Summary: New research shows that low levels of vitamin B12 can contribute to cognitive decline, even within normal ranges. The researchers found that older adults with low biologically active B12 meet current nutritional requirements, but still have slower cognitive processing and slower white matter lesions.
These findings suggest that the definition of B12 deficiency may require modification to incorporate functional biomarkers rather than relying on fixed thresholds. Researchers recommend further research and potential supplementation in older adults to prevent cognitive impairment.
Important facts
Subtle cognitive decline: Elderly people with low active B12 levels had poor performance on cognitive tests that measured processing speed and response time. Brain lesions: An increase in white matter lesions in participants with low B12 was revealed. Guidelines: Researchers suggest that current B12 recommendations may be insufficient to prevent neurological decline and guarantee reassessment.
Source: UCSF
Meeting the minimum requirements for vitamin B12 required to make DNA, red blood cells, and nerve tissue may not be enough in practice. It may even put you at risk of cognitive impairment.
A new study led by researchers at UC San Francisco found that older healthy volunteers with low B12 concentrations but still in the normal range showed signs of neurological and cognitive deficiency.
Video Credit: Neuroscience News
These levels are associated with reduced cognitive and visual processing speeds compared to those with higher B12, with nerve fibers that allow for communication between brain white matter, i.e. brain regions. It was associated with more damage.
The study was published in the Annals of Neurology on February 10th.
Researchers led by UCSF School of Neurology and Ophthalmology and Senior Author Ari J. Green, MD, of Weill Institute for Neurosciences, raised questions about current B12 requirements and suggested that recommendations need to be updated. He said that.
“Previous studies that defined healthy doses of B12 may have missed high or low levels of subtle functional symptoms that could affect people without causing obvious symptoms.” said that clear defects in vitamins are generally related to types of anemia.
“Reviewing the definition of B12 deficiency to incorporate functional biomarkers could lead to previous interventions and prevention of cognitive decline.”
Low B12 correlates with slow processing speeds and brain lesions
In this study, the researchers enrolled 231 healthy participants without dementia or mild cognitive impairment. The average age was 71 years old. They were recruited through the Brain Aging Network for Cognitive Health (Branch) Research at UCSF.
Their blood B12 averages 414.8 pmol/L, well above the minimum of 148 pmol/L. Adjusting for factors such as age, gender, education, and cardiovascular risk, researchers looked at the biologically active ingredients of B12. This provides a more accurate measure of the amount of vitamins your body has access to.
Cognitive tests showed that participants with low active B12 had slower processing speeds associated with subtle cognitive decline. The effects were amplified by age. They also show significant delays in response to visual stimuli, indicating slow visual processing speeds and slow general brain conductivity.
MRI revealed more lesions in the white matter of participants. This may be related to cognitive decline, dementia, or stroke.
While the research volunteers are older and may have certain vulnerabilities to lower levels of B12, co-author Alexandra Beaudry-Richard, MSC, said that these lower levels were previously thought to be “previously thought.” He said it could have a more cognitive impact than we had, and it could have an impact on a much larger population than we were aware of.”
Beaudry-Richard currently holds a PhD in Research and Medicine from the Department of Neurology and the Department of Microbiology and Immunology at the University of Ottawa.
“In addition to redefining B12 deficiency, clinicians should consider supplementing older patients with neurological symptoms, even if their levels are within normal range,” she said.
“In the end, we need to invest in more research into the underlying biology of B12 deficiency, as it could be a preventable cause of cognitive decline.”
Author: Co-first authors are Ahmed Abdelhak, MD, and PhD of UCSF Neurologies and Weill Institute for Neurosciences. For a complete list of authors, see this study.
Funding and Disclosure: Westridge Foundation and the Canadian Institute of Health. There are no conflicts of interest to report.
About this news on this cognitive decline research.
Author: Suzanne Lee
Source: UCSF
Contact: Suzanne Leigh – UCSF
Image: Image credited to Neuroscience News
Original research: Open access.
“Vitamin B12 levels are associated with functional and structural biomarkers of central nervous system damage in elderly people,” Ari J. Green et al. Chronicles of Neurology
Abstract
Association with vitamin B12 levels with functional and structural biomarkers of central nervous system damage in elderly people.
Objective
Vitamin B12 (B12) plays an important role in fat and amino acid metabolism and nucleotide synthesis. The association between B12 deficiency and neurological dysfunction is well known, but the exact threshold of validity remains undefined in terms of dysfunction and evidence of injury. The aim was to assess whether B12 levels within the current normal range in a cohort of healthy elderly people are associated with measurable evidence of neurological damage or dysfunction.
method
231 healthy elderly volunteers (median age 71.2 years old) were enrolled to have a median B12 blood concentration of 414.8 pmol/L (measured by automated chemiluminescence assay). Multifocal visual evoked potential tests, processing speed tests, and magnetic resonance imaging were performed to assess neurological conditions. Additionally, serum biomarkers of neural axis disorders, astrocyte involvement, and amyloid pathology were measured.
result
Low (log-transformed) B12, in particular, decreased holotranscobalamin, caused by visually induced latency delay (estimated = -0.04; p = 0.023), processing speed disorders (age-dependent methods; standardized β = -2.39; p = 0.006) and massive white matter superstrength of MRI (β=−0.21; P=0.039). Surprisingly, high levels of holohaptocholine (a biologically inactive percentage of B12) were correlated with serum levels of Tau, a biomarker of neurodegeneration (β=0.22, P=0.015).
interpretation
Healthy elderly subjects exhibit neurological changes at both ends of the measurable “normal” B12 spectrum. These findings challenge the current understanding of optimal serum B12 levels and propose to reexamine how appropriate nutritional recommendations can be established.
