Freddd
Senior Member
- Messages
- 5,184
- Location
- Salt Lake City
Hi Sergio,
Now 12.5 years after starting.
Better late than never. I got put back under it with partial methylation failure caused by copper deficiency, measured at 74 with 72 being the bottom of the "range".
I want to bring the B-vitamins up to date. B1, B2, B3 and inositol all cause selected methylation block in that they each affect a slightly different cross section of folate deficiency symptoms. I don't know what dose of inositol is helpful. It too had a specific cross section of methylation symptoms it shut down.
P5P drove my hematocrit too high, 54 and rising prior to discovering the copper problem and my doc wanted to reduce testosterone which was a titrated amount. Reducing P5P brought my hematocrit down to 47 in 3 months. Addied 15mg/day copper amino acid chelate (Solgar) and my testosterone went up 300ng/L in one month so I have started down titrating the testosterone. The copper also increased my need for potassium by 400mg daily and is making literally visible changes on my body slowly fading out the spider veins. I hope all my varicose veins also rebuild like the spider veins. Lack of copper damages connective tissue at the very least as well as causing sub acute combined degeneration type lesions and affects the upper motor neurons more. increasing the feeling of fatigue in the muscles. My doc is just amazed at these changes as am I. My gums dissolved in 5 years and I have had to have all my upper teeth removed. We are waiting a year on the lowers. In 2 months the color of the gums went to normal from cyanotic and the inflammation cleared up. Both the oral surgeon and my dentist were amazed at the changes in my gums and that my healing has been excellent, far better than expected. Maybe I will get to keep the other half my teeth.
I'm going to answer your numbered questions but not in your order.
4- Why do you think GSH may be dangerous?
I KNOW now. I have been diagnosed with adult onset CblC disease on the basis of my 2 hour reaction of going into methyltrap from glutathione. Glutathione causes catastrophic B12 deficiency in hours with the genetic differences. Also for me it takes very little to clean out all circulating active b12s by converting them to glutathionylcobalamin and excreting in the urine several multiples faster than normal. However, with our N=10 trials, 100% had the same problems in the end but some people took 3 weeks to get the effect I got in 2 hours.
1- What do you think is the cause of CFS?
2- What's the role of the methylation cycle in CFS?
6- In short, in what do you think Rich V. Konyneburg's theory failed, and why? and how your proposed treatment corrects these mistakes?
First, let me say that add in FMS and ME. I think the distinctions are more of an order of the Deadlock Quartet breaking down. Then let's add another symptom in common. CFS, FMS, Parkinson's, MS, Supra Nuclear Palsy,
ALS, autism and Alzheimer's all have low cerebral spinal fluid cobalamin and each of these disease has a different balance of too much HCY and MMA causing damages as well as the demyelination common to everything through ALS on that list.
If by "cause" you want to know the ultimate root cause of CFS it is genetics. Before folic acid and CyCbl invaded the food chain, the people getting these things had an inability to use vegetable folates. My grandfather (adoptive-step, so not related) was diagnosed with ALS in 1942 and wasn't expected to live out the year. My grandmother's "old family cook" from Germany made her "nerve tonic stew". Every day she reduced 5 pounds of liver to concentrated extract for the next days food,, and added meat and vegetables and he ate that 3 times a day. He died about 1972 after my grandmother got lung cancer and the cook was long dead and he ended up in a nursing home in which he died in less than 6 months without his tonic. The disease progressed very slowly; one cane in the early 50s, moving to 2 canes later and then crutches by 1960 and a wheelchair in 1964. He got more MeCbl, AdoCbl and l-methylfolate every day than anybody else in the world. At that time the fear factor "treatment" for pernicious anemia (B12 deficiency, don't you know that is all it is?) was 2 liters per day of pureed liver and most choose to die instead. They didn't think of the concentrate until later but it was for pernicious anemia, not ALS.
So when vitamin cereals and breads and all white flour products and even soft drinks now have folic acid and CyCbl, we have two things happening, CyCbl going into people that is perhaps as much as 1% active as MeCbl/AdoCbl and folic acid that 20% can't use at all, 30% use poorly and 50% use to the 800-1000 mcg biological channel limit. Unfortunately unconverted folic acid accumulates and blocks l-methylfolate. CyCbl puts everybody at the edge of functionality, and folic acid can kick them over, or any strain on the system such as physical trauma or viruses or bacteria.
Rich and I exchanged some raw data of our work, or at least the rawest he had from the study. We were able to discuss it privately without an audience and compare some notes. I got some uncombined variables (symptoms that had been grouped together) because of the doctor in charge needs and so on. Also, I have discussed the problem of getting the real working treatment past an institutional review committee with various researchers. Every one of them has told me it is impossible for a number of reasons. So the study couldn't be done the way he actually wanted to do it. Further, the doctor limited the symptoms list to his needs, not CFS needs. I did something else with the data, I grouped it differently so it was in order of my data. I also did numbers of each responding rather than percentage because 1 person was 50% or even 100% in some cases were only 1 or 2 had the symptom. As my list was validated and had two versions, one of ALL symptoms people reported and the other list, all the symptoms that responded to the deadlock quartet and half a dozen additional nutrients and high dose injected MeCbl (10mg sc 3x per day).
So the study used HyCbl and folic acid. HyCbl is only a little better than CyCbl. A flaw in his working hypothesis was that only HTC2 B12 mattered, not that 99% of the healing is done with free active B12s in the serum via diffusion, and therefor HyCbl was fine I don't believe that Metafolin was available at the time the study was planned or was way too expensive and too hard to come by. So in the simplified methylation he changed to folinic acid or at least optioned it.
I don't think that anybody is going to untangle the paradoxical folate deficiency and methyltrap situation without experiencing it. I can't say that I would have recognized it second or third hand if I also hadn't experienced it first hand. I had to work through it the hard way and untangle it all; the difference in meanings between what happens with folic acid, folinic acid and vegetable folates.
to be continued