Vitamin B12 Guidelines Fall Short of Neuroprotective Effects: Study

For older adults, the low end of the current accepted normal range for vitamin B12 blood levels may not be enough to offer neuroprotective effects seen with higher levels, according to a new study published in Annals of Neurology. The findings, according to the authors, suggest that people may be told their B12 status is fine, even though their brains are showing early signs of strain.

In the study, the authors looked at adults who didn’t have dementia or mild cognitive impairment with an average age of 71; lower levels of active B12 in this group were linked to slower thinking, slower visual processing, and more visible injury to the brain’s white matter.

The minimum threshold used to define vitamin B12 deficiency may not be serving older adults, according to the authors, as the lower end of the accepted normal range may be associated with “measurable evidence of neurological injury or dysfunction.”

Early Signs of Cognitive Decline

Researchers enrolled 231 healthy participants through the Brain Aging Network for Cognitive Health (BrANCH) study at UCSF. At baseline, no participants had dementia or mild cognitive impairment. They were administered a battery of cognitive tests and received MRI scans to assess their neurological status.

The average blood B12 level was 414.8 pmol/L, well above the minimum cutoff of 148 pmol/L, which is used to define deficiency. Instead of relying on total B12, the researchers looked at the biologically active form of the vitamin (methylcobalamin) to account for the amounts of the vitamin actually being used by the body.  

Participants with lower active B12 showed impaired processing speed and visual latency delay, per the cognitive tests. MRI scans revealed that participants with lower active B12 had a higher volume of white matter lesions.

“Current parameters for defining adequate B12 levels may be inappropriate when considering neurophysiological, neuropsychological, serological, and neuroradiological outcomes,” the authors concluded. It’s especially important to consider how much vitamin B12 is being metabolized into methylcobalamin, they noted. Importantly, this study captured a “precursor” stage of low vitamin B12 levels, without diagnosable neurological disorders, where microstructural changes were already present and impairing neurological function.