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Towards Dietary Reference Intakes for EPA and DHA

Towards Establishing Dietary Reference Intakes for Eicosapentaenoic and Docosahexaenoic Acids^1,2

³ Cardiovascular Health Research Center, Sanford Research/USD and Sanford School of Medicine at University of South Dakota, Sioux Falls, SD 57105 ⁴ Division of Cardiovascular Medicine and Channing Laboratory at Brigham and Women's Hospital and Harvard Medical School and Departments of Epidemiology and Nutrition at Harvard School of Public Health, Boston, MA 02115 ⁵ Center for Advanced Nutrition, Utah State University, Logan, UT 84322 ⁶ CDT Consulting, LLC, Fairfax, VA 22033 ⁷ Department of Psychology and Schiefelbusch Institute for Life Span Studies at University of Kansas, Lawrence, KS 66045 ⁸ Research Center on Aging, Université de Sherbrooke, Sherbrooke, QC, Canada J1H 4C4 ⁹ Food Composition and Methods Development Laboratory and Nutrient Data Laboratory, Beltsville Human Nutrition Research Center, Agriculture Research Service, USDA, Beltsville, MD 20705 ¹⁰ Agricultural Research Service, USDA, Beltsville, MD 20705 ¹¹ Internal Medicine and Preventive Medicine at Rush University Medical Center, Chicago, IL 60612 ¹² Department of Nutrition at University of Tennessee, Knoxville, TN 37996

There is considerable interest in the impact of (n-3) long-chain PUFA in mitigating the morbidity and mortality caused by chronic diseases. In 2002, the Institute of Medicine concluded that insufficient data were available to define Dietary Reference Intakes (DRI) for eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), noting only that EPA and DHA could contribute up to 10% toward meeting the Adequate Intake for -linolenic acid. Since then, substantial new evidence has emerged supporting the need to reassess this recommendation. Therefore, the Technical Committee on Dietary Lipids of the International Life Sciences Institute North America sponsored a workshop on 4–5 June 2008 to consider whether the body of evidence specific to the major chronic diseases in the United States—coronary heart disease (CHD), cancer, and cognitive decline—had evolved sufficiently to justify reconsideration of DRI for EPA+DHA. The workshop participants arrived at these conclusions: 1) consistent evidence from multiple research paradigms demonstrates a clear, inverse relation between EPA+DHA intake and risk of fatal (and possibly nonfatal) CHD, providing evidence that supports a nutritionally achievable DRI for EPA+DHA between 250 and 500 mg/d 2) because of the demonstrated low conversion from dietary ALA, protective tissue levels of EPA+DHA can be achieved only through direct consumption of these fatty acids 3) evidence of beneficial effects of EPA+DHA on cognitive decline are emerging but are not yet sufficient to support an intake level different from that needed to achieve CHD risk reduction; 4) EPA+DHA do not appear to reduce risk for cancer; and 5) there is no evidence that intakes of EPA+DHA in these recommended ranges are harmful.

^* To whom correspondence should be addressed. E-mail: harrisw{at}sanfordhealth.org.