Journal Name:
Am J Cardiol

Article Title:
Comparison of effects of n-3 to n-6 fatty acids on serum level of lipoprotein(a) in patients with coronary artery disease

Date Written:
1995

Volume:
76

Number:

Page:
459

Author(s):
Herrmann, W.; Biermann, J.; Kostner, G.M.

Article:
Lipoprotein(a) (Lp[a]) is a LDL particle with a specific protein, apo(a), attached to it. Serum levels of Lp(a) are highly correlated to increased risk of CHD. Recent research has indicated that Lp(a) is not influenced to a significant extent by diet, although levels have been shown to be increased by trans fatty acids and by SFA. The effects of n-3 PUFAs on Lp(a) levels has not been established. The objective of the present study was to ascertain the influence of dietary supplementation with n-3 PUFAs on plasma Lp(a) levels. The diets of 35 male hospitalized patients with CHD were supplemented for 4 weeks with 12 g/day of fish oil (approximately 8.5 g of n-3 PUFAs). Eighteen patients were fed the same diet supplemented with 12 g/day of CO. Diets were comprised of 30% fat, 45% carbohydrate and 25% protein. All patients had elevated Lp(a) levels and were chosen because this population could benefit the most from reductions on Lp(a).

Following the completion of the supplementation period, TC, LDL-C, and apo B levels decreased significantly in both the CO (-14.4%, -20.3%, -15.2%, respectively) and fish oil (-12.2%, 16.0%, and -14.2%, respectively) groups. TGs decreased (-20.3%) and HDL-C increased (+8.3%) significantly in the patients treated with fish oil. Plasma Lp(a) levels were reduced by 14% in the fish oil group. In the CO group, all patients had minor, but nonsignificant, reductions in Lp(a). Patients treated with fish oil could be categorized into 2 subgroups: "responders, with a reduction in Lp(a) by 24% and "nonresponders, with a small nonsignificant increase in serum Lp(a). No significant changes were found in platelet and clotting factors, except for tissue plasminogen activator, which was significantly reduced by 16% in both groups.

The data suggests that CHD patients differ in their responses to dietary modification of Lp(a) and to effects of dietary supplementation of n-3 PUFAs. In the responder group, the authors speculated that Lp(a) reductions may be due to a lowering of apo(a) synthesis and/or secretion from the liver or possibly through impaired assembly of LDL particles. Further research is necessary to determine the role of n-3 PUFAs on Lp(a) levels in patients with CHD.,

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