Summary: Even when within the ordinary selection, lower levels of vitamin B12 may help to cognitive decline, according to a new study. Despite meeting existing nutritional needs, scientists discovered that older people with lower physiologically active B12 had slower cognitive control and more white problem lesions.
These results suggest that useful biomarkers may need to be changed in order to replace the use of set thresholds in the description of B12 deficiency. Experts advise further investigation and possible treatment for older adults to stop cognitive decline.
Major Information
- Lower Active B12 levels in older adults performed worse on mental tests that evaluated processing speed and response times.
- Lesions in the head: MRI scans revealed more light issue lesions in individuals with lower B12, which may increase the risk of dementia and strokes.
- Revisiting B12 Guidelines: Analysts suggest present B12 recommendations may be inappropriate for preventing neural decline and permit readjustment.
Origin: UCSF
Even if you are older, it might not be enough to meet the minimum requirement for supplement B12, which is needed to produce DNA, red blood cells, and muscle tissue. It may even put you at risk for cerebral damage.
A new research, led by UC San Francisco experts, found that older, healthy individuals, with lower amounts of B12, but still in the normal range, showed evidence of neurological and mental deficiency.
Video Credit: Neuroscience News
These levels were linked to higher B12 levels, higher mental light matter levels, higher brain light matter damage, and test scores that suggested slower mental and physical processing speeds.
The research published in , Annals of Neurology , on Feb. 10.
The experts led by top author , Ari J. Green, MD, of the UCSF Departments of Neurology and Ophthalmology and the , Weill Institute for Neurosciences, said that the findings raise concerns about recent B12 requirements and advise the comments need updating.  ,
Prior studies that identified good B12 levels “may have missed simple efficient manifestations of high or low levels that may influence people without causing explicit symptoms,” said Green, noting that obvious deficiencies of the vitamin are frequently linked to a type of anemia.
” Revisiting the definition of B12 deficiency to incorporate functional biomarkers could facilitate earlier intervention and the reduction 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 UCSF study called Brain Aging Network for Cognitive Health ( BRANCH).  ,
Their blood B12 amounts averaged 414.8 pmol/L, well above the U. S. minimum of 148 pmol/L. Researchers examined the biologically active component of B12, which provides a more accurate gauge of the vitamin’s potency when age, sex, education, and cardiovascular risks were adjusted for.
In cognitive testing, participants with lower active B12 were found to have slower processing speed, relating to subtle cognitive decline. The older you get, the more it impacts you. Additionally, they revealed significant delays in responding to visual stimuli, which suggests slower brain conductivity and slower visual processing speeds.  ,
A higher volume of lesions in the participants ‘ white matter was discovered by MRIs, which may be linked to cognitive decline, dementia, or a stroke.  ,
Although the study’s volunteers were older adults who may have a particular vulnerability to lower B12 levels, co-first author Alexandra Beaudry-Richard, MSc, claimed that these lower levels “may have an impact on cognition in a much larger proportion of the population than we realize”
At the University of Ottawa’s Department of Microbiology and Department of Microbiology and Immunology, Beaudry-Richard is currently working toward the end of her doctorate in research and medicine.
” Comedical professionals should take into account 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. No potential conflicts of interest should be reported.
About this research on cognitive decline
Author: Suzanne Leigh
Source: UCSF
Contact: Suzanne Leigh – UCSF
Image: The image is credited to Neuroscience News
Original Research: Open access.
Ari J.” Central Nervous System Injury in older adults is correlated with vitamin B12 levels in both functional and structural biomarkers..” Green et al. Annals of Neurology
Abstract
Central Nervous System Injury in older adults is correlated with vitamin B12 levels in both functional and structural biomarkers.
Objective
Vitamin B12 ( B12 ) plays a critical role in fatty- and amino-acid metabolism and nucleotide synthesis. The precise threshold for adequacy remains ambiguous in terms of functional impairment and injury evidence, despite the well-known link between B12 deficiency and neurological dysfunction. In a cohort of healthy older adults, the goal was to find out if B12 levels within the current normal range have any bearing on the presence of observable evidence of neurological dysfunction or injury.
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 ). To assess neurological status, we performed multiplexed visual evoked potential testing, processing speed testing, and magnetic resonance imaging. 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 suggest that we should revisit how to establish appropriate nutritional recommendations and challenge our current understanding of optimal serum B12 levels.
