The most likely mechanism by which ALA may prevent coronary heart disease (CHD) mortality is by reducing cardiac arrhythmia. In Western populations, almost 50% of all deaths from cardiovascular disease can be attributed to sudden cardiac death and the majority of sudden deaths are directly caused by acute ventricular arrhythmia (Brouwer et al 2004). A review in 2001 (Lanzmann-Petithory) and a meta-analysis of three studies in 2004 (Brouwer et al) both found in favour of a protective effect from increased ALA consumption against fatal CHD (RR 0.24). The dose associated with this trend was small; only 1-3 g/day ALA higher than controls (Brouwer et al 2004). A study published in 2005, which derived data from the Nurses' Health Study (Albert et al), found that women consuming ALA in the highest two quintiles had a 38-40% lower risk of sudden cardiac death than women in the lowest quintile; however, the protective effect did not extend to other fatal forms of CHD or non-fatal myocardial infarction.
Much criticism has been directed at those researchers wanting to extrapolate prescriptive advice from these findings. An editorial by Harris (2005) notes that only one primary prevention study with ALA in CHD has been conducted and that was in the 1960s. The 1 -year trial involved 13,578 Norwegian men and compared 10 g of FSO (providing 5.5 g/day ALA) with a sunflower seed placebo. In the analysis there was no demonstrable difference in end-points between the two groups. Recent attempts to explain this lack of effect, such as high baseline n-3 consumption by this population, appear to be well founded (Mozaffarian et al 2005).
There is an urgent need for RCTs using FSO in suitable populations to clarify the Flaxseed oil 455
relationship between ALA and CHD mortality.
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