Riboflavin — also known as vitamin B2 — is crucial to the formation of myelin, a fatty white substance that surrounds the axon of certain nerve cells with an electrically insulating layer and is necessary for the nervous system to function properly.
MS, on the other hand, is an inflammatory demyelinating disease of the central nervous system. Because of this, riboflavin deficiency is considered a risk factor in MS.
Based on this information, researchers from several Iranian universities, as well as from Western Sydney University, conducted a systematic review of previous papers on the effects of riboflavin on MS patients.
They included human and animal clinical trials and case-control and experimental studies from 1976 to 2017 found on four main databases.
They found that in experimental studies, riboflavin deficiency was shown to trigger neurological abnormalities associated with peripheral neuropathies, such as demyelinating neuropathy.
In RCTs and case-control studies where MS patients had been supplemented with riboflavin or given a higher dietary dose of the vitamin, patients displayed improvements in neurological motor function.
In addition, riboflavin was found to promote protein and gene levels of brain-derived neurotrophic factor (BDNF) in the central nervous system in an animal model of MS, making BDNF a possible mediator for riboflavin’s positive impact on neurological motor disability.
Riboflavin is also a co-factor of the enzyme xanthine oxidase, which generates reactive oxygen species (ROS). As such, its deficiency worsens copper-induced low uric acid levels, which leads to myelin degeneration.
The researchers further wrote: "The vitamin additionally plays a significant role in the normal functioning of glutathione reductase as an antioxidant enzyme, and conditions of riboflavin deficiency lead to oxidative damage."
They added that while studies so far generally support riboflavin's effects against MS and that it might help alleviate the impact of MS-induced neurological impairment, "further observational and interventional studies on human populations are warranted to validate the effects of riboflavin".
In conclusion, the researchers stated: "The mechanism by which riboflavin protects the body against demyelination possibly involves neurotrophins, especially BDNF, a crucial agent for neuronal maturation and protection.
"Since the majority of research in this area to date is limited to experimental studies, further interventional studies on human populations are required to establish the effects of riboflavin."
Source: Iranian Journal of Medical Sciences
"Update on riboflavin and multiple sclerosis: a systematic review"
Authors: Mahshid Naghashpour, et al.