Interesting research published in JAMA last month refuted omega-3s’ role in cognitive function (2015;314(8):791-801). The well-known Age-Related Eye Disease Study 2 (AREDS2), conducted by the National Institutes of Health (NIH), is one of the largest—4,000 patients—and longest—five years—of its kind. There is substantial research supporting omega-3 fatty acid’s ability to protect the brain, but this study showed supplementing omega-3s did not slow cognitive decline in older patients.
Omega-3s are a popular inclusion in all types of functional foods—and beverages, too—such as eggs, cereals, sports-nutrition drinks and more. In fact, the functional foods market is slated to hit $2.5 billion by 2020. But will this new study cause consumers to doubt the need to supplement and/or eat omega-3 fatty acids? Let’s take a closer look at the study design and results.
In the double-masked randomized clinical trial, retinal specialists in 82 U.S. academic and community medical centers enrolled and observed participants who were at risk for developing late age-related macular degeneration (AMD) from October 2006 to December 2012. In addition to annual eye examinations, several validated cognitive function tests were administered via telephone by trained personnel at baseline and every two years during the five-year study.
Long-chain polyunsaturated fatty acids (LCPUFAs) (1 g) and/or lutein (10 mg)/zeaxanthin (2 mg) versus a placebo were tested in a factorial design. All participants were also given varying combinations of vitamins C, E, beta carotene and zinc.
The main outcome was the yearly change in composite scores determined from a battery of cognitive function tests from baseline. The analyses, which were adjusted for baseline age, sex, race, history of hypertension, education, cognitive score and depression score, evaluated the differences in the composite score between the treated versus untreated groups. The composite score provided an overall score for the battery, ranging from −22 to 17, with higher scores representing better function.
A total of 89 percent (3,741/4,203) of AREDS2 participants consented to the ancillary cognitive function study and 93.6 percent (3,501/3,741) underwent cognitive function testing. The mean age of the participants was 72.7 (7.7) years and 57.5 percent were women. There were no statistically significant differences in change of scores for participants randomized to receive supplements versus those who were not. The yearly change in the composite cognitive function score was −0.19 for participants randomized to receive LCPUFAs versus −0.18 for those randomized to no LCPUFAs. Similarly, the yearly change in the composite cognitive function score was −0.18 for participants randomized to receive lutein/zeaxanthin versus −0.19 for those randomized to not receive lutein/zeaxanthin. Analyses were also conducted to assess for potential interactions between LCPUFAs and lutein/zeaxanthin and none were found to be significant.
According to the researchers, among older persons with AMD, oral supplementation with LCPUFAs or lutein/zeaxanthin had no statistically significant effect on cognitive function.
“Contrary to popular belief, we didn’t see any benefit of omega-3 supplements for stopping cognitive decline," said Emily Chew, deputy director of the Division of Epidemiology and Clinical Applications and deputy clinical director at the National Eye Institute (NEI), part of NIH.
“The AREDS2 data add to our efforts to understand the relationship between dietary components and Alzheimer’s disease and cognitive decline," said Lenore Launer, Ph.D. senior investigator in the Laboratory of Epidemiology and Population Science at the National Institute on Aging. “It may be, for example, that the timing of nutrients, or consuming them in a certain dietary pattern, has an impact. More research would be needed to see if dietary patterns or taking the supplements earlier in the development of diseases like Alzheimer’s would make a difference."