B vitamin supplements slow brain atrophy in cognitively impaired patients
The results of a double-blinded clinical trial reported online on September 8, 2010 in the journal PLoSONE revealed that men and women with mild cognitive impairment who were supplemented with vitamin B6, vitamin B12 and folic acid experienced a reduction in the rate of brain atrophy compared with those who received a placebo. Brain atrophy, which involves the loss of neurons and their connections, occurs in older individuals and has been linked with elevated plasma homocysteine, a toxic amino acid that is lowered by specific B vitamins.
The study included 168 men and women aged 70 and older diagnosed with mild cognitive impairment who participated in the Homocysteine and B Vitamins in Cognitive Impairment (VITACOG) trial. A. David Smith and colleagues at the University of Oxford in England randomized the subjects to receive 20 milligrams vitamin B6, 500 micrograms vitamin B12 and 800 micrograms folic acid per day for 24 months. Cognitive testing, blood sample analysis, and magnetic resonance imaging (MRI) scans of the brain to assess the rate of atrophy were conducted before and after the treatment period.
Cognitive test results associated an increased rate of atrophy with lower final scores. The age-adjusted rate of brain atrophy per year was 29.6 percent less and homocysteine levels were 31.7 percent lower by the end of the trial in the active treatment group compared to the placebo group. Higher plasma homocysteine levels at the beginning of the trial predicted a greater rate of atrophy among those who did not receive B vitamins, however, this effect was not observed among the treatment group. Among those who received the vitamins and whose baseline homocysteine levels were among the top 25 percent, a 53 percent reduction in the rate of atrophy occurred compared to the placebo group. Additionally, reduction in the rate of atrophy was associated with improvement in folate or vitamin B12 levels. The authors remark that while elevated homocysteine could be a direct cause of the brain atrophy observed in the study, it may alternately be the result of reduced levels of folate, vitamin B6 and vitamin B12, with increased homocysteine only serving as a marker of these insufficiencies.
"The accelerated rate of brain atrophy in elderly with mild cognitive impairment can be slowed by treatment with homocysteine-lowering B vitamins," the authors conclude. "Since accelerated brain atrophy is a characteristic of subjects with mild cognitive impairment who convert to Alzheimer’s disease, trials are needed to see if the same treatment will delay the development of Alzheimer’s disease."
Elevated homocysteine levels (along with reduced levels of B vitamins such as folate, vitamin B12, and vitamin B6) are persistently associated with Alzheimer’s disease and mild cognitive impairment (Quadri P et al 2005; Ravaglia G et al 2005; Tucker KL et al 2005). Based on the association between elevated homocysteine and Alzheimer’s disease, strategies that lower homocysteine levels to safe ranges, including supplementation with B vitamins, are recommended.
Vitamin B12. Research has suggested that low cobalamin (vitamin B12) levels are related to dementias in general. In a study evaluating levels of vitamin B12 in patients who had Alzheimer’s disease or frontotemporal dementia, researchers found a significant negative correlation (the lower the level of vitamin B12, the more the deterioration) between vitamin B12 and degree of cognitive deterioration (Engelborghs S et al 2004). A population-based longitudinal study in Sweden of 370 people aged 75 years or older who did not have dementia found that subjects who had low levels of vitamin B12 or folate had twice the risk of developing Alzheimer’s disease over the 3-year period of the study (Wang HX et al 2001).
Vitamin B6. A study found significantly lower consumption of vitamin B6 after age 60 years in patients with Alzheimer’s disease compared to control subjects (Mizrahi EH et al 2003). Low vitamin B6 levels are also associated with elevated numbers of lesions on the brains of patients with Alzheimer’s disease (Mulder C et al 2005).
Folate. 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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