Increased folic acid intake linked with lower Alzheimer’s disease risk
The January 2007 issue of American Medical Association journal Archives of Neurology published the finding of José A. Luchsinger, MD, of Columbia University Medical Center, and colleagues that older men and women with a higher intake of folate from diet and supplements have a reduced risk of Alzheimer’s disease compared to those who consume less.
The researchers followed 965 Medicare recipients aged 65 or older for an average of 6 years. The study population was 45.3 percent Hispanic, 32.6 percent African American and 22.1 percent Caucasian. Dietary questionnaires completed at the beginning of the study were analyzed for folate, vitamin B6, and vitamin B12 from diet and supplements. Participants were without dementia upon enrollment and were evaluated for the development of Alzheimer’s disease approximately every 18 months.
One hundred ninety-two participants developed Alzheimer’s disease over the follow up period. Although the researchers did not find a correlation between the development of Alzheimer’s disease and the intake of vitamin B6, B12, or folate from either food or supplements alone, greater intake of folate from diet and supplements combined was associated with a reduced risk of the disease. Participants in the top one-fourth of total folate intake experienced half the adjusted risk of developing Alzheimer’s disease than those in the lowest quarter. A modest association between lower homocysteine levels and greater total folate intake as well as serum folate was observed, "indirectly suggesting that a lower homocysteine level is a potential mechanism for the association between higher folate intake and a lower Alzheimer's disease risk," the authors remark.
It is possible that the evident lack of benefit found in this study for vitamin B12, a nutrient that is also known to reduce homocysteine levels, is due to the animal source of the vitamin, which links a higher intake of B12 with a diet that contains more meat. Previous research has found that diets that have a lower meat and higher vegetable content are associated with a lower risk of Alzheimer’s disease.
To the authors’ knowledge this is the first published study to explore the relationship between vitamins related to homocysteine and Alzheimer’s disease in a population that is mainly African American and Caribbean Hispanic. They introduce their article by observing that “By the year 2047, the prevalence of Alzheimer's disease is expected to quadruple.” Any measure that could help delay its onset will decrease the tremendous burden that the disease is projected to inflict on Alzheimer’s disease sufferers, caregivers, and the nation’s healthcare system.
Compelling and growing evidence links inflammation and oxidative stress to Alzheimer’s disease. According to the inflammation theory (discussed in dozens of recent clinical trials), inflammatory cytokines gather at the neurons of people who have Alzheimer's. These cytokines set off an inflammatory cascade. The inflammation generates high levels of free radicals that contribute directly to the formation of beta-amyloid plaques. The result is more inflammation, free radicals, and beta-amyloid plaques. Iron has also been linked to the generation of free radicals. Studies have shown that free iron accumulates on the surface of dying neurons, where it generates oxygen-derived free radicals that hasten the spread of the disease (Mandel S et al 2006).
Other possible causes include high levels of homocysteine in the brain and specific nutrient deficiencies. Although these ideas are still developing, they have opened up exciting new targets for therapy. In clinical studies, the most cutting-edge researchers are turning to therapies such as anti-inflammatory nutrients, antioxidants that reduce oxidative stress, and metal chelating agents (such as green tea) that reduce the levels of free iron in the brain.
Folic acid is needed for DNA synthesis and to make S-adenosylmethionine (SAMe). A study of 126 patients, including 30 who had Alzheimer’s disease, found that the levels of folate in cerebrospinal fluid were significantly lower in patients with late-onset Alzheimer’s disease (Serot JM et al 2001). Another longitudinal analysis of people between the ages of 70 and 79 years found that people who had high levels of homocysteine or low levels of folate had impaired cognitive function. The strongest association between abnormal levels and dementia was found in people who had low folate levels, leading researchers to suggest that folate might reduce the risk of cognitive decline (Kado DM et al 2005).
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