For what it's worth, this article directly challenges the idea that fish
oils are more suseptible to oxidation, at least in relation to some
other oils and with respect to LDL -- I suppose that's been a fear in
the literature.

Liz

Journal of Lipid Research, Vol. 42, 407-418, March 2001
Copyright © 2001 by Lipid Research, Inc.

Original Article

Supplementation of postmenopausal women with fish oil does not increase
overall oxidation of LDL ex vivo compared to dietary oils rich in oleate
and linoleate
J. V. Higdon a,  S. H. Du a,  Y. S. Lee a,  T. Wu a, and  R. C. Wander a
aDepartment of Nutrition and Food Management, Oregon State University,
Corvallis, OR 97331

Correspondence to:  R. C. Wander, at current address: Dept. of Nutrition
and Foodservice Systems, University of North Carolina at Greensboro, 318
Stone Building, 1000 Spring Garden St., Greensboro, NC 27402-6170.,
[log in to unmask] (E-mail)

Although replacement of dietary saturated fat with monounsaturated and
polyunsaturated fatty acids (MUFA and PUFA) has been advocated for the
reduction of cardiovascular disease risk, diets high in PUFA could
increase low density lipoprotein (LDL) susceptibility to oxidation,
potentially contributing to the pathology of atherosclerosis. To
investigate this possibility, 15 postmenopausal women in a blinded
crossover trial consumed 15 g of sunflower oil (SU) providing 12.3 g/day
of oleate, safflower oil (SA) providing 10.5 g/day of linoleate, and
fish oil (FO) providing 2.0 g/day of eicosapentaenoate (EPA) and 1.4
g/day of docosahexaenoate (DHA). During CuSO 4-mediated oxidation, LDL
was depleted of -tocopherol more rapidly after FO supplementation than
after supplementation with SU ( P=0.0001) and SA ( P=0.05). In LDL
phospholipid and cholesteryl ester fractions, loss of n-3 PUFA was
greater and loss of n-6 PUFA less after FO supplementation than after SU
and SA supplementation ( P< 0.05 for all), but loss of total PUFA did
not differ. The lag phase for phosphatidylcholine hydroperoxide (PCOOH)
formation was shorter after FO supplementation than after
supplementation with SU ( P=0.0001) and SA ( P=0.006), whereas the lag
phase for cholesteryl linoleate hydroperoxide (CE18:2OOH) formation was
shorter after FO supplementation than after SU ( P=0.03) but not SA. In
contrast, maximal rates of PCOOH and CE18:2OOH formation were lower
after FO supplementation than after SA ( P=0.02 and 0.0001,
respectively) and maximal concentrations of PCOOH and CE18:2OOH were
lower after FO supplementation than after SA ( P=0.03 and 0.0006,
respectively).

Taken together, our results suggest that FO supplementation does not
increase the overall oxidation of LDL ex vivo, especially when compared
with SA supplementation. Consequently, health benefits related to
increased fish consumption may not be offset by increased LDL oxidative
susceptibility.— Higdon, J. V., S. H. Du, Y. S. Lee, T. Wu, and R. C.
Wander. Supplementation of postmenopausal women with fish oil does not
increase overall oxidation of LDL ex vivo compared to dietary oils rich
in oleate and linoleate. J. Lipid Res. 2001. 42: 407;–418.

http://www.jlr.org/cgi/content/abstract/42/3/407