Hi,
I just want to say up front that I'm sorry that the B12 book is scary. The whole brain damage subject came up in the context of a discussion of whether waiting to treat CFS until more is known would be a good idea. I was just trying to say that I understand this point of view, but at the same time, people should be aware that there might be a down side to waiting, also, because of the ongoing excitotoxicity in CFS. Having made this point, though, I want to suggest some things that I think might give you some hope.
Here's the picture on long-term effects in the brain in CFS as I see it:
We have evidence that there is excitotoxicity in both CFS and FM now. It is known that excitotoxicity can kill neurons. It is known that neurons are generally not replaced. There is published evidence from quantitative MRI studies that the gray matter volume decreases over time in CFS, FM, and most recently, in Gulf War Illnesses. The gray matter is composed of neurons. In view of these facts, I think it is reasonable to suspect that excitotoxicity is responsible for the decrease in gray matter volume in CFS. This last statement is, however, an unproven hypothesis.
In my opinion, it is also known now that there is a chronic partial methylation cycle block in many or most cases of CFS. This is based on my review of over 45 methylation panel results from PWCs at this time,
and it is also supported by urine organic acids tests, including MAP panel results, showing elevated methylmalonate and figlu in many PWCs. It is known that methylation is necessary to synthesize myelin basic
protein, which is important in the formation of myelin. It is known that myelin is important for promoting rapid transmission of nerve impulses. As was pointed out by Dr. Gudrun Lange in the brain session
at the IACFS meeting in January, 2007, the most well-founded observation on abnormality in brain function in CFS is a slowed processing speed. I think it is reasonable to suspect that the slowed processing speed in CFS is caused by defects in the myelin sheaths on nerve axons, and that these defects result from normal wear and tear,
which is not repaired because of insufficient synthesis of myelin basic protein, secondary to the partial methylation cycle block. This last statement is, again, an unproven hypothesis.
So what are the long term prospects for correcting these problems? We have no experience to look at here, so all I can do is to theorize based on what I believe is well established.
First, it would seem to be important to stop the excitotoxicity damage process. Dr. Yasko has suggested a number of supplements in her Phase I that may help with this. It seems that it would also be important to restore the methylation capacity. That's what Dr. Yasko's step 2 and the simplified treatment approach that I have suggested (with Trina's help) are intended to do. So I think these things are important first steps.
Then, it would seem to me that if there are living neurons that are lacking well-constructed myelin sheaths, this should be correctable. In the brain, the myelin sheaths are formed by cells called oligodendrocytes, which collapse and wrap themselves around the axons, sort of like a jelly roll. I suspect that the myelin basic proteins are used to fasten this "jelly roll" together. In the peripheral nerves (outside the brain), the same sort of thing is done by Schwann cells. Though I have not looked into this in detail, I suspect that these cells are capable of repairing the myelin if they have what they need to do it, including healthy methylation. Dr. Yasko's step 3 is aimed at helping remyelination.
Now, what about the decrease in the neuron population due to excitotoxicity? Again, we don't have much experience to go on, but I will just note that brain size has not been found to correlate well
with intelligence. As I understand it, it is not so much dependent on the total number of neurons, but on the degree to which they are interconnected, forming neural networks. So it would seem that to repair this kind of damage, there might be two possible courses of action. One would be to try to increase the interconnection of the remaining neurons, while the other might be to try to form new neurons. I'm not sure how the first could be done, but I would think that supplying the brain all the raw materials it is known to need, together with exercising the brain (such as by "brain teasers" or puzzles, or memory exercises) might help.
There are some particular supplements that are supposed to help brain function. I haven't looked into the details of them, but I can tell you that I have personally experimented with Cognitex, which is sold by the Life Extension Foundation. It has several ingredients, so it isn't possible to say which one or ones are producing effects, but I can say that I can tell a difference in how my brain works when I take this supplement. In particular, when I awaken in the morning, I can tell that my brain is more active, in terms of thoughts that pop up, than when I don't take it. Note that I am not recommending this supplement for CFS, because I don't know what its effects would be in CFS, but I
am just pointing out that there may be some possibilities in the supplements that are claimed to help the brain. People must proceed cautiously and under the care of a doctor if they are going to try such
supplements.
In regard to developing new neurons, Prof. Richard Deth has suggested to me that the reason neurons normally have long lifetimes and are not replaced is that removing and replacing neurons would break these
interconnections, on which memory and other brain functions depend. He shared with me a paper in which it is suggested that the redox potential in cells determines whether they will proliferate or not, and he suggested that the neurons normally operate at a more oxidizing redox potential than other cells that are periodically replaced, and
particularly at a more oxidizing potential than cancer cells, which proliferate out of control. So perhaps there might be a way to make the redox potential in the neurons somewhat more reducing (but not too much so!), and perhaps nerve growth factors might be another thing to look at. Note that I'm just speculating here, but I just want to note
that there might be some possibilities.
I guess that's all I have to say at this point, but I just want to urge you not to lose hope about your long-term brain function. Once the damage processes are stopped, it does seem that there are some possibilities that could be explored.
Best regards,
Rich
