The role of essential fatty acids in the control of coronary heart disease
The role of essential fatty acids in the control of coronary heart disease
Year: 2012
Authors: Vedtofte, M.S. Jakobsen, M.U. Lauritzen, L. Heitmann, B.L.
Publication Name: Clin. Nutr.
Publication Details: Volume 15; Issue 6
Abstract:
Evidence from various research paradigms supports the cardiovascular benefits of a high intake of n3 polyunsaturated fatty acids (PUFAs), especially the long chain, marine derived n3 PUFA, eicosapentaenoic acids and docosahexaenoic acids. The effect of the plant derived alpha linolenic acid (ALA) is, however, not clear. Concerns about a high n6 PUFA intake has been raised, because n6 PUFA may weaken the effects of n3 PUFA. Most previous observational studies on the intake of PUFA and the risk of coronary heart disease (CHD) did not specify the replacement nutrient. A recent meta analysis of cohort studies suggested that replacing saturated fatty acids with PUFA may lower the risk of CHD. On the other hand, recently published studies do not suggest that higher linoleic acid intake is associated to a lower risk of CHD or to give support for a negative association between ALA and CHD. Furthermore, recent studies do not suggest that the association between ALA and CHD is modified by linoleic acid. Recent meta analyses of cohort studies have reported a lower risk of CHD when PUFA replaces SFA in the diet. However, recent studies do not suggest that a higher linoleic acid intake is related to a lower risk of CHD. The effect of ALA on the risk of CHD is not clear. (Authors abstract)
In the present article, the results from observational and randomized clinical trials published since 2010 that have investigated the effect of essential fatty acids on mortality and morbidity of CHD will be reviewed. A meta analysis from 2004 including five prospective cohort studies showed that ALA intakes of approximately 2 g/day were associated with a borderline significant 21 percent lower risk of fatal CHD, compared with intakes of 0.8 g/day It is possible that ALA may have cardioprotective effects in populations with higher intakes or in populations with lower intakes of n3 LCPUFA and linoleic acid. It has been suggested that the conflicting results between the more recent and the previous studies could be because the health effect of ALA depends on intake of both n3 LCPUFA and linoleic acid, and that linoleic acid intake has been markedly increased in recent decades. As linoleic acid and ALA compete for the same enzymes when they are being metabolized, ALA conversion to n3 LCPUFA are influenced by linoleic acid levels and high intakes of n6 PUFA (relative to n3 PUFA) may therefore attenuate the beneficial effect of n3 PUFA. As the dietary intake of n6 PUFA greatly exceeds that of n3 PUFA, the scientific debate has emerged as to whether the high intake of n6 PUFA might weaken the beneficial effect of n3 PUFA. The conclusion from an expert meeting in 2010 Healthy Fats for Healthy Hearts was that more evidence is still needed and that a 5 year RCT comparing the effects of historically low (2 percent) and currently high (7.5 percent) linoleic acid intakes on cardiac outcomes is warranted. Despite plausible biological pathways suggesting that ALA like n3 LCPUFA may be cardioprotective, although possibly in higher doses than actually consumed, results from recent as well as previous cohort studies are inconsistent, and whether a higher intake of ALA is associated with a lower risk of CHD needs to be confirmed. (Editors comments)
In the present article, the results from observational and randomized clinical trials published since 2010 that have investigated the effect of essential fatty acids on mortality and morbidity of CHD will be reviewed. A meta analysis from 2004 including five prospective cohort studies showed that ALA intakes of approximately 2 g/day were associated with a borderline significant 21 percent lower risk of fatal CHD, compared with intakes of 0.8 g/day It is possible that ALA may have cardioprotective effects in populations with higher intakes or in populations with lower intakes of n3 LCPUFA and linoleic acid. It has been suggested that the conflicting results between the more recent and the previous studies could be because the health effect of ALA depends on intake of both n3 LCPUFA and linoleic acid, and that linoleic acid intake has been markedly increased in recent decades. As linoleic acid and ALA compete for the same enzymes when they are being metabolized, ALA conversion to n3 LCPUFA are influenced by linoleic acid levels and high intakes of n6 PUFA (relative to n3 PUFA) may therefore attenuate the beneficial effect of n3 PUFA. As the dietary intake of n6 PUFA greatly exceeds that of n3 PUFA, the scientific debate has emerged as to whether the high intake of n6 PUFA might weaken the beneficial effect of n3 PUFA. The conclusion from an expert meeting in 2010 Healthy Fats for Healthy Hearts was that more evidence is still needed and that a 5 year RCT comparing the effects of historically low (2 percent) and currently high (7.5 percent) linoleic acid intakes on cardiac outcomes is warranted. Despite plausible biological pathways suggesting that ALA like n3 LCPUFA may be cardioprotective, although possibly in higher doses than actually consumed, results from recent as well as previous cohort studies are inconsistent, and whether a higher intake of ALA is associated with a lower risk of CHD needs to be confirmed. (Editors comments)
