Why Biotin May Help Multiple Sclerosis, An Update
Previous research has shown that biotin may be a potentially important treatment for progressive multiple sclerosis. In this new review, a team of experts have hypothesized two complementary reasons why this natural approach may work.
Review of results from two earlier studies
In two studies whose results were reported earlier in 2015, researchers used a high-dose biotin drug (MD1003) that delivered 100 to 600 milligrams (mg) of the vitamin or a placebo to the participants, all of whom had been diagnosed with progressive multiple sclerosis. The usual recommended daily dose of biotin is much less, a mere 30 to 100 micrograms (mcg) daily.
In the first pilot, uncontrolled study, 23 individuals were given 100 to 600 mg daily for a mean of 9.2 months. Overall:
- EDSS scores improved significantly in 22 percent of the patients
- There were marked improvements in various signs and symptoms, including fatigue, swallowing problems, sensory signs, gait problems, dysarthria (speech difficulties), visual acuity, Uhthoff’s phenomenon, and motor coordination
- Eighty-nine percent of patients with prominent spinal cord involvement experience improvement
- More than 90 percent (21 of 23) demonstrated some level of clinical improvement, including a reduction in MS-related disability
In the second, larger study (154 participants), 103 patients took 300 mg biotin (as the drug MD1003) and 51 received placebo daily for 48 weeks. At nine and 12 months, a “significant proportion” of individuals who took biotin achieved the primary endpoint, which was at least a 1 point reduction in EDSS for those with a score of 5.5 or less or a 0.5 point reduction for those with a 6.0 score or higher or a 20 percent improvement in a timed walk. None of those in the placebo group reached the primary endpoint.
Note: Data from a 12-month extension of the larger study are expected in January 2016. During this extension, all of the participants took high-dose biotin.
New information on biotin for MS
In the new review, the authors suggest that high-dose biotin offers a therapeutic effect via two mechanisms:
- By promoting remyelination through enhanced formation of myelin by the oligodendrocytes, which are special cells involved in the production of myelin; and
- Enhancing production of brain energy, which in turn protects demyelinated axons (the threadlike portion of a nerve cells which serves as a pathway for nerve impulses to travel from one cell to another) from becoming damaged and destroyed
More specifically, the investigators hypothesize that high doses of biotin trigger the formation of myelin in oligodendrocytes through its role as a cofactor for ACC (acetyl-CoA carboxylase). There’s a high level of ACC activity in oligodendrocytes in the brain.
ACC is necessary for the synthesis of malonyl-CoA, which is a critical ingredient for making fatty acids. Experts believe that high doses of biotin may lead to increased production of fatty acids necessary for myelin repair.
The second way high-dose biotin may help involves how the vitamin targets cellular energy levels. According to the authors, there is evidence to suggest that “cellular energy deprivation secondary to demyelination is responsible for the progressive irreversible neuronal degeneration” associated with progressive multiple sclerosis.
The explanation of this process is complex, but essentially biotin boosts production of ATP (adenosine triphosphate, a high-energy molecule that stores energy for life) in axonal mitochondria (energy “organs” in cells). Biotin is a co-enzyme for three enzymes expressed in neurons and their activity ultimately leads to key factors in a cycle that produces ATP. Thus the scientists suggest that “high doses of biotin may result in increased ATP production in demyelinating neurons.”
More high-dose biotin studies
There’s more good news: three multicenter phase III placebo-controlled trials of high-dose biotin in individuals with progressive multiple sclerosis are currently underway. Completion dates are 2016.
Each of the three studies focuses on a different set of patients; one involves individuals with spinal cord loss, another with chronic visual loss following optic neuritis, and the third with adrenomyeloneuropathy (AMN).
The use of biotin for multiple sclerosis treatment appears to be an exciting and promising approach that definitely deserves to be monitored carefully. Anyone who is interested in taking biotin should discuss this possibility with a knowledgeable healthcare provider.
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