“Normal” vitamin B12 levels may not prevent brain decline

Study -Letters accepted vitamin B12 levels, which revealed hidden neurological risks, even within the ‘normal’ reach.

Study: Vitamin B12 -levels Association with functional and structural biomarkers of injury in the central nervous system in older adults. Image Credit: Lightspring / Shutterstock.com

A recent study published in the Annals of Neurology Uses a multimodal test approach to identify associations between B12 levels that are currently accepted as normal and markers of neurological injury or disorders.

Vitamin B12 -deficit

Vitamin B12, which is also known as cobalamin, is an essential vitamin in the diet that can be obtained from the consumption of animal products, certain dry fruit, food fermentation and reinforced food. Vitamin B12 deficiency can lead to blood cell abnormalities such as megaloblastic anemia and dysfunction of the neurological system, including subacute combined degeneration of the spinal cord (SACD).

Some symptoms associated with SACD are sensory ataxia, paraesthesia and weakness. Previous pathological analyzes indicate that SACD arises as a result of degeneration of the myelin sheath, which ultimately leads to the destruction and vacuolization of the white matter (WM) of the spinal cord.

B12 deficiency is also associated with cognitive impairment, memory loss, dementia and psychosis. However, vitamin B supplementation has been shown that it reduces the speed of brain atrophy in older people with mild cognitive disorders (MCI).

In the United States, the B12 deficiency is defined as a total blood level of less than 148 pmol/l, which are three standard deviations among the population average. Due to a lack of agreement on which blood levels form a B12 deficiency, clinical characteristics are often considered a better indication for supplementation.

B12 absorbed from the gastrointestinal tract is bound by transport proteins in the blood, including haptocorrin (HC) and transcobalamine (TC). The B12-TC complex (Holo-TC) is the only bioactive form of this vitamin, because B12 is bound to HC (HOLO-HC) not available for cell intake and is considered inactive.

About the study

Visual called potentials (VEP) offer a more sensitive and non-invasive method to identify early changes in the myeline function in the visual path. The current study used multifocal VEP (MFVEP) to assess the impact of low B12 on neurological health.

A total of 231 healthy people with a median age of 71 years who were part of the Brain Aging Network for Cognitive Health (branch) at the University of California, San Francisco (UCSF) memory and the aging center were included in the study. In addition to B12 measurements, all participants in the study were tested annually for neurological function, cognitive performance and magnetic resonance formation (MRI) to detect signs of inflammation, axonal damage or amyloid-related disease.

Study findings

The study cohort had a median blood B12 concentration of 415 pmol/l, with Holo-TC and Holo-HC Mediane values ​​of 93 and 298 pmol/l respectively. Vitamin B12 levels were stratified in above and below the geometric average value of 408 pmol/l.

To this end, low levels of B12, in particular Holo-TC, were associated with neurological dysfunction. At low B12 levels, MFVEP was 0.04 slower, indicating a slower conduction of nerve impulses in the brain.

Lower Holo-TC was inversely proportional to latency, which showed that insufficient B12-biological availability was responsible for greater latency of nerve conduction. Low vitamin B12 levels were associated with a reduced spatial processing speed, which demonstrates that brain dysfunction correlated with reduced total B12 and Holo-TC, but not Holo-HC.

This negative association was dependent on the age, perhaps because older people at a younger age are at a greater risk of low biological available B12 or suboptimal cognitive test performance.

Increased Holo-HC correlated with Serum Tau protein and Ubiquitine C-Terminal Hydrolase L1 (UCH-L1) levels. B12 prevents the formation of the Tau fibril, which precedes the formation of neurofibrillary tangles (NFT) in Alzheimer’s dementia (AD). Thus high levels of non-bio-available B12 were predictive for increased neurodegeneration markers.

Low B12 levels were associated with higher WMH volumes, despite the fact that all participants have levels within the currently accepted limits of Normaal. No correlation was observed with total B12; Lower Holo-TC levels, however, were associated with higher WMH load.

Implications

With low B12 levels, especially organic available B12, white dust injury occurs in the spinal cord. The injury mechanism remains unclear; However, it may be due to high homocysteine ​​levels secondary to B12.

B12 supplementation for hematological symptoms often leads to their resolution; However, this therapeutic approach is usually not effective for reducing neurological symptoms associated with B12 deficiency. Thus subtle neurological dysfunction can continue to exist, despite normal B12 levels of blood.

In general, the research results emphasize the crucial need to determine optimum B12 levels and requires a broader reconsideration of food guidelines.