Folic acid supplementation could effectively prevent dementia in some people, recent research suggests.
The possibility that low folic acid is a modifiable risk factor for dementia has been extensively studied. Dementia is linked to the natural age-related decline in information processing speed and memory, and data suggests that low folic acid levels are linked to this process. This new evidence supports a protective effect of supplementary folic acid, even indicating that it can improve cognitive function.
A team led by Dr. Jane Durga of Wageningen University and Wageningen Center for Food Sciences, the Netherlands examined this possible link among men and women enrolled in a trial focusing on folic acid and atherosclerosis (hardening of the arteries), called the Folic Acid and Carotid Intima-media Thickness (FACIT) trial.
The team gave 818 adults ages 50 through 70 either 800 micrograms of folic acid or a placebo every day for three years. At the start of the experiment, all the participants all had raised levels of homocysteine, indicating that they had low folic acid levels in the blood. Both groups were tested on memory, movement speed, information processing speed, and word fluency.
In the medical journal The Lancet, the researchers reported that the participants given folic acid showed significantly better changes on the cognitive tests than the placebo group. They suggest that folic acid might simultaneously affect memory and speed, because high levels of homocysteine are linked to damage to the hippocampus the area of the brain important for memory formation.
“[Our study was conducted] in older adults with raised total homocysteine concentrations,” the researchers pointed out. “Trials similar to our own should be repeated in other populations to provide greater insight into the clinical relevance of folic acid supplementation, such as in populations with mild cognitive impairment and dementia.”
In a commentary, Dr. Martha C. Morris and Dr. Christy C. Tangney from Rush University, Illinois, agree with the need for further trials, and ask why folic acid intakes are often so low.
It may be because 50 to 95 percent of folate content in food is estimated to be lost in storage, preparation, or manufacturing processes, according to the two doctors. The best sources of folate are yeast, organ meats (e.g., liver), green leafy vegetables (e.g., spinach), legumes, beans, and some fruits.
“To make more informed dietary recommendations for optimum folate intake, we need randomized trials that take the approach of the current trial,” they concluded.
A large study in 2005 added to the evidence of a link between folic acid intake and cognitive decline. Researchers from Johns Hopkins University, Baltimore, concentrated on homocysteine, which is elevated when a person’s folic acid intake is too low. The team measured blood homocysteine levels and cognitive function, using 20 neurobehavioral tests, in 1,140 men and women ages 50 to 70 enrolled in the Baltimore Memory Study.
Researchers found a clear link between homocysteine levels and cognitive ability, even when taking into account many related variables such as ethnicity and socioeconomic status. Homocysteine was “consistently and strongly associated with poorer neurobehavioral test performance,” they said. The closest links were found between homocysteine and speed of movement, eye-hand coordination, dexterity, verbal memory, and learning.
The researchers concluded that “higher homocysteine levels were associated with worse function across a broad range of cognitive domains, and the magnitude of the associations was large. The data suggest that homocysteine may be a potentially important modifiable cause of cognitive dysfunction.”
With recent studies from Greece and China supporting a homocysteine/cognitive impairment link, the evidence is stacking up in favor of folic acid supplementation for older people with a deficiency or other risk factors.
However, a 2003 review of the findings on folic acid supplementation showed no overall beneficial effect on cognitive performance or mood. But the authors added that many of the trials used small numbers of participants, gave supplements only for a short time, or used cognitive tests which could not detect subtle changes in cognitive function (such as the Mini-Mental State Examination).
A long-term study in the United States, in which Dr. Morris was involved, appeared to find greater cognitive decline in people with a high folic acid intake than in those with low intakes, in areas where folic acid fortification of foods was routine. The researchers remarked that these findings were “unexpected” and called for further study.
Neurologist Sudha Seshadri of Boston University, put it this way: “The role of homocysteine-lowering treatments [such as folic acid] in the primary prevention of dementia, as well as their role in preserving cognition among persons with mild cognitive impairment and early dementia deserves to be fully pursued.”
Durga J. et al. Effect of 3-year folic acid supplementation on cognitive function in older adults in the FACIT trial: a randomized, double blind, controlled trial. The Lancet, Vol. 369, Jan. 20, 2007, pp. 208-16.
Morris M. C. and Tangney C. C. Is dietary intake of folate too low? The Lancet, Vol. 369, Jan. 20, 2007, pp. 166-67.
Schafer J. H. et al. Homocysteine and Cognitive Function in a Population-Based Study of Older Adults. Journal of the American Geriatrics Society, Vol. 53, March 2005, pp. 381-388.
Morris M. C. et al. Dietary folate and vitamin B12 intake and cognitive decline among community-dwelling older persons. Archives of Neurology, Vol. 62, April 2005, pp. 641-45.
Malouf M. et al. Folic acid with or without vitamin B12 for cognition and dementia. Cochrane Database of Systematic Reviews (online) 2003; 4: CD004514.
Seshadri S. Elevated plasma homocysteine levels: risk factor or risk marker for the development of dementia and Alzheimer’s disease? The Journal of Alzheimers Disease, Vol. 9, August 2006, pp. 393-98.