A new population-based study of antioxidants, appearing in the June 26, issue of the Journal of the American Medical Association (JAMA), suggests that a diet rich in foods containing vitamin E may help protect some people against Alzheimer's disease (AD). The latest in a series of reports on vitamin E and dementia, the findings heighten interest in the outcome of clinical trials now underway to test the effectiveness of vitamin E and other antioxidants in preventing or postponing cognitive decline and AD.
"This and a number of important population studies have pointed to vitamin E as possibly protective against oxidative damage or other mechanisms associated with cognitive decline and dementia," says Neil Buckholtz, Ph.D., head of the Dementias of Aging Branch at the National Institute on Aging (NIA). "The only way this association can really be tested is through clinical studies and trials now underway. These will help us determine whether vitamin E in food or in supplements — or taken together — can prevent or slow down the development of mild cognitive impairment or AD."
The JAMA study was conducted by Martha Clare Morris, Sc.D., and colleagues from the Rush Institute for Healthy Aging at Rush-Presbyterian-St.Luke's Medical Center, Chicago. The 815 people participating in the study were part of the Chicago Health and Aging Project (CHAP), a study of a large, diverse community of people age 65 and older. Participants were free of dementia at the start of the study and followed for an average of 3.9 years. At an average of 1.7 years from their baseline assessment, participants completed a questionnaire, asking them in detail about the kinds and quantities of foods consumed in the previous year.
Some 131 participants had been diagnosed with AD by the end of the study period, when researchers examined the relationship between intake of antioxidants, including dietary and supplemental vitamins E and C, beta carotene, and a multivitamin, and development of AD. The most significant protective effect was found among people in the top fifth of dietary vitamin E intake (averaging 11.4 IU/d), whose risk of AD was 67 percent lower when compared to people in the group with the lowest vitamin E consumption from food (averaging 6.2 IU/d). (The recommended dietary allowance of vitamin E is 22 IU/d.)
The data were also analyzed to see if age, gender, race, education, or possible genetic risk for AD would influence the findings. Only the presence or lack of apoE-e4, one form of a protein associated with increased risk of late-onset AD, seemed to matter: the protective effect of vitamin E from food was strongest among people who did not have the apoE-e4 risk factor.
"Dietary vitamin E may protect against Alzheimer's disease," says Morris, "but the protection may only occur among people without the apoE-e4 allele."
No significant change in risk of AD was found when the scientists looked at vitamin E supplements, the other antioxidants and their supplements, or a general multivitamin. There was some evidence, though not statistically significant, that increased intake of dietary vitamin C and beta carotene was moving in a "protective direction," the researchers said.
Morris suggests that further study in key areas is needed to confirm and explain some of the study's findings, including the link with apoE status and the study's striking distinction between dietary intake of vitamin E and use of supplements. For example, the lack of a protective effect for the supplements could be explained by several factors. Some participants in the study started taking supplements only recently and there may not have been sufficient time for the supplement to be found effective. Also, people who believe they have memory problems could be more likely to take the supplements in the first place. Another possible explanation might be variations in the forms of vitamin E, scientists note. Most vitamin E supplements consist of alpha tocopherol while foods are generally richer in gamma tocopherol. These forms of vitamin E scavenge different types of free radicals, with one possibly more important than another in potentially reducing risk of cognitive decline. To help determine whether vitamin E might play a role in preventing AD, or at least in delaying its onset, a number of clinical trials are now being supported by the NIA.
It is not recommended, based on current evidence, that people take high-dose vitamin E supplements or other antioxidant pills in an effort to prevent mental decline, Buckholtz says. While population-based studies and animal research have suggested that antioxidants may be neuroprotective, clinical trials to test that notion are currently in progress. Little is known about safety, effectiveness, and dosages of various antioxidant supplements that are proposed for neuroprotective purposes, Buckholtz emphasizes. In excessively high doses (above 2,000 International Units daily, or IU/d), for example, vitamin E may be associated with increased risk of bleeding, and patients taking anti-coagulant medications may be especially at risk. Interactions with other medications commonly taken by older people are also of potential concern. People are advised to consult with their physicians before taking high doses of supplemental vitamin E or other antioxidants.