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St Luke's Hospital, Lipid and Diabetes Research Center, 4320 Wornall, Suite 128, Kansas City, MO 64111, E-mail: wharris{at}saint-lukes.org
Dear Sir:
One of us (DWTN) previously reported the results of a study carried out in Stavanger, Norway, of the effects of daily treatment with 3.4 g eicosapentaenoic acid plus docosahexaenoic acid (EPA+DHA) for 12–24 mo on endpoints of clinical coronary heart disease (CHD) (1). The subjects were patients with a history of acute myocardial infarction (n = 300), and the median follow-up time was 18 mo. In contrast with observations from the Diet and Reinfarction Trial (2) and the GISSI-Prevenzione trial (3), increased intakes of n-3 fatty acids in the Stavanger study had no beneficial effect. It was suggested that the background dietary intake of n-3 fatty acids in this Norwegian population may have produced sufficiently high blood concentrations of these fatty acids such that no further benefit from supplementation could have been achieved.
Further data from the Stavanger study have now been published (4). In a subset of 28 patients from each treatment group, the frequency of fish consumption, the proportion of patients taking fish oil supplements before the study, and serum phospholipid EPA+DHA concentrations were assessed (Table 1). Because some of the patients had taken EPA and DHA supplements before the study began, the baseline values shown in Table 1 may misrepresent the effect of the Norwegian background diet alone on EPA+DHA concentrations. To address this question, serum from patients who had not taken an EPA or DHA supplement before the study began was analyzed and was shown to have a mean of 6.3% EPA+DHA in the phospholipid fraction. This value was not materially different from the baseline values shown in Table 1; therefore, supplement consumption did not have a significant effect on baseline concentrations.
View this table:
TABLE 1. Serum phospholipid eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) concentrations in the Stavanger study and in cases and controls from published epidemiologic investigations1
The EPA+DHA content of the phospholipids in the Stavanger study were compared with those reported in epidemiologic studies on fish intake and CHD risk (Table 1). It was immediately obvious that the patients in the Stavanger study had concentrations that were approximately twice those reported by others, not only after treatment but also before treatment began. These data support the original suggestion that the failure of supplemental n-3 fatty acids to alter the future risk of CHD was probably due to the presence of high n-3 concentrations in the background diet. More important, these data also imply that there may be an upper limit of tissue n-3 fatty acid concentrations above which further CHD benefit will not be realized.
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