B vitamins are well known for their energy boosting abilities. Thiamin (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxine (B6) and biotin (B7) all play important supportive roles in the energy-producing reactions performed when our body breaks down carbohydrates, fats and proteins (Groff & Gropper, 1999).  Without these B vitamins we are often left feeling worn out, stressed and in some cases of severe deficiency, experience neurological symptoms such as muscle weakness and numbness. 

 Other B vitamins, such as folic acid (B9), cobalamin (B12,) along with B5 and B6, contribute to our red blood cell production (Groff & Gropper, 1999). When we have healthy red blood cells we are delivering oxygen efficiently, keeping our brain, muscles and nervous system happy.

As of late there are a lot of questions as to whether or not B vitamins are effective in helping those experiencing cognitive decline or neurodegeneration. Several forms of B vitamins have shown to be protective for the brain and beneficial in repairing damaged nerves (Wu & Ren, 2006) (Nishimoto, et al. 2015). Methylcobalamin, the methylated form of B12, has been shown to be helpful after nerve injury by assisting to rebuild myelin. This improves speed and delivery of signalling through the nerve (Nishimoto, et al., 2015). Another B vitamin that has been shown to be neuroprotective is Benfotiamine, a more bioavailable form of B1. Benfotiamine has been suggested to help decrease symptoms of diabetic retina and nervous system damage caused by excess blood sugar which, if left unmanaged, can result in vision impairment and loss of sensation (Wu & Ren, 2006).  We understand that B vitamins have a role in supporting nervous system function as well as providing some protection from damage; thus, it would be helpful to investigate whether or not these energy boosting vitamins can be useful in slowing cognitive decline.

 Folate and Vitamin B12 in patients diagnosed with Alzheimer’s disease.

One approach to studying cognitive decline has been to investigate non-genetic risk factors that are believed to be associated with developing Alzheimer’s disease (AD). One of these risk factors is high blood levels of the amino acid homocysteine (Aisen, et al., 2008). When homocysteine is significantly elevated in our body it results in physiological stress that can increase inflammation, as well as damage our cardiac and nervous systems. Folate and B12 are known to assist in the removal of homocysteine from the blood and coincidentally these vitamins have been found to be low in individuals diagnosed with AD. In one study, a high-dose B vitamin treatment including folic acid, B6 and B12 slowed shrinkage of whole brain volume over two years compared to placebo (Douaud, et al., 2013). It is important to note that not all cases of AD feature elevated homocysteine levels and that studies that have looked at the combination of Folate, B12, and B6 have not been shown to slow cognitive decline in those with normal homocysteine levels (Aisen, et al., 2008).

Omega-3 fatty acids in combination with B vitamins

One retrospective study looked at the use of omega-3 fatty acids with B6, B12, and folate in elderly individuals over the age of 70 with mild cognitive impairment (Jerneren, et al., 2015). It is interesting to note that B vitamin intervention was only found to be beneficial in those with high baseline omega-3 levels, slowing brain atrophy by 40% compared with the placebo group. The researchers also acknowledged that AD patients with high homocysteine levels were less likely to respond to B vitamin intervention if the individual’s omega-3 fatty acid levels were low.

It appears as though an individual’s use of omega-3 fatty acids prior to AD development may augment the effect of B vitamins in slowing cognitive decline and brain atrophy. Additional research is warranted, and with larger treatment groups, in orde r to begin to understand the lifestyle factors that may contribute to the progression of cognitive decline. While B vitamins may help slow decline it is important to point out that the goal should be to reduce homocysteine levels earlier in life to control inflammation, and reduce the risk factors that are within our control.

Works Cited

Aisen, P. S., Schneider, L. S., Sano, M., Diaz-Arrastia, R., van Dyck, C. H., Weiner, M. F., et al. (2008, October 15). High-dose B vitamin supplementation and cognitive decline in Alzheimer Disease a randomized control trial. JAMA, 1774-1783.

Douaud, g., Refsum, H., de Jager, C. A., Jacoby, R., Nichols, T. E., Smith, S. M., et al. (2013, June 4). Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment. PNAS, 110(23), 9523-9528.

Groff, J. L., & Gropper, S. S. (1999). The Water-Soluble Vitamins. In J. L. Groff, & S. S. Gropper, Advanced Nutrition and Human Metabolism (pp. 245-303). Wadsworth Thomson Learning.

Jerneren, F., Elshorbagy, A. K., Oulhaj, A., Smith, S. M., Refsum, H., Smith, et al. (2015). Brain atrophy in cognitively impaired elderly: the importance of long chain w-3 fatty acids and B vitamin status in a randomized controlled trial. The Americal Journal of Clinical Nutrition, 102(1), 215-221.

Nishimoto, S., Tanaka, H., Okamoto, M., Okada, K., Murase, T., & yoshikawa. (2015). Methylcobalamin promotes the differentiation of schwann cells and remyelination in lysophosphatidylcholine-induced demyelination of the rat sciatic nerve. Frontiers in Cellular Neuroscience, 9(298), 1-13.

Wu, S., & Ren, J. (2006). Benfotiamine alleviates diabetes-induced cerebral oxidative damage independent of advanced glycation end-product, tissue factor and TNF-a. Neuroscience Letters, 394(2), 158-162.