The Content of Favorable and Unfavorable Polyunsaturated Fatty Acids Found in Commonly Eaten Fish


      Changes in diet during the past century have caused a marked increase in consumption of saturated fatty acids and n-6 polyunsaturated fatty acids (PUFAs) with a concomitant decrease in the intake of n-3 PUFAs. Increased fish consumption has been shown to be the only realistic way to increase dietary quantities of beneficial long-chain n-3 PUFAs such as eicosapentaenoic acid and docosahexaenoic acid and re-establish more balanced n-6:n-3 ratios in the diets of human beings. Our objective in this research was to characterize some of the relevant fatty acid chemistry of commonly consumed fish, with a particular focus on the four most commonly consumed farmed fish. To do this, 30 commonly consumed farmed and wild fish were collected from supermarkets and wholesalers throughout the United States. Fatty acid composition of samples from these fish was determined using gas chromatography. The 30 samples studied contained n-3 PUFAs ranging from fish having almost undetectable levels to fish having nearly 4.0 g n-3 PUFA per 100 g fish. The four most commonly farmed fish, Atlantic salmon, trout, tilapia, and catfish, were more closely examined. This analysis revealed that trout and Atlantic salmon contained relatively high concentrations of n-3 PUFA, low n-6:n-3 ratios, and favorable saturated fatty acid plus monounsaturated fatty acid to PUFA ratios. In contrast, tilapia (the fastest growing and most widely farmed fish) and catfish have much lower concentrations of n-3 PUFA, very high ratios of long chain n-6 to long chain n-3 PUFAs, and high saturated fatty acid plus monounsaturated fatty acid to PUFA ratios. Taken together, these data reveal that marked changes in the fishing industry during the past decade have produced widely eaten fish that have fatty acid characteristics that are generally accepted to be inflammatory by the health care community.
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      K. L. Weaver is with the Department of Internal Medicine, Section on Molecular Medicine, P. Ivester is a research coordinator, and J. A. Chilton and P. Prandey are laboratory assistants, Department of Physiology and Pharmacology, M. D. Wilson is a research associate, Department of Pathology, Section on Lipid Sciences, and F. H. Chilton is a professor, Department of Physiology and Pharmacology, and director, Wake Forest Center for Botanical Lipids, Wake Forest University School of Medicine, Winston-Salem, NC.

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      • Erratum
        Journal of the American Dietetic AssociationVol. 108Issue 10
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          In the July 2008 Perspectives in Practice article, “The Content of Favorable and Unfavorable Polyunsaturated Fatty Acids Found in Commonly Eaten Fish,” pp 1178-1185, the name of one of the authors was misspelled in the biographical information paragraph on page 1178. “P. Prandey” should have been listed as “P. Pandey.” The Journal apologizes to the author for the error.
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      • Regarding Favorable and Unfavorable PUFA in Fish
        Journal of the American Dietetic AssociationVol. 108Issue 10
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          We would like to thank Dr Harris for his thoughtful comments regarding our paper on favorable and unfavorable polyunsaturated fatty acids found in commonly eaten fish in the July 2008 issue of the Journal (1). Harris is a world-recognized and respected nutritionist, and his thoughts in the form of a Research Editorial (2) are greatly appreciated.
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      • Concerning PUFA in Fish
        Journal of the American Dietetic AssociationVol. 108Issue 11
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          It was surprising to read in the Journal that certain n-6 polyunsaturated fatty acids (PUFAs), long considered essential nutrients, were deemed unfavorable (1). For years, Americans have been urged to substitute unsaturated fatty acids, including polyunsaturated ones, for saturated ones, with the result that the US consumption of PUFAs is about 7% of energy or more, most of which comes from linoleic acid (2). This increase has been associated with decreased mortality from coronary heart disease and lower incidence of myocardial infarction (3).
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      • Author's Response
        Journal of the American Dietetic AssociationVol. 108Issue 10
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          I appreciate the opportunity to comment on Dr Chilton's comments about my Research Editorial. He indicates that I disagreed with the statement that: “Several studies indicate that there is a strong in vivo correlation between AA [arachidonic acid] consumption and eicosanoid production.” In fact, I do not dispute that higher arachidonic acid intakes lead to higher production levels of eicosanoids. The Ferretti study (1) confirms this. What I dispute is the assumption that this is harmful. An increase in “vasoactive” eicosanoids can mean vaso-constrictive (adverse) and/or vaso-dilatory (beneficial) species.
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