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J Nutr. 1991 Apr;121(4):484-91. Related Articles, Links

Effect of long-term fish oil supplementation on vitamin E status and

lipid peroxidation in women.

Meydani M, Natiello F, Goldin B, Free N, Woods M, Schaefer E,

Blumberg JB, Gorbach SL.

U.S. Department of Agriculture Human Nutrition Research Center on

Aging, Tufts University, Boston, MA 02111.

Fifteen young (22-35 y) and 10 older (51-71 y) women received six

capsules of fish oil (Pro-Mega)/d, providing a total of 1,680 mg

eicosapentaenoic (EPA), 720 mg docosahexaenoic (DHA), 600 mg other

fatty acids, and 6 IU vitamin E. Blood was collected before and after

1, 2 and 3 mo of supplementation. Compliance was confirmed by the

significant increase in plasma EPA and DHA in all women. Older women

had a significantly higher increase in EPA and DHA than did young

women (10-fold increases in EPA and 2.5-fold increases in DHA vs. 8-

fold in EPA and 2-fold in DHA for older and young women,

respectively). The decrease in the arachidonic acid:EPA ratio was

more dramatic in the older women. Plasma total triglycerides (TG)

decreased significantly, and the ratio of polyunsaturated fatty acids

to saturated fatty acids was significantly (P less than 0.01)

increased. Plasma vitamin E levels did not change significantly after

supplementation; however, after 3 mo of supplementation by young

women, plasma vitamin E was significantly lower than after 1 mo. The

vitamin E: TG ratio was significantly increased and vitamin E:(EPA +

DHA) significantly decreased. All women showed a significant increase

in plasma lipid peroxide through mo 2 of supplementation. After 2 mo,

older women had significantly higher lipid peroxide levels than young

women. The lipid peroxide:TG ratio, which declined by mo 3, was still

significantly higher than baseline. These data indicate that although

long-term fish oil supplementation may be beneficial in reducing

plasma total TG, susceptibility of plasma lipids to free radical

attack is potentiated.(ABSTRACT TRUNCATED AT 250 WORDS)

=========================================================

Lipid peroxidation during n-3 fatty acid and vitamin E

supplementation in humans.

Allard JP, Kurian R, Aghdassi E, Muggli R, Royall D.

Department of Medicine, University of Toronto, Ontario, Canada.

The purpose of this study was to investigate in healthy humans the

effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)

intake, alone or in combination with dL-alpha-tocopherol acetate

(vitamin E) supplements on lipid peroxidation. Eighty men were

randomly assigned in a double-blind fashion to take daily for 6 wk

either menhaden oil (6.26 g, n-3 fatty acids) or olive oil

supplements with either vitamin E (900 IU) or its placebo.

Antioxidant vitamins, phospholipid composition, malondialdehyde

(MDA), and lipid peroxides were measured in the plasma at baseline

and week 6. At the same time, breath alkane output was measured.

Plasma alpha-tocopherol concentration increased in those receiving

vitamin E (P < 0.0001). In those supplemented with n-3 fatty acids,

EPA and DHA increased in plasma phospholipids (P < 0.0001) and plasma

MDA and lipid peroxides increased (P < 0.001 and P < 0.05,

respectively). Breath alkane output did not change significantly and

vitamin E intake did not prevent the increase in lipid peroxidation

during menhaden oil supplementation. The results demonstrate that

supplementing the diet with n-3 fatty acids resulted in an increase

in lipid peroxidation, as measured by plasma MDA release and lipid

peroxide products, which was not suppressed by vitamin E

supplementation.

Lipid peroxidation during n-3 fatty acid and vitamin E

supplementation in humans.

Allard JP, Kurian R, Aghdassi E, Muggli R, Royall D.

Department of Medicine, University of Toronto, Ontario, Canada.

