Hi, all.
As some of you know, I have become fairly sure that ME/CFS and autism are essentially the same disorder at the biochemical level. For a long time I have tried to understand what the link might be between ME/CFS and fibromyalgia. We know that many people who have one also have the other. Lately I've also been trying to understand why some people with ME/CFS also have EMH (electromagnetic hypersensitivity). And then there's multiple sclerosis, the cause of which is still not understood, but which is known to involve an autoimmune reaction and damage to the myelin on the nerves.
I'm starting to think that there might be a link between all of these disorders, involving a deficit in methylation, which in turn causes problems in repair of myelin, the fatty insulating material on nerve axons.
There are at least three substances in myelin that require methylation for their synthesis: myelin basic protein, phosphatidylcholine, and choline plasmalogen. There is good evidence in the published literature that a deficit in methylation will cause problems with maintaining the myelin.
Myelin is vital to the function of the nervous system. It serves as electrical insulation on the axons of the neurons. This prevents leakage of current and dissipation of nerve impulses (action potentials) and it also allows fast transmission of nerve impulses via the axons.
In ME/CFS, we now know that just as in autism, there is a deficit in methylation due to inhibition of the activity of methionine synthase in the methylation cycle. We also know that in ME/CFS the best documented brain-related features are slow processing speed and slow reaction time. These would be consistent with disrepair of myelin.
Perhaps fibromyalgia also results from myelin disrepair in at least some cases. It has been found that fibromyalgia involves an elevated sensitivity to stimuli within the central nervous system. It would seem that a myelin problem might account for this.
Recent work in MS has shown that treatment to improve methylation has produced improvement in some patients. What if the problem starts with a methylation deficit, followed by myelin degradation, and then the immune system responds to that, rather than being responsible for the initial insult to the myelin?
Some PWMEs/PWCs experience hypersensitivity to electromagnetic fields (EMH). I'm starting to believe that this may also be due to myelin damage, secondary to the methylation deficit. If the electrical insulation provided by myelin normally prevents loss of current from action potentials within the axons, it seems reasonable to me to suspect that myelin also normally protects the nerves from external currents. We can expect that environmental electromagnetic radiation is constantly generating currents in the human body, just as it does in receiving antennas. Perhaps when the myelin falls into disrepair because of the methylation deficit, it becomes electrically "leaky," and external currents can then enter the nervous system. I think that could account for the variety of neurologically related symptoms that people with EMH are reporting.
Anyway, this methylation deficit link to myelin damage looks to me as though it has the potential to explain several disorders, and if that's true, then treatment to support the methylation cycle and related pathways might have the potential to help other groups of sufferers beyond those who are already being helped.
Of course, a lot of work would need to be done to find out if this is true, but I think it is an avenue worth pursuing.
Best regards,
Rich
As some of you know, I have become fairly sure that ME/CFS and autism are essentially the same disorder at the biochemical level. For a long time I have tried to understand what the link might be between ME/CFS and fibromyalgia. We know that many people who have one also have the other. Lately I've also been trying to understand why some people with ME/CFS also have EMH (electromagnetic hypersensitivity). And then there's multiple sclerosis, the cause of which is still not understood, but which is known to involve an autoimmune reaction and damage to the myelin on the nerves.
I'm starting to think that there might be a link between all of these disorders, involving a deficit in methylation, which in turn causes problems in repair of myelin, the fatty insulating material on nerve axons.
There are at least three substances in myelin that require methylation for their synthesis: myelin basic protein, phosphatidylcholine, and choline plasmalogen. There is good evidence in the published literature that a deficit in methylation will cause problems with maintaining the myelin.
Myelin is vital to the function of the nervous system. It serves as electrical insulation on the axons of the neurons. This prevents leakage of current and dissipation of nerve impulses (action potentials) and it also allows fast transmission of nerve impulses via the axons.
In ME/CFS, we now know that just as in autism, there is a deficit in methylation due to inhibition of the activity of methionine synthase in the methylation cycle. We also know that in ME/CFS the best documented brain-related features are slow processing speed and slow reaction time. These would be consistent with disrepair of myelin.
Perhaps fibromyalgia also results from myelin disrepair in at least some cases. It has been found that fibromyalgia involves an elevated sensitivity to stimuli within the central nervous system. It would seem that a myelin problem might account for this.
Recent work in MS has shown that treatment to improve methylation has produced improvement in some patients. What if the problem starts with a methylation deficit, followed by myelin degradation, and then the immune system responds to that, rather than being responsible for the initial insult to the myelin?
Some PWMEs/PWCs experience hypersensitivity to electromagnetic fields (EMH). I'm starting to believe that this may also be due to myelin damage, secondary to the methylation deficit. If the electrical insulation provided by myelin normally prevents loss of current from action potentials within the axons, it seems reasonable to me to suspect that myelin also normally protects the nerves from external currents. We can expect that environmental electromagnetic radiation is constantly generating currents in the human body, just as it does in receiving antennas. Perhaps when the myelin falls into disrepair because of the methylation deficit, it becomes electrically "leaky," and external currents can then enter the nervous system. I think that could account for the variety of neurologically related symptoms that people with EMH are reporting.
Anyway, this methylation deficit link to myelin damage looks to me as though it has the potential to explain several disorders, and if that's true, then treatment to support the methylation cycle and related pathways might have the potential to help other groups of sufferers beyond those who are already being helped.
Of course, a lot of work would need to be done to find out if this is true, but I think it is an avenue worth pursuing.
Best regards,
Rich