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Review
. 1986;25(1-4):437-50.
doi: 10.1016/0163-7827(86)90089-5.

Serum fatty acids and coronary heart disease in Finnish populations

Affiliations
Review

Serum fatty acids and coronary heart disease in Finnish populations

T Nikkari. Prog Lipid Res. 1986.

Abstract

Finland has one of the highest coronary heart disease (CHD) rates in the whole world, and within the country, the rates are higher in men and eastern Finland than in women and western Finland, respectively. The differences are not wholly explained by the 3 classical risk factors. Several cross-sectional and longitudinal studies suggest that the intake of dietary linoleate (18:2), as reflected in the composition of serum and tissue fatty acids, has an inverse association with CHD, although there are also studies with negative results. Our own retrospective study failed to show any differences in the fatty acid composition of serum CE, TG or PL between men who had died of CHD and age- and risk factor-matched controls, but the negative finding may be due to changes in the fatty acids during storage. Among Finnish populations, most serum CE fatty acids had highly significant correlations with those in other serum lipid fractions, adipose tissue and platelets, and they had good "tracking" for up to 4 yr. Serum CE and TG 18:2, and total omega 6 polyunsaturated fatty acids (PUFA) had strong correlations with dietary 18:2 and PUFA, and can thus be used in the evaluation of population differences in the intake of PUFA. CE fatty acids were analyzed in a total of 2820 free-living 1- to 85-yr-old males and females. The percentages of serum fatty acids were age-dependent. West-Finnish populations had higher contents of 18:2 than those in eastern Finland, and middle-aged women had higher proportions of 18:2 than men. The content of 18:2 in adipose tissue and/or serum CE of middle-aged men was comparable to that in Scotland and lower than those in Italy and Sweden. These findings are compatible with the idea that 18:2 is a negative risk factor of CHD, but the evidence is only circumstantial. Possible mechanisms whereby 18:2 could affect CHD have been discussed. The contents of omega 3 fatty acids in CE were opposite to those of omega 6 fatty acids in that eastern Finnish and male populations had higher contents of 18:3 omega 3 and 20:5 omega 3 than western Finns and females, respectively. This finding is apparently due to substitution of vegetable fat for milk fat in the diet, resulting in a relative deficiency of the omega 3 fatty acids at the expense of 18:2. Experimental evidence for such a mechanism was obtained in an intervention study.(ABSTRACT TRUNCATED AT 400 WORDS)

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