All values are increased.
All but two values have come into the normal range. (Last October, before I started the nutritional protocol to support methylation, only two values were in the normal range.)
Until I figure out how to upload pictures of the files (I scanned them as .tif files and my upload attempts have failed), you can look at the spreadsheet with numbers crunched to show gains (losses) and percentage increases.
Compare VD Methyl Panels 1 and 2
Sometimes the ratio between two or more values is more important that the actual value on tests. This is the case for SAMe and SAH, listed on the test results as S-adenosylmethionine (RBC) and S-adenosylhomocysteine (RBC). SAMe acts as a methyl donor in the methylation cycle, giving its methyl group (CH3) to other molecules so they can function properly. SAH is what is left after SAMe gives away its methyl group, and too much SAH inhibits the production of SAMe in one of those nifty feedback cycles the body uses to maintain homeostasis. In the methylation cycle, SAH then gets converted to homocysteine, high levels of which have been associated with heart disease. Consequently, a ratio of SAMe to SAH above 4.5 is good.
On my first panel, my ratio was 5.72:1. Now, it has decreased to 5.67:1. This change took place before I started adding a small amount of SAMe (1/32 of a capsule) into my daily supplement regimen. Many questions arise: Is higher better, or is there an ideal ratio? Should I discontinue taking all supplemental SAMe or will taking a tiny amount support the optimization of the SAMe:SAH ratio?
Psst: If you know the answer, please write it in the comments section.
Another significant ratio is between oxidized and reduced glutathione. Reduced glutathione is available as an antioxidant. Oxidized glutathione has already been used. Since reduced glutathione binds toxic metals and protects B12, a high level of reduced to oxidized glutathione indicates improved B12 metabolism and lowering of toxic load. My first test was 11.78 to 1; my second test was 13.0 to 1.
So how does this translate into real life? Do I feel any better?
I've noticed over the past few weeks that a few issues have started to resolve. My blood sugar control is better. I can go longer between meals and no longer get that "I'm-going-to-die-if-I-don't-get-food-right-now" feeling (Okay, I did have it a little on Wednesday and Sunday this week after substitute teaching two yoga classes and using up a lot more energy than I am used to putting out).
The second area in which I've improved is electrolyte balance. For more than a year, on the advice of James Wilson, N.D. in Adrenal Fatigue , I've started my days with a quart of salt water. Like many PWC's, I've had frequent and prolific urination, which has led to dehydration, and contributed to orthostatic intolerance (also called dysautonomia) and waking at night. About a month ago, the water started to taste unpleasantly salty; consequently, I eliminated it from my protocol. I rarely have dry mouth and excessive urination now.
Rich Van Konynenberg addresses these issues in his 2007 IACFS paper "Glutathione Depletion-Methylation Cycle Block: A Hypothesis for the Pathogenesis of Chronic Fatigue Syndrome"
Diabetes insipidus (excessive urination, thirst, decrease in blood volume): According to this Hypothesis, glutathione depletion inhibits production of arginine vasopressin (141), which has one disulfide bond (142), by the same biochemical mechanism by which it inhibits perforin and ACTH synthesis (102).
Low cardiac output (145): According to this Hypothesis, this occurs because depletion of reduced glutathione in the heart muscle cells lowers the rate of production of ATP, as in the skeletal muscle cells. This produces diastolic dysfunction as observed by Cheney (146, 147). Both low blood volume (see Diabetes insipidus, above), which produces low venous return, and diastolic dysfunction, which decreases filling of the left ventricle, produce low cardiac output. In addition, in some cases, as observed by Lerner et al., viral infections produce cardiomyopathy (148). According to the GD-MCB Hypothesis, this is a result of depletion of reduced glutathione and suppression of cell-mediated immunity. This is another factor that can decrease cardiac output in CFS.
Orthostatic hypotension and orthostatic tachycardia (149): According to this Hypothesis, these occur because of low blood volume, low cardiac output and HPA axis blunting (See Diabetes insipidus, Low cardiac output, and HPA axis blunting, above.)
Notice that my reduced gluathione is just about the low normal. If I can raise it to the mid range, will more symptoms diminish? Will some completely disappear?
I hope so. I have just ordered Life-Wave glutathione and carnosine patches which are supposed to raise glutathione naturally by working on the acupuncture meridians of the body according to some kind of mysterious principle (voodoo? prayer?) that is not explained in their literature. But I'm a sucker for non-toxic remedies.
Desire: The symptoms I would like to change most are the production of energy and the ability to stand for lengths of time. I would like to be able to take walks and bike ride, to go someplace for a full day without needing a nap, to attend a party in the evening and even, someday, to travel and visit museums. David would like me to have the energy to wash the dinner dishes! The prospect is not exciting...
The second unanswered question: Why is folic acid higher when I am avoiding all supplements with folic acid?
Here are the pics, thanks to my new Spanish friend Sergio, who made them into jpgs.
As always, I welcome comments. Please click on the word comments below and let me know what you think!