Association of atherosclerosis-related markers and its relationship to n-3 polyunsaturated fatty acids levels with a prevalence of coronary artery disease in an urban area in Japan

Abstract

Higher intakes of fish and n-3 polyunsaturated fatty acids (n-3PUFAs: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) are associated with a reduced risk of coronary artery disease (CAD). We investigated the relationships between fish-derived n-3PUFAs and prevalence of CAD, and to assess the association of n-3PUFAs with atherosclerosis-related markers in an urban area. This study was designed as a hospital-based cross-sectional study on 649 consecutive outpatients who had undergone regular examinations between April 2009 and October 2009. After adjustments for the coronary risk factors in a multilogistic regression analysis of variables for which a significant difference was identified between the group of patients with a prevalence of CAD and the group with no prevalence of CAD, the multivariable odds ratio (95 % confidence interval) was 0.394 (0.205/0.760; P = 0.005) for the highest (92.4-373.5 μg/ml) versus lowest (6.2-40.0 μg/ml) quartile of serum EPA values and 0.433 (0.228/0.824; P = 0.011) for the highest (160.7-451.8 μg/ml) versus lowest (35.7-100.7 μg/ml) quartile of serum DHA values. Multivariate regression analyses after adjustment for risk factors showed that higher serum EPA and DHA levels were independent variables of a higher level of serum apolipoprotein A-1, a major compound of high-density lipoprotein. However, the results suggested that there might be conflicting effects of EPA and DHA in regard of the serum levels of other lipid markers. This cross-sectional study suggests that higher serum levels of n-3PUFAs were associated with a lower prevalence of CAD and an increase in serum apolipoprotein A-1 level, even in an urban area.

Association of Fish Consumption-Derived Ratio of Serum n-3 to n-6 Polyunsaturated Fatty Acids and Cardiovascular Risk With the Prevalence of Coronary Artery Disease

“…19,20) Our cross-sectional study, reported recently, demonstrated an association between elevated serum EPA and a decrease of serum TRLs. 6) Linoleic acid, which is a precursor of AA, is abundantly contained in the TG fraction, and it seems likely that the effect of EPA in lowering the serum TG may lead to a decrease of the serum AA, and consequently, elevation of the serum EPA/AA ratio. 13) For this reason, evaluation of the extent of influence of the EPA/AA ratio on atherosclerosis may be more accurate than the evaluation based on the serum EPA level alone.…”

“…6) Exclusion criteria included refusal to provide consent for participation in the study, current treatment with n3PUFAs, and/or a diagnosis of acute coronary syndrome (ACS) within 3 months prior to the study.…”

“…In a recent report, we indicated that the prevalence of CAD was lower in a population with higher serum EPA and DHA levels, although it was not possible in that study to stratify the risk for CAD according to the EPA and DHA levels. 6) However, we may now say that the n-3 PUFA/AA ratio is probably useful in stratification of the risk for CAD. Study limitations: First, this was a cross-sectional study, which made it difficult to establish a cause-effect relationship.…”

“…4,5) Recently, we reported findings from a hospital-based cross-sectional study that indicated the incidence of CAD was lower in a group of individuals with high serum EPA and DHA levels. 6) Although belonging to the same n-3PUFA family, EPA and DHA differ from one another in molecular structure 4,5) and it is known that the percentage of EPA and DHA contained in each organ differs depending on the difference in the percent uptake by the respective cell membranes. 7) It seems therefore likely that in vivo, EPA and DHA exhibit different physiological activities.…”

“…[8][9][10][11] A strong positive correlation is known to exist between serum EPA and DHA levels, and this was also shown in our study cited above. [4][5][6] Because serum EPA and serum DHA levels serve as confounding factors for each other, there are limits to discussing their effects on the incidence of coronary artery disease.…”