Dietary a-linolenic acid, linoleic acid, and n�3 long-chain PUFA and risk of ischemic heart disease1�3
Dietary a-linolenic acid, linoleic acid, and n�3 long-chain PUFA and risk of ischemic heart disease1�3
Year: 2011
Authors: Vedtofte, M.S. Jakobsen, M.U. Lauritzen, L. Heitmann, B.L.
Publication Name: Am. J. Clin. Nutr.
Publication Details: doi: 10.3945/ajcn.111.018762
Abstract:
n-3 (omega-3) PUFA has been proposed as having health-promoting effects, primarily in relation to ischemic heart disease (IHD). Whether these benefits can be achieved by both a-linolenic acid (ALA, 18:3n-3) and n-3 long-chain PUFA (LCPUFA) is debatable. The objective was to examine the association between ALA intake and risk of IHD in healthy subjects and to see if this was modified by intake of n-3 LC-PUFA or linoleic acid (LA, 18:2 n-6).This was a prospective cohort study of 3277 healthy Danish women and men free of known IHD. Four hundred seventy-one cases of IHD were observed during a median follow-up period of 23.3 y. Higher intake of ALA was not significantly associated with decreased risk of IHD among women or men. Although the HR of IHD was stepwise decreased with increasing ALA intake in men [0.84 (95% CI: 0.62, 1.14) in the medium compared with the lowest tertile (reference) and 0.83 (95% CI: 0.56, 1.24) in the highest compared with the lowest tertile], this change was far from significant (P-trend: 0.39). No evidence of effect modification by n-3 LC-PUFA or LA was observed. High n-3 LC-PUFA intake, in comparison with low intake, was inversely associated with risk of IHD; this trend was significant in women (P = 0.04; HR: 0.62; 95% CI: 0.40, 0.97) but not in men (P = 0.15; HR: 0.74; 95% CI: 0.51, 1.06). No associations were observed between intake of LA and risk of IHD. This study suggests that there is no association between ALA intake and risk of IHD, but a high intake of n-3 LCPUFA had a significant cardioprotective effect in women. (Author�s abstract)
Whether ALA could be a possible alternative cardioprotective n-3 fatty acid is of public health ALA may particularly reduce the risk of IHD among subjects with a low n-3 LCPUFA intake. High intake of n-3 LC-PUFA may also blur the effect of ALA. In the present study, data from the Glostrup Population Studies was used to investigate the association between intake of ALA and risk of IHD, with the following hypothesis. 1) Intake of ALA is inversely associated with the risk of IHD and 2) the inverse association between ALA and the risk of IHD is modified by the dietary intake of n-3 LCPUFA and/or LA. Previous studies have mainly used food frequency questionnaires to assess ALA intake, whereas in the present study we used data from 7-d weighed food records. The study included a heterogeneous group of healthy men and women with a wide range of ALA intakes (0.7�2.6 g/d). Unlike previous studies, no association between ALA intake and risk of IHD was shown. Such a cardioprotective has been reported in a number of observational studies. The present study did not include sudden cardiac death and may thus have missed that type of cardioprotective effect. It is possible that ALA may particularly reduce the risk of IHD among subjects with a low n-3 LC-PUFA intake. In other research, each 1 g ALA intake/d was associated with a 47% lower risk of IHD among men with little or no n-3 LC-PUFA intake (<1g/d). In men, those who were in the highest category for both ALA and n-3 LC-PUFA had the lowest risk. This indicates that there may have been both an effect modification and an additive effect. The lack of an association between ALA and risk of IHD may be explained by the competitive actions of LA and a high intake of LA may thus inhibit the effect of ALA on IHD risk. A limitation in the study is the use of weighed food record which was limited in the number of days. The estimated median daily intake of ALA in the present study was 1.2 g/d and 1.6 g/d among women and men, respectively. And about one-half of the study population was under the minimum requirement, whereas others had intakes well above 2 g/d. Further larger studies are warranted to examine potential effect modification by different PUFA. (Editor�s comments)
Whether ALA could be a possible alternative cardioprotective n-3 fatty acid is of public health ALA may particularly reduce the risk of IHD among subjects with a low n-3 LCPUFA intake. High intake of n-3 LC-PUFA may also blur the effect of ALA. In the present study, data from the Glostrup Population Studies was used to investigate the association between intake of ALA and risk of IHD, with the following hypothesis. 1) Intake of ALA is inversely associated with the risk of IHD and 2) the inverse association between ALA and the risk of IHD is modified by the dietary intake of n-3 LCPUFA and/or LA. Previous studies have mainly used food frequency questionnaires to assess ALA intake, whereas in the present study we used data from 7-d weighed food records. The study included a heterogeneous group of healthy men and women with a wide range of ALA intakes (0.7�2.6 g/d). Unlike previous studies, no association between ALA intake and risk of IHD was shown. Such a cardioprotective has been reported in a number of observational studies. The present study did not include sudden cardiac death and may thus have missed that type of cardioprotective effect. It is possible that ALA may particularly reduce the risk of IHD among subjects with a low n-3 LC-PUFA intake. In other research, each 1 g ALA intake/d was associated with a 47% lower risk of IHD among men with little or no n-3 LC-PUFA intake (<1g/d). In men, those who were in the highest category for both ALA and n-3 LC-PUFA had the lowest risk. This indicates that there may have been both an effect modification and an additive effect. The lack of an association between ALA and risk of IHD may be explained by the competitive actions of LA and a high intake of LA may thus inhibit the effect of ALA on IHD risk. A limitation in the study is the use of weighed food record which was limited in the number of days. The estimated median daily intake of ALA in the present study was 1.2 g/d and 1.6 g/d among women and men, respectively. And about one-half of the study population was under the minimum requirement, whereas others had intakes well above 2 g/d. Further larger studies are warranted to examine potential effect modification by different PUFA. (Editor�s comments)