The purpose of this study was to investigate in healthy humans the

effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)

intake, alone or in combination with dL-alpha-tocopherol acetate

(vitamin E) supplements on lipid peroxidation. Eighty men were

randomly assigned in a double-blind fashion to take daily for 6 wk

either menhaden oil (6.26 g, n-3 fatty acids) or olive oil

supplements with either vitamin E (900 IU) or its placebo.

Antioxidant vitamins, phospholipid composition, malondialdehyde

(MDA), and lipid peroxides were measured in the plasma at baseline

and week 6. At the same time, breath alkane output was measured.

Plasma alpha-tocopherol concentration increased in those receiving

vitamin E (P < 0.0001). In those supplemented with n-3 fatty acids,

EPA and DHA increased in plasma phospholipids (P < 0.0001) and plasma

MDA and lipid peroxides increased (P < 0.001 and P < 0.05,

respectively). Breath alkane output did not change significantly and

vitamin E intake did not prevent the increase in lipid peroxidation

during menhaden oil supplementation. The results demonstrate that

supplementing the diet with n-3 fatty acids resulted in an increase

in lipid peroxidation, as measured by plasma MDA release and lipid

peroxide products, which was not suppressed by vitamin E

supplementation.

Lipid peroxidation during n-3 fatty acid and vitamin E

supplementation in humans.

Allard JP, Kurian R, Aghdassi E, Muggli R, Royall D.

Department of Medicine, University of Toronto, Ontario, Canada.

The purpose of this study was to investigate in healthy humans the

effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)

intake, alone or in combination with dL-alpha-tocopherol acetate

(vitamin E) supplements on lipid peroxidation. Eighty men were

randomly assigned in a double-blind fashion to take daily for 6 wk

either menhaden oil (6.26 g, n-3 fatty acids) or olive oil

supplements with either vitamin E (900 IU) or its placebo.

Antioxidant vitamins, phospholipid composition, malondialdehyde

(MDA), and lipid peroxides were measured in the plasma at baseline

and week 6. At the same time, breath alkane output was measured.

Plasma alpha-tocopherol concentration increased in those receiving

vitamin E (P < 0.0001). In those supplemented with n-3 fatty acids,

EPA and DHA increased in plasma phospholipids (P < 0.0001) and plasma

MDA and lipid peroxides increased (P < 0.001 and P < 0.05,

respectively). Breath alkane output did not change significantly and

vitamin E intake did not prevent the increase in lipid peroxidation

during menhaden oil supplementation. The results demonstrate that

supplementing the diet with n-3 fatty acids resulted in an increase

in lipid peroxidation, as measured by plasma MDA release and lipid

peroxide products, which was not suppressed by vitamin E

supplementation.

Lipid peroxidation during n-3 fatty acid and vitamin E

supplementation in humans.

Allard JP, Kurian R, Aghdassi E, Muggli R, Royall D.

Department of Medicine, University of Toronto, Ontario, Canada.

The purpose of this study was to investigate in healthy humans the

effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)

intake, alone or in combination with dL-alpha-tocopherol acetate

(vitamin E) supplements on lipid peroxidation. Eighty men were

randomly assigned in a double-blind fashion to take daily for 6 wk

either menhaden oil (6.26 g, n-3 fatty acids) or olive oil

supplements with either vitamin E (900 IU) or its placebo.

Antioxidant vitamins, phospholipid composition, malondialdehyde

(MDA), and lipid peroxides were measured in the plasma at baseline

and week 6. At the same time, breath alkane output was measured.

Plasma alpha-tocopherol concentration increased in those receiving

vitamin E (P < 0.0001). In those supplemented with n-3 fatty acids,

EPA and DHA increased in plasma phospholipids (P < 0.0001) and plasma

MDA and lipid peroxides increased (P < 0.001 and P < 0.05,

respectively). Breath alkane output did not change significantly and

vitamin E intake did not prevent the increase in lipid peroxidation

during menhaden oil supplementation. The results demonstrate that

supplementing the diet with n-3 fatty acids resulted in an increase

in lipid peroxidation, as measured by plasma MDA release and lipid

peroxide products, which was not suppressed by vitamin E

supplementation.

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