B vitamin supplementation can lower plasma homocysteine but does not significantly reduce rates of age-related cognitive decline, according to the findings of a recent meta-analysis.
Observational studies have shown that elevated plasma homocysteine may be a modifiable risk factor for cognitive aging, noted Robert Clarke and colleagues in their report for The American Journal of Clinical Nutrition (2014;100:657-666).
As the investigators explained, cognitive function and its component domains of memory, speed, and executive function decline more quickly in some individuals, and some prospective studies have shown that healthy older persons with homocysteine concentrations of 14 µmol/L or higher had a twofold greater risk of Alzheimer disease after adjustment for known risk factors.
With high homocysteine levels being a marker for vitamin B insufficiency, several studies have been designed to evaluate whether supplementation with folic acid and vitamin B12 could lower homocysteine concentrations and slow the rate of age-related cognitive decline.
Clarke’s team used data from 11 large trials, involving 22,000 participants, to determine the cognitive effects of treatment with B vitamins compared with placebo. Most aspects of cognitive function declined during the studies evaluated and vitamin B supplementation reduced circulating homocysteine concentrations, as expected.
However, there was no coordinated effect of vitamin B supplementation on cognitive outcomes. “…[T]he discrepant results of the observational studies and the randomized trials for the effects of B vitamins on cognitive function suggest that elevated plasma homocysteine is probably a marker of underlying cognitive aging rather than a causal risk factor,” concluded Clarke and coauthors