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1 127 Courser Road Canada E-mail: vos{at}health-heart.org
2 Department of Nutritional Sciences Faculty of Medicine University of Toronto Toronto, Ontario M5S 3E2 Canada
Dear Sir:
The study by Djoussé et al (1) concludes that a higher intake of both -linolenic (18:3n-3) and linoleic acid (18:2n-6) is inversely related to the risk of coronary artery disease (CAD) in a high-risk population. The authors report about one-half the risk of CAD in going from the lower to the upper quintiles of -linolenic acid intake. As mentioned by the authors, this result is consistent with a growing body of evidence indicating the overall health benefit of -linolenic acid and, indeed, of all n-3 fatty acids.
Interestingly, the most protective intake of -linolenic acid in this study was the mean -linolenic acid intake in the United States. This intake is about one-half of the adequate intake of 2.2 g/2000 kcal (1% of energy) proposed in the consensus document (Internet: http://www.issfal.org.uk/adequateintakes.htm) from the working group that met under the auspices of the International Society for the Study of Fatty Acids and Lipids (ISSFAL). This suggests that the benefits of -linolenic acid increase at intakes > 1 g/d. The benefit is more likely to be optimal at an intake closer to 2 g/d, as indicated by the cardioprotective effects of the -linolenic acid–enriched (and linoleic acid–reduced) diet studied by de Lorgeril et al (2).
Djoussé et al report correctly that -linolenic acid is found mainly in flaxseed, soybeans, canola oil, and English walnuts. However, contrary to what they state, almonds and hazelnuts contain no -linolenic acid, and corn oil is a very poor source. Although it contains 59% linoleic acid, corn oil provides only 0.7% -linolenic acid (Internet: http://www.nal.usda.gov/fnic/cgi-bin/nut_search.pl). The ratio between these fatty acids is 84:1, whereas the ratio for an adequate intake proposed by ISSFAL is 2:1. Hence, corn oil should not be seen as contributing in any meaningful way to -linolenic acid intake because 1 tbsp provides 8 g linoleic acid but only 0.1 g -linolenic acid.
The conclusion that linoleic acid reduces the risk of CAD needs to be examined carefully. This conclusion seems to be based on the data in Table 8 of Djoussé et al’s article, in which the tertile for the highest linoleic acid intake and the lowest -linolenic acid intake was of insufficient size to provide a stable estimate. The next tertile for -linolenic acid, at the same high linoleic acid intake, did not show a decreased risk, whereas only in the group with the highest -linolenic intake and high linoleic acid intake was a reduced risk found. Also, tertiles seem to be a relatively crude measure for changes in dietary fatty acid intakes, whereas the close association of linoleic acid with -linolenic acid in foods makes it difficult to separate adequately their individual effects. Therefore, we think that this association, although perhaps statistically valid, is tenuous. Nevertheless, on the basis of the conclusion of Djoussé et al’s study and some other recent dietary recommendations (3), there would appear to be no prudent upper limit of linoleic acid intake.
However, this widespread public health support for a high linoleic acid intake is not borne out by the literature, as carefully scrutinized by Ravnskov (4). High linoleic acid intakes are not associated with reduced all-cause mortality, as are high -linolenic acid intakes (5). Indeed, Yam et al (6) suggest that the Israeli Paradox—a high incidence of CAD, cancer, and other degenerative diseases in Israel—may well be related to high linoleic acid intakes. Therefore, epidemiologic studies covering < 2 decades are, at best, unconvincing about the benefits of high linoleic acid intakes.
In addition, the results of 2 blinded clinical intervention trials of linoleic acid supplementation clearly question the overall health benefit of high linoleic acid intakes (7, 8). In both trials, animal and saturated fats were essentially replaced with corn oil. The first trial, by Rose et al (7), found that after 2 y, 75% of the control group remained free of coronary events as opposed to only 52% of those who consumed high–linoleic acid corn oil. They concluded that ".. under the circumstances of this trial, corn oil cannot be recommended in the treatment of ischaemic heart disease."
The second trial, by Pearce and Dayton (8), is also known as the Veterans Trial. These authors reported, as did many others in the 1960s and 1970s, on the replacement of saturated fatty acids with polyunsaturates but ignored the confounding role of n-3 fatty acids in some of the oils used. However, the dietary analysis in the Veterans Trial clearly shows that it was a linoleic acid trial in which the mean linoleic acid contents were 10% and 38% of total fats (11 and 41 g/d, respectively) and the mean -linolenic acid contents were 0.7% and 1.6% of total fats (0.8 and 1.7 g/d, respectively) in the control and experimental groups, respectively. The ratios of n-6 (linoleic acid) to n-3 (-linolenic acid) fatty acids were 14:1 and 24:1, respectively.
Pearce and Dayton (8) reported that the reduction in CAD with increased linoleic acid intakes was offset by twice the cancer incidence in the second half of this 8-y trial (8). Total mortality was unchanged; 59% survived (250 of 424 subjects) in the linoleic acid–supplemented group and 58% survived (244 survivors of 422 subjects) in the control group. This trial raises the crucial issue of overall mortality, which is often ignored in the evaluation of specific endpoints such as CAD.
In summary, we believe that Djoussé et al’s conclusion is well supported, ie, that high -linolenic acid intakes are inversely related to the risk of CAD, as they are with overall mortality (5). However, blinded clinical trials of the effects of high linoleic acid intakes (7, 8) indicate potential deleterious effects on long-term health. These clinical trials and others (9, 10) suggest caution regarding the high amounts of linoleic acid in Western diets. The uncertainties about the merits of unlimited linoleic acid intake caused ISSFAL to recommend an upper limit of linoleic acid intake of 6.7 g/d (3% of energy). We therefore wish to stress the importance of trials of longer duration and the evaluation of endpoints that must include noncardiac effects and total mortality.
We encourage people to abandon the overly simple concept of the ratio of polyunsaturated to saturated fatty acids. We suggest that dietary studies be specific regarding the respective amounts of these 2 families of polyunsaturates. We have outlined some of the evidence for questioning the overall health merits of current linoleic acid intakes in Western societies. Because linoleic acid constitutes most of the polyunsaturated fatty acid component of the ratio of polyunsaturated to saturated fatty acids, we suggest that reports be specific and refer to high intakes of linoleic acid if it is the main fatty acid under study.
Prior to the introduction of solvent-extracted vegetable oils and soy- rand corn-based animal husbandry over approximately the past 70 y, no population had been exposed to the current intakes of linoleic acid. We may well be experiencing the "linoleic acid paradox," in which a supposedly healthy fatty acid (ie, one that lowers total cholesterol) is associated with increasing rates of cancer and inflammatory and cardiovascular diseases during these same decades. Compounding and confounding this paradox are low intakes of -linolenic acid and other n-3 (fish) oils.
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