet, and day to day variations in tissue levels cannot be excluded either.

Several prospective cohort studies have evaluated the association between ALA intake and CHD risk and obtained inconsistent results. The current findings are in line with those of a recent meta analysis of thirteen prospective studies carried out in 2012 showing that higher ALA intakes (each 1 g per d increment) are associated with a 10 per cent  lower risk of incident CVD. However, in the evaluation of the association between the intake of ALA and the risk of CVD subtypes, CHD events and CHD deaths, only three studies were included in the meta analysis of CHD events and six studies in the analysis of CHD deaths and the association was found to be significant only for ALA intake and CHD deaths.  Of these nine studies, four used cohorts that were also included in the present study (NHS, HPFS and ATBC). Only two of the nine studies were conducted in women (data from the NHS) and six were conducted solely in men, whereas the last study was conducted in a sample of both the sexes, with 27 per cent  women and 73 per cent men. In the present study, different results for women and men were found. Whether the different results obtained for women and men reflect true biological differences or are due to power or are caused by some kind of bias remains to be determined. On the other hand, an inverse association between ALA intake and CHD risk is theoretically more likely among women than among men, as several studies have shown that the conversion of ALA into n 3 LCPUFA is stimulated by oestrogen and is greater in women. In this large pooled study on the association between dietary ALA intake and CHD risk, an inverse association was observed among men; however, it was not significant. No consistent association was observed among women. This is the largest and most powerful study to evaluate the association between ALA intake and CHD risk to date. Given that a higher intake of ALA was found to reduce the risk of CHD, although only among men, from a public health point of view, it may be feasible to increase ALA intake. Rapeseed oil (which is rich in ALA) is the cheapest oil in many countries and thus can be used in household cooking by a majority of populations.  However, rapeseed oil is best for raw use (i.e. salad dressing) and not for heating due to its degree of unsaturation. Other sources of ALA are, for instance, walnuts and flaxseeds, although their use is not very common in all populations.  To obtain 1 g of ALA, one has to consume two teaspoons of rapeseed oil or 15 g of walnuts or 6 g of flaxseeds. Sex differences in prospective cohort studies have received little attention and deserve further investigation. (Editors comments)