BO2 - Brain Fog in a Bottle? Exploring High Vitamin B12 and Neuronal Stress
Abstract
Vitamin B12 is an essential nutrient in our diets since it is a necessary cofactor for an enzyme, Methionine Synthase, to function at its maximum capacity. Methioinine synthase function is necessary to convert folic acid to a one-carbon methyl group that can be added to DNA, RNA, and histone proteins to regulate gene expression. Many studies have indicated the dangers of low serum Vitamin B12 in humans, but few studies have been done to determine the possible negative outcomes of high serum Vitamin B12 in humans. Human serum Vitamin B12 levels should be 200-900pg/mL (which has an average of 550pg/mL), while optimum levels are reported as 300-350pg/mL. Clinically, a higher serum Vitamin B12 level at around 2x the average “normal” Vitamin B12 level has been correlated with poor prognosis in cancer patients and higher incidence of new solid tumors, and it can indicate liver disease when at up to 10x the average “normal” Vitamin B12 level. Anecdotally, persons taking very high levels of Vitamin B12 have reported mild cognitive impairment or “brain fog”, and preliminary data indicates a clinical correlation between mild cognitive impairment and higher serum Vitamin B12. Our prior studies in the lab have focused a human neuronal model in culture (SH-SY5Y cells), and we have found that a 2x Vitamin B12 treatment increases oxidative stress, increased generation of free radicals, and a loss of ubiquitination, which theoretically leaves old and misfolded proteins in the cell. Because our oxidative stress and ubiquitination data centered around metabolic genes’ expression levels, we sought this year to determine if metabolism is affected in these human neuronal cells that are exposed to 2x Vitamin B12 in culture. We performed mitochondrial stress, glycolytic stress, ATP production rate, and glycolytic rate assays using the Seahorse metabolic analyzer. Our data indicate no change to glycolysis but did indicate mitochondrial stress. Our findings highlight a need to further investigate the negative consequences of high Vitamin B12 in humans since it could impact how practitioners view this diagnosis.
BO2 - Brain Fog in a Bottle? Exploring High Vitamin B12 and Neuronal Stress
CASB 101
Vitamin B12 is an essential nutrient in our diets since it is a necessary cofactor for an enzyme, Methionine Synthase, to function at its maximum capacity. Methioinine synthase function is necessary to convert folic acid to a one-carbon methyl group that can be added to DNA, RNA, and histone proteins to regulate gene expression. Many studies have indicated the dangers of low serum Vitamin B12 in humans, but few studies have been done to determine the possible negative outcomes of high serum Vitamin B12 in humans. Human serum Vitamin B12 levels should be 200-900pg/mL (which has an average of 550pg/mL), while optimum levels are reported as 300-350pg/mL. Clinically, a higher serum Vitamin B12 level at around 2x the average “normal” Vitamin B12 level has been correlated with poor prognosis in cancer patients and higher incidence of new solid tumors, and it can indicate liver disease when at up to 10x the average “normal” Vitamin B12 level. Anecdotally, persons taking very high levels of Vitamin B12 have reported mild cognitive impairment or “brain fog”, and preliminary data indicates a clinical correlation between mild cognitive impairment and higher serum Vitamin B12. Our prior studies in the lab have focused a human neuronal model in culture (SH-SY5Y cells), and we have found that a 2x Vitamin B12 treatment increases oxidative stress, increased generation of free radicals, and a loss of ubiquitination, which theoretically leaves old and misfolded proteins in the cell. Because our oxidative stress and ubiquitination data centered around metabolic genes’ expression levels, we sought this year to determine if metabolism is affected in these human neuronal cells that are exposed to 2x Vitamin B12 in culture. We performed mitochondrial stress, glycolytic stress, ATP production rate, and glycolytic rate assays using the Seahorse metabolic analyzer. Our data indicate no change to glycolysis but did indicate mitochondrial stress. Our findings highlight a need to further investigate the negative consequences of high Vitamin B12 in humans since it could impact how practitioners view this diagnosis.