Determining levels of homocysteine may be one way to intervene in mild cognitive deficit early in the adult life-cycle

Sep 28 2005

Determining levels of homocysteine may be one way to intervene in mild cognitive deficit early in the adult life-cycle, according to a recent study by a research team led by Merrill F. Elias, a professor of epidemiology in the Statistics and Consulting Unit of the Department of Mathematics and Statistics at Boston University.

Normally present in blood plasma, homocysteine is an amino acid by-product of the biological process that converts food to the chemical compounds that keep the body running.

Other studies, as well as early results from clinical trials, indicate that preventive measures for homocysteine-related cognitive deficit might be as simple and convenient as daily supplements of folate, and B12 and B6 vitamins.

Drawing participants from the Framingham Offspring Study, the team analyzed data from 2,096 individuals who were determined to be free of dementia. According to the analysis, high levels of homocysteine correlated with decreased performance levels on cognitive tests that measured a range of abilities that included abstract reasoning, visual and verbal memory, organization, attention, executive ability, tracking, and global ability.

Research has shown that high levels of homocysteine may, over time, adversely affect cognitive performance, but, until this study, no research has cleanly teased out homocysteine's link to cognitive functioning. For this study, the researchers were able to focus on homocysteine's effects on cognitive measures because they were able to statistically eliminate other factors that could affect cognitive function -- the confounding factors of risk for future stroke, cardiovascular disease, cardiovascular risk factors, and the vitamin cofactors (folate, B12, and B6 ) that play a role in high levels of homocysteine.

The investigators discovered an inverse relationship between high blood levels of homocysteine and cognitive performance in persons over 60 years of age. Specifically, the team found that regardless of what statistical adjustments they made to the data to account for a range of factors (e.g., age; sex; education; vitamin B12, vitamin B6, and folate; cardiovascular disease or risk factors for cardiovascular disease), the higher the levels of homocysteine, the lower the levels of cognitive performance. Conversely, they found that the higher the levels of vitamin B12, the higher the levels of cognitive performance.

For participants under the age of 60, however, the data showed no such associations, leading the researchers to speculate that use of vitamins by individuals under age 60 may be useful in lowering homocysteine levels since such an intervention would take place prior to lowered cognitive performance.

The team's findings of a relationship between homocysteine and mild cognitive dysfunction are reported in the recent issue of the American Journal of Epidemiology.

Participants in this study were drawn from the Framingham Offspring Study, a group of individuals who have, over a 30-year period, been studied to identify risk factors for cardiovascular and cerebrovascular disease. A spin-off of the Framingham Heart Study, which began in 1948, participants in the offspring study have at least one biological parent or one of their spouse's parents participating in the Framingham Heart Study.

"We were excited to find this result because it indicates that preventing cognitive difficulties down the road might be something individuals can take charge of well before they reach the age of 60," says Elias. "Taking vitamins B12, B6, and folate in the dosages currently recommended by the U.S. Food and Drug Administration could offer a side-effect-free way to prevent difficulties in memory and recall later in life."