DHA Supplementation Found Not to Slow Alzheimer Disease
Quinn, J. F. et al., J. Am. Medical Assoc., 304: 1903-1911 , 2010
Dept. Of Neurology, Oregon Health and Science University, Portland , Oregon, USA
A total of 402 individuals (52 % female) with mild to moderate Alzheimer disease (having Mini-Mental State Examination (MMSE) scores of 14-26) and an average age of 76 years were randomized to receive a placebo supplement (minus DHA) or encapsulated algal DHA omega-3 (docosahexaenoic acid) at 2000 mg/day for a duration of 18 months. The chief aim of this clinical trial was to determine if DHA supplementation (free of EPA) could retard the rate of cognitive and functional decline in this patient population. Analyses of DHA levels in blood (plasma phospholipid fraction) and cerebrospinal fluid at baseline and up to 18 months showed marked increases which were generally consistent with overall expected compliance to the targeted DHA supplementation regimen (for those completing the trial).
Based on the clinical measures undertaken , the authors concluded that there was no evidence for benefit of DHA supplementation in this population of patients with mild to moderate Alzheimer disease. When analyzing their results from sub-groups within the patients, they found some exploratory support to suggest that those participants who were found (genetically) to be APOE epsilon 4-negative appeared to exhibit a moderate but significantly-lower decline in their cognitive scores when receiving DHA relative to the placebo controls.
Dr. Holub's Comments:
Previous studies in the relevant literature have indicated that the regular consumption of fish containing DHA omega-3 over extended time periods (longer than that used above) may reduce the risk of developing Alzheimer disease in an aging population (Morris et al., Arch. Neurol., 60: 923 (2003)). Also, there is some published support to suggest that supplementation with DHA plus EPA (eicosapentaenoic acid) in sub-groups with very mild Alzheimer disease (MMSE scores above 27) may reduce the MMSE decline rate (Freund-Levi et al., Arch. Neurol., 63: 1402 (2006)). It should be pointed out that the investigators above found no effect of DHA when breaking their patients into groups with MMSE scores above or below 21. Although only speculative, it is possible that supplementation with a mixture of DHA plus EPA , which gives rise to a wider range of oxygenated bioactive products in brain tissue (including resolvins and protectins) than formed from DHA alone with anti-inflammatory neuroprotective properties , may offer benefit in long-term studies if introduced very early.