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Methylation, Acumen vs. EDL tests questions for Rich V K

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3
Hi, eric (and the group).

I have seen the results of quite a few AcumenLab panels on people with ME/CFS, and the types of results you have received are very typical.

As you may know, I believe that the origin of the mito dysfunction that is so well documented by these tests is the vicious circle mechanism involving glutathione depletion, a functional B12 deficiency, a partial block of the methylation cycle, and loss of folates.

Dr. Howard does do a glutathione measurement, but it is a red blood cell total glutathione measurement. While many PWMEs have a low value from this measurement, many are only low-normal or even normal. The problem here, as I see it, is that this type of test is not very reflective of the levels of reduced glutathione in the tissue cells. First of all, it is run on the red blood cells, which are normally producers and net exporters of glutathione. They can thus be expected to have a better glutathione status than cells that do not have this capability. Second, total glutathione includes oxidized glutathione, and it is a liability rather than an asset in maintaining the redox status of the cells.

As far as I know, only the European Laboratory of Nutrients in the Netherlands and its subsidiary, the Health Diagnostics and Research Institute in New Jersey, USA, have the capability to measure both reduced and oxidized glutathione in blood plasma, which is more reflective of the situation in tissue cells. Most PWMEs are found to have low reduced glutathione with this testing.

In the clinical study of methylation treatment that Dr. Nathan and I performed, the patients reported a statistically significant increase in energy level on a visual analog rating scale. I think this indicates that methylation treatment improved the function of their mitochondria, since the mitochondria are mainly responsible for producing the ATP that powers biochemical reactions, including the contraction of the muscles.

I think that the theoretical basis for this connection between the vicious circle mechanism and mito dysfunction is also pretty solid. Oxidative stress, which is associated with glutathione depletion, is known to inhibit mito function. Carnitine, coenzyme Q10, phosphatidylcholine, and creatine are all needed by the mitochondria and the ATP system, and all of them require methylation for their synthesis. When glutathione goes down, toxins build up, as are found in the mitochondria in ME/CFS. When there is a shortage of ATP, due to mito dysfunction, the proper levels of essential minerals cannoth be maintained in the cells, because sufficient energy is not available for the cell membrane ion pumps.

Based on all of this, I believe that the methylation treatment is necessary to bring the mitochondria back to full normal operation. I hope this is helpful.

Best regards,

Rich

Hi Rich
I've taken the liberty of copying one of your posts into this new thread as I had a few questions and did not want to go off topic in the original one.
I have had those mitochondrial tests for years and I agree they are not helpful. They haven't proven helpful at all I must say (I'm not as diplomatic).
Least so the treatment with all those vitamins, minerals and cofactors. If anything I got worse and so I stopped everything some time ago.
Whilst certain treatments helped reduce my toxic load, these were replaced by "aldehydes, products of oxidative stress" in hindering mitochondria and ATP production.
From what you write, I infer that getting the methylation cycle up to speed is more important than supplementing with CoQ10, carnitine, glutathione, magnesium etc. because the body then should be able to manufacture those and help maintain a better mineral balance. In my instance for e.g., no matter how much magnesium I take, my tests always show lowish levels.

I have a few questions concerning the topics that you flagged.
Tests:
Have you seen EDL tests showing low blood plasma glutathione even though RBC glutathione may be normal?
I'm trying to assess whether it's worth having tests at EDL (my RBC glutathione is normal and so are peroxidase and s-transferase.)

Methylation protocol:
From your study and experience, is the methylation block reversible or one has to stay on the protocol for life? Is it safe very long-term?
My doctor says that SOD is very important in protecting mitochondria from oxidative stress, would the methylation protocol boost SOD in addition to the other effects you wrote about (my levels remain low no matter what)?
My tests have consistently reported high intracellular calcium and aldehydes, is this a product of a blocked methylation cycle notwithstanding the reported normal glutathione levels?

Best regards
Jo