Summary: Even when within the normal range, lower levels of vitamin B12 may contribute to cognitive decline, according to a new study. Researchers found that older adults with lower biologically active B12 had slower cognitive processing and more white matter lesions, despite meeting current nutritional requirements.
These findings suggest that the definition of B12 deficiency may need revision to incorporate functional biomarkers rather than relying on fixed thresholds. Researchers recommend further study and potential supplementation for older adults to prevent cognitive impairment.
Key Facts
- Subtle Cognitive Decline: Older adults with lower active B12 levels performed worse on cognitive tests measuring processing speed and reaction times.
- Brain Lesions: MRI scans revealed increased white matter lesions in participants with lower B12, which may contribute to dementia and stroke risk.
- Revisiting B12 Guidelines: Researchers suggest current B12 recommendations may be insufficient for preventing neurological decline and warrant reassessment.
Source: UCSF
Meeting the minimum requirement for vitamin B12, needed to make DNA, red blood cells and nerve tissue, may not actually be enough – particularly if you are older. It may even put you at risk for cognitive impairment.
A new study, led by UC San Francisco researchers, found that older, healthy volunteers, with lower concentrations of B12, but still in the normal range, showed signs of neurological and cognitive deficiency.
Video Credit: Neuroscience News
These levels were associated with more damage to the brain’s white matter – the nerve fibers that enable communication between areas of the brain – and test scores associated with slower cognitive and visual processing speeds, compared to those with higher B12.
The study published in Annals of Neurology on Feb. 10.
The researchers led by senior author Ari J. Green, MD, of the UCSF Departments of Neurology and Ophthalmology and the Weill Institute for Neurosciences, said that the results raise questions about current B12 requirements and suggest the recommendations need updating.
“Previous studies that defined healthy amounts of B12 may have missed subtle functional manifestations of high or low levels that can affect people without causing overt symptoms,” said Green, noting that clear deficiencies of the vitamin are commonly associated with a type of anemia.
“Revisiting the definition of B12 deficiency to incorporate functional biomarkers could lead to earlier intervention and prevention of cognitive decline.”
Lower B12 correlates with slower processing speeds, brain lesions
In the study, researchers enrolled 231 healthy participants without dementia or mild cognitive impairment, whose average age was 71. They were recruited through the Brain Aging Network for Cognitive Health (BrANCH) study at UCSF.
Their blood B12 amounts averaged 414.8 pmol/L, well above the U.S. minimum of 148 pmol/L. Adjusted for factors like age, sex, education and cardiovascular risks, researchers looked at the biologically active component of B12, which provides a more accurate measure of the amount of the vitamin that the body can utilize.
In cognitive testing, participants with lower active B12 were found to have slower processing speed, relating to subtle cognitive decline. Its impact was amplified by older age. They also showed significant delays responding to visual stimuli, indicating slower visual processing speeds and general slower brain conductivity.
MRIs revealed a higher volume of lesions in the participants’ white matter, which may be associated with cognitive decline, dementia or stroke.
While the study volunteers were older adults, who may have a specific vulnerability to lower levels of B12, co-first author Alexandra Beaudry-Richard, MSc, said that these lower levels could “impact cognition to a greater extent than what we previously thought, and may affect a much larger proportion of the population than we realize.”
Beaudry-Richard is currently completing her doctorate in research and medicine at the UCSF Department of Neurology and the Department of Microbiology and Immunology at the University of Ottawa.
“In addition to redefining B12 deficiency, clinicians should consider supplementation in older patients with neurological symptoms even if their levels are within normal limits,” she said.
“Ultimately, we need to invest in more research about the underlying biology of B12 insufficiency, since it may be a preventable cause of cognitive decline.”
Authors: Co-first author is Ahmed Abdelhak, MD, PhD, of the UCSF Department of Neurology and the Weill Institute for Neurosciences. For a full list of authors, please see the study.
Funding and Disclosures: Westridge Foundation and the Canadian Institutes of Health and Research. There are no conflicts of interest to report.
About this cognitive decline research news
Author: Suzanne Leigh
Source: UCSF
Contact: Suzanne Leigh – UCSF
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Vitamin B12 Levels Association with Functional and Structural Biomarkers of Central Nervous System Injury in Older Adults” by Ari J. Green et al. Annals of Neurology
Abstract
Vitamin B12 Levels Association with Functional and Structural Biomarkers of Central Nervous System Injury in Older Adults
Objective
Vitamin B12 (B12) plays a critical role in fatty- and amino-acid metabolism and nucleotide synthesis. While the association between B12 deficiency and neurological dysfunction is well-known, the exact threshold for adequacy remains undefined in terms of functional impairment and evidence of injury. The objective was to assess whether B12 levels within the current normal range in a cohort of healthy older adults may be associated with measurable evidence of neurological injury or dysfunction.
Methods
We enrolled 231 healthy elderly volunteers (median age 71.2 years old) with a median B12 blood concentration of 414.8 pmol/L (as measured by automated chemiluminescence assay). We performed multifocal visual evoked potential testing, processing speed testing, and magnetic resonance imaging to assess neurological status. Moreover, we measured serum biomarkers of neuroaxonal injury, astrocyte involvement, and amyloid pathology.
Results
Low (log-transformed) B12, especially decreased holo-transcobalamin, was associated with visual evoked potential latency delay (estimate = −0.04; p = 0.023), processing speed impairment (in an age-dependent manner; standardized β = −2.39; p = 0.006), and larger volumes of white matter hyperintensities on MRI (β = −0.21; p = 0.039). Remarkably, high levels of holo-haptocorrin (biologically inactive fraction of B12) correlated with serum levels of Tau, a biomarker of neurodegeneration (β = 0.22, p = 0.015).
Interpretation
Healthy older subjects exhibit neurological changes at both ends of the measurable “normal” B12 spectrum. These findings challenge our current understanding of optimal serum B12 levels and suggest revisiting how we establish appropriate nutritional recommendations.
