Recently a study that was published in the prestigious Proceedings of the National Academy of Sciences (PNAS) discussed how B vitamins (specifically folic acid, B6 and B12) may be able to slow the development of Alzheimer’s disease, slowing the shrinkage of brain volume (Douaud et al. 2013). This is not the first study of its kind, but is one piece of the mounting pile of evidence that suggests that one of the biggest causative factors of Alzheimer’s is elevated homocysteine levels, and that controlling homocysteine may be a viable treatment.
It all started over 15 years ago, with the observation that Alzheimer’s patients had higher homocysteine levels (Clarke et al. 1998). These patients also had lower than average folic acid and vitamin B12 levels, which are key components of the body’s system for dealing with homocysteine.
This connection has been bolstered over the years from numerous angles, including an increased risk for Alzheimer’s being noted in those with mutations in the gene MTHFR, which is required for conversion of supplemental folic acid into the active 5-methyltetrahydrofolate (5-MeTHF; Mansoori et al. 2012). These individuals are unable to effectively convert the folic acid found in fortified foods, and as a result, may have higher homocysteine levels. This mutation is present in between 10% and 40% of the population, with the highest frequency in Caucasians, and the lowest in those of African descent. In these individuals, normal supplemental folic acid is less effective at reducing homocysteine levels, and active folates like 5-MeTHF are required for full benefit.
So where does this leave us? Ongoing research is showing us that homocysteine is involved in some of the biggest health dangers of our time, Alzheimer’s, diabetes, cardiovascular disease, and even osteoporosis, but the message is only getting to the public very slowly. Supplements containing 5-MeTHF, vitamin B6 and vitamin B12 are clinically proven to reduce elevated homocysteine, and, as found in the recent study, can slow the development of disease.
You may also be interested in: “Homocysteine Reduction with Vitamin B”
Clark et al. (1998) Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol 55(11):1149-1455.
Douaud et al. (2013) Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment. PNAS June 4, 2013 vol. 110 no. 23.
Mansoori et al. (2012) MTHFR (677 and 1298) and IL-6-174 G/C genes in pathogenesis of Alzheimer’s and vascular dementia and their epistatic interaction. Neurobiol Aging May 33(5):1003 e1-8.