Vitamin B12 Deficiency Mimics Symptoms of Multiple Sclerosis

[ad_1]

Recent research sheds light on a molecular link between B12 deficiency and multiple sclerosis, opening the door to the possibility of new ways to treat MS.

Multiple sclerosis (MS), especially in its early stages, shares overlapping symptoms with many other conditions. Unfortunately, this makes it easy to misdiagnose. One of these conditions, which is gaining attention in the medical community, is vitamin B12 deficiency.

Vitamin B12 deficiency is relatively common in the United States, affecting between 1.5 and 15 percent of the adult population, according to Cleveland Clinic. Older adults, those who follow a vegan or vegetarian diet, and those with medical conditions that hamper the absorption of B12 (also known as cobalamin) are most at risk of becoming deficient in B12. Certain diabetes and acid-lowering medications can also hinder the absorption of B12.
Since the body stores significant amounts of vitamin B12, “about 1 to 5 mg vitamin B12 (or about 1,000 to 2,000 times as much as the amount typically consumed in a day,” according to the National Institutes of Health, symptoms of a deficiency, which can be physical, neurological, or psychological, can be years in the making and easy to miss.

Multiple Sclerosis–Cause Unknown

Multiple sclerosis, on the other hand, is thought to be an autoimmune disorder in which the immune system attacks the central nervous system, damaging the protective myelin sheath that surrounds nerve fibers (a process known as demyelination). This damage results in scar tissue (sclerosis) around the nerve fibers, and disrupted communication between the brain and other parts of the body.

Researchers have suspected a connection between multiple sclerosis (MS) and vitamin B12 deficiency for decades, due to the similarity of neurological symptoms that are common to both conditions, such as muscle weakness, numbness, tingling, fatigue, and cognitive dysfunction. Also, being deficient in vitamin B12 is considered a risk factor for MS. However, studies attempting to confirm a direct relationship between the two have been inconsistent. There are numerous other possible causes of MS, such as viruses, autoimmune diseases, and environmental factors. The exact cause, or causes, of MS, are unknown.

Significantly, vitamin B12 deficiency can also cause demyelination. A review published in the April–June 2017 edition of Cell Journal indicates that “Vitamin B12 is an important factor in the generation of myelin shell components. Thus, deficiency of this vitamin can be a major cause for neurological diseases such as MS.” These findings have prompted some doctors to recommend that older patients with symptoms of neuropsychiatric disorders be tested for B12 in the early stages of diagnoses and treatment.

Link Between B12 Deficiency and MS

A recent study, conducted by researchers from Sanford Burnham Prebys, in collaboration with others, and published in the December 2023 issue of Cell Reports, sheds more light on the subject, revealing a molecular link between vitamin B12 deficiency and multiple sclerosis. The researchers suggest the possibility of new ways to treat MS via specific brain-targeting B12 formulations.

Sanford Burnham Prebys News reported that “Working with an animal model of MS as well as human post-mortem brains, the researchers found that [FDA-approved MS drug] fingolimod suppresses neuroinflammation by functionally and physically regulating B12 communication pathways, … This known process was newly identified for its interactions with fingolimod within astrocytes [glial cells in the brain].” Fingolimod’s role in enhancing the brain’s uptake of B12 is of particular interest.

Related Stories

Researchers Identify Potential Precursors to Multiple Sclerosis
The Essential Guide to Multiple Sclerosis: Symptoms, Causes, Treatments, and Natural Approaches
Senior study author Dr. Jerold Chun, professor and senior vice president of Neuroscience Drug Discovery at the Center for Genetic Disorders and Aging Research, and Yasuyuki Kihara, research associate professor of the Degenerative Diseases Program at Sanford Burnham Prebys and co-corresponding study author, told the Epoch Times:

“Our study provides a molecular link between MS and vitamin B12 in the brain. This link is accessed by the MS drug fingolimod (Gilenya)—known as an S1P receptor modulator—that was found to enhance vitamin B12 entry into brain cells (called astrocytes) while concomitantly reducing neuroinflammation. For MS patients, these results support treatments that could increase the brain’s vitamin B12 levels, especially if they are using S1P receptor modulator therapy.”

The study also noted the significant fact that levels of the B12 receptor CD320 are known to be reduced in MS plaques and that lower levels of CD320, or a dietary restriction of B12, worsened the disease course in animal models and reduced the effectiveness of fingolimod.

Previous research had already found that patients with chronic autoimmune diseases, including MS, seem to have an increased need for vitamin B12, and that, while not all patients with MS are deficient in B12, they do seem to be deficient at higher rates than that of the general population. These findings have led to a chicken-and-egg discussion of whether a vitamin B12 deficiency may cause MS, or whether the onset of MS may lead to a B12 deficiency.

B12 for the Brain

While vitamin B12 supplementation has generally been recommended only for those MS patients who have been found to be deficient, this study highlights the importance of B12 for the brain, even when blood levels appear within a normal range, and offers hope for the development of specific, brain-targeted B12 therapies.

Dr. Chun and Mr. Kihara note:

“B12 deficiency as determined by blood tests can share signs and symptoms associated with MS. However, blood tests can not directly assess the brain’s vitamin B12 levels. Our study implicates reduced B12 in the brains of MS patients as another variable that could be corrected by B12 supplementation—possibly not detected by blood levels—especially in conjunction with S1P receptor modulator therapies (we used fingolimod, known commercially as Gilenya), and this may be even more critical in patients with evidence of B12 deficiency as well as those with normal blood levels but who may have unappreciated B12 deficiency within the brain.

“While oral B12 supplementation may help, other routes (e.g., injection) should be considered; further research on brain B12 delivery into appropriate brain cells is needed.”

[ad_2]

Source link

Leave a Reply

Your email address will not be published. Required fields are marked *