Journal Name:
Circulation
Article Title:
Alpha-Linolenic Acid and Risk of Nonfatal Acute Myocardial Infarction.
Date Written:
2008
Volume:
118
Number:
NA
Page:
339
Author(s):
Campos, H.; Baylin, A.; Willett, W.C.
Article:
In many regions of the world, the availability of fish and other marine products that are the main sources of long-chain fatty acids are limited. Alpha-linolenic acid (ALA) could be a viable cardioprotective alternative to these fatty acids in these countries.
Coronary heart disease is generally high in countries where the estimated intake of EPA and DHA is extremely low (long-chain n-3 fatty acid intake about 0.07% energy). Because of price, availability, or cultural preference, many of these countries have little or no possibility of increasing fish intake. European countries with extremely low EPA and DHA intakes such as Bulgaria and Romania also can have low intakes of ALA from vegetable oils because they almost exclusively use sunflower oil, which does not contain ALA. Similarly, low intakes of ALA can be found in developing countries where cardiovascular disease is on the rise because they almost exclusively consume palm oil.
Since the early 1980s, Costa Rica has experienced a decrease in the intake of palm oil and an increase in the intake of soybean oil which has lead to increased intake of ALA in the population. In a previous analysis, data from these investigators suggested that ALA in adipose tissue is associated with a decreased risk of MI in the Costa Rican population. The objective of this study is to test the hypotheses that ALA (assessed both by questionnaire and in adipose tissue) is associated with reduced risk of MI in a larger population, that the maximum benefit of ALA is obtained within a specific range of intake, and that the association between ALA and MI is independent of fish intake.
Cases (n=1819) with a first nonfatal acute myocardial infarction and population-based controls (n=1819) living in Costa Rica matched for age, sex, and area of residence were studied.
ALA in adipose tissue ranged from 0.36% in the lowest decile to 1.04% in the highest decile. The corresponding median levels of intake were 0.42% and 0.86% energy. Greater ALA (assessed either in adipose or by questionnaire) was associated with lower risk of myocardial infarction. The odds ratios for nonfatal myocardial infarction for the highest compared with the lowest deciles were 0.41 (0.25 to 0.67) for ALA in adipose tissue and 0.61 (0.42 to 0.88) for dietary ALA. The relationship between ALA and myocardial infarction was nonlinear; risk did not decrease with intakes of 0.65% energy (1.79 g/d). Fish or eicosapentaenoic acid and docosahexaenoic acid intake at the levels found in this population did not modify the observed association.
Both dietary and adipose levels of ALA acid were associated with a large and significant reduction in the risk of nonfatal acute MI. These results suggest that increasing intake of vegetable oils rich in ALA acid could reduce the risk of MI. The data indicate that ALA acid is associated with decreased MI risk at low intake levels and that the amount of ALA associated with maximum benefit is small.
The data suggests that only a small amount of either soybean oil or canola oil, about 2 teaspoons daily, would contain enough ALA to reduce the risk of nonfatal acute MI when the baseline level of intake is low. The association between ALA acid and MI observed in this study could be due to the potential anti-inflammatory properties of ALA acid. In epidemiological studies, increased ALA acid intake in the range observed in this study (0.6 g/d) was associated with decreased plasma concentration of markers of inflammation (C-reactive protein, vascular cell adhesion molecule-1, and E-selectin). Consistent with these findings, intervention studies found that ALA acid lowers C-reactive protein plasma concentration, vascular cell adhesion molecule-1, and E-selectin.
The potential anti-inflammatory effects of ALA acid could be mediated in part through its conversion to EPA and DHA by the action of desaturase and enlongase enzymes. It has been shown that ALA acid decreases the nuclear transcription factor B, a major transcription factor involved in the regulation of inflammatory genes. Furthermore, ALA acid inhibits the production of nitric oxide and downregulates inducible nitric oxide synthase, cyclooxygenase-2, and tumor necrosis factor-R gene expression in murine macrophage. It is possible that ALA acid would have a more prominent role among populations with low fish intake because EPA can inhibit the action of delta-5 and delta-6 desaturase activity, which is required for ALA acid conversion. The data strongly supports that the consumption of vegetable oils rich in ALA acid could confer important cardiovascular protection. The apparent protective effect of ALA acid is most evident among subjects with low intakes.
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