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By Greg Arnold, DC, CSCS, January 9, 2007, abstracted from Relation of Higher Folate Intake to Lower Risk of Alzheimer Disease in the Elderly” in the January 2007 issue of the Archives of Neurology

Expected to quadruple by the year 2047,1 Alzheimer disease (AD) currently costs our healthcare system $100 billion each year2 and affects 4 million Americans.3 Because inflammation has been found to be a significant contributor to the onset of AD,4 supplementing your diet with fish oil5 has been found to reduce inflammation and help maintain mental health.

Homocysteine, a known risk factor for cardiovascular disease6 and stroke,7 is also thought to be related to an increased risk for AD.8 Now a new study9 has found that folic acid deficiency, which leads to increased homocysteine levels,10 may increase the risk for AD.

In the study, researchers followed 965 persons 65 years or older without dementia for an average of 6 years. They analyzed their responses to food frequency questionnaires concerning total, dietary, and supplement intake of folate and vitamins B6 and B12 and calorie intake.

While they found no association between vitamin B6 and B12 intake and AD risk, they found that those with the highest intakes of folic acid (greater than 487.9 micrograms per day) had a 50% decreased risk of AD compared to those with the lowest intakes (less than 292.9 micrograms per day). For those with intakes of 365.1 to 487.8 micrograms per day, AD risk was reduced by 30%.

For the researchers, “higher folate intake may decrease the risk of AD independent of other risk factors and levels of vitamins B6 and B12.”

Greg Arnold is a Chiropractic Physician practicing in Danville, CA. You can contact Dr. Arnold directly by emailing him at mailto:ChiroDocPSUalum@msn.com or visiting his website.

Reference:

1 Brookmeyer R. Projections of Alzheimer's disease in the United States and the public health impact of delaying disease onset. Am J Public Health. 1998;88:1337-1342.

2 Ernst, RL; Hay, JW. “The U.S. Economic and Social Costs of Alzheimer’s Disease Revisited.” American Journal of Public Health 1994; 84(8): 1261 – 1264

3 Hebert, LE. “Alzheimer Disease in the U.S. Population: Prevalence Estimates Using the 2000 Census.” Archives of Neurology August 2003; 60 (8): 1119 – 1122

4 Potter, H., I. M. The inflammation-induced pathological chaperones ACT and apo-E are necessary catalysts of Alzheimer amyloid formation. Neurobiol Aging 2001; 22(6): 923-30

5 Wurtman RJ. Synaptic proteins and phospholipids are increased in gerbil brain by administering uridine plus docosahexaenoic acid orally. In Press, Corrected Proof, Available online 21 April 2006 in Brain Research

6 Yusuf S. Homocyst(e)ine and cardiovascular disease: a critical review of the epidemiologic evidence. Ann Intern Med. 1999;131:363-375

7 Chambless LE, et al. Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) Randomized Controlled Trial. JAMA. 2004;291:565-575

8 Selhub J, et al. Plasma homocysteine as a risk factor for dementia and Alzheimer's disease. N Engl J Med. 2002;346:476-483

9 Luchsinger JA. Relation of Higher Folate Intake to Lower Risk of Alzheimer Disease in the Elderly. Arch Neurol. 2007;64:86-92

10 Leboeuf R. Homocysteine and Alzheimer's disease. J Am Diet Assoc. 2003;103:304-307
Disclaimer: Claims made by NOW Foods for Folic Acid as a dietary supplement are regulated by the FDA, and any claims made in the above article are not made by NOW Foods. NOW makes no claims for the effect of Folic Acid on cognitve functioning or the risk of Alzheimer Disease.