To Nicola re: Co Q10 and methylation
Hi, Nicola.
I'll offer a few comments in response to your experience and your question, for what they are worth.
First, the synthesis of Co Q10 in the body requires methylation. In CFS, people commonly are found to have partial blocks in their methylation cycle, using the Vitamin Diagnostics methylation pathways panel. In the GD-MCB hypothesis, the reason for the deficit in Co Q10 in CFS is the partial methylation cycle block. This also accounts for deficits in a variety of other important substances, including carnitine, choline, and creatine, and many other effects as well.
So I think that your observation that by supplementing B12, you no longer needed to supplement Co Q10, can be explained by improvement in the operation of the methylation cycle. When you dropped your B12 intake, you may have lowered your methylation capacity and also lowered the rate of production of Co Q-10.
The main role of Co Q10 in the cells of the body is in coupling the Krebs cycle to the respiratory chain, which is responsible for most of the ATP production in cells.
Co Q10 is particularly important in the heart muscle cells, because of their high, continuous requirement for ATP to power the contractions of the heart muscle. Dr. Cheney has reported finding diastolic dysfunction in the hearts of most (or maybe all) of his CFS patients. The cause of diastolic dysfunction is too low a rate of production of ATP, which prevents the heart muscle from relaxing fast enough to allow enough blood to enter the left ventricle (the main chamber of the heart) in the time before the next contraction. This lowers the cardiac output, and affects the body in general.
The following is also part of the GD-MCB hypothesis: Improving the operation of the methylation cycle in a person in whom it has been partially blocked for a long time will cause the immune system and the detox system to come back into more normal operation, and begin working on the backlogs of infections and toxins that have accumulated during this time. The result is mobilization of toxins into the bloodstream, which bathes all the cells of the body. This can result in a variety of unpleasant symptoms until these backlogs are cleared.
With regard to the POTS (orthostatic tachycardia), in the GD-MCB hypothesis, this is caused in CFS by a combination of low cardiac output and HPA axis dysfunction.
The low cardiac output in turn results from the diastolic dysfunction, and also from a low total blood volume, which decreases the venous return to the heart (the rate at which blood is returned to the heart from the body). The low total blood volume in turn is caused by diabetes insipidus (not the same as diabetes mellitus, which involves blood sugar and insulin). the diabetes mellitus is caused by insufficient rate of production of antidiuretic hormone by the hypothalamus. This causes the kidneys to dump too much water into the urine, and though the person is thirsty and drinks a lot of fluids, they don't keep up with this loss, so the total blood volume goes below normal.
The HPA axis dysfunction is caused by insufficient production of ACTH by the pituitary, which causes the adrenals to secrete insufficient amounts of cortisol. The adrenals normally control the circulatory system, and adjust the distribution of blood flow when a person stands up. When cortisol is insufficient, epinephrine steps in to rescue the situation. That's what causes the tachycardia. It's an effort to maintain sufficient blood flow to the brain in the presence of low total cardiac output and poor control of distribution, which can cause blood pooling in the legs.
I hope this is helpful.
Rich
