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CME Released: 2/11/2005
Valid for credit through: 2/11/2006
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Feb. 11, 2005 — Intake of a mixture of vitamin E tocopherols from food sources rather than from supplements is associated with a reduced risk of Alzheimer's Disease (AD), according to the results of a large prospective study published in the February issue of the American Journal of Clinical Nutrition. Randomized trials therefore appear to be warranted.
"High intake of vitamin E from food (tocopherol), but not from supplements (which usually contain α-tocopherol), is inversely associated with Alzheimer disease," write Martha Clare Morris, ScD, PhD, from the Rush Institute for Healthy Aging in Atlanta, Georgia, and colleagues. "Because vitamin E is composed of four different tocopherol forms (α-, γ, δ, and β-tocopherols) and four corresponding tocotrienols, and because vitamin E supplements usually consist of α-tocopherol only, one possible explanation for the seeming inconsistency is that the effect is not due to α-tocopherol alone but to another tocopherol form or to a combination of tocopherol forms."
The investigators studied whether food intakes of vitamin E, α-tocopherol equivalents (a measure of the relative biologic activity of tocopherols and tocotrienols), or individual tocopherols would protect against incident AD and cognitive decline for six years in subjects enrolled in the Chicago Health and Aging Project (CHAP). This study of community residents aged 65 years or older took place from 1993 to 2002, and it included a battery of four cognitive tests, clinical evaluations for AD, and dietary assessment by food frequency questionnaire (FFQ).
Logistic regression revealed that tocopherol intake from food was directly related to the four-year incidence of AD in 1,041 participants who were clinically evaluated (n = 162 incident cases). Tocopherol intake from food was also positively associated with change in a global cognitive score determined by mixed models in 3,718 participants.
In separate multiple-adjusted models that included intakes of saturated and trans fats and docosahexaenoic acid, higher intakes of vitamin E and α-tocopherol equivalents were associated with a reduced incidence of AD. Relative risk was 0.74 per 5 mg/day increase for vitamin E (95% confidence interval, 0.62-0.88) and 0.56 per 5 mg/day increase for α-tocopherol equivalents (95% confidence interval, 0.32-0.98). α- and γ-Tocopherols were independently associated with risk of AD. Separate mixed models showed that a slower rate of cognitive decline was associated with intakes of vitamin E, α-tocopherol equivalents, and α- and γ-tocopherols.
The main study limitation was the questionable validity of intakes of some of the different tocopherol forms.
"The results suggest that various tocopherol forms rather than α-tocopherol alone may be important in the vitamin E protective association with Alzheimer disease," the authors write. "This may explain the absence of association reported in some studies between Alzheimer disease and use of vitamin E supplements, which have traditionally contained only α-tocopherol. Additional testing through randomized controlled clinical trials appears warranted to more firmly establish the effects of various tocopherol forms on the prevention of age-related cognitive decline and Alzheimer disease."
The authors report no conflict of interest.
Am J Clin Nutr. 2005;81:508-514
