Ema
Senior Member
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- Midwest USA
Has anyone tried adenosine monophosphate injections a la the Dr Harvey Sklar protocol?
http://www.legerepharm.com/uploads/CFS_6-1-12_PP.pdf
I'm really interested in adenosine since it seems like it can cause almost all the problems most of experience in ME/CFS.
I originally thought that my adenosine was too high - it was over range on the methylation panel - and not degrading properly into uric acid. My uric acid levels are below range.
When I take inosine (an intermediary), my uric acid levels rise so that part seems to work OK.
I think that my adenosine is not breaking down by adenosine deaminase into inosine possibly due to a genetic defect. When people are homozygous recessive for that gene, they can develop severe combined immune deficiency (ie bubble boy).
I'm wondering if being heterozygous is not simply being a nonsymptomatic carrier as is commonly thought, but actually can produce symptoms.
High adenosine produces fatigue, vasodilation, migraines, orthostatic intolerance, increased neurotransmitters and there are a lot of adenosine receptors in the hypothalamus which might explain why so many of us have endocrine abnormalities.
Adenosine is also displaced by caffeine temporarily which may explain why caffeine helps some of us. It blocks the adenosine which makes us feel more alert.
There is also a relationship with nicotine - but it seems to be the opposite one. Nicotine enhances the circulatory effects of adenosine apparently.
But these two thoughts don't seem to work together - is it high adenosine failing to break down into uric acid? Or just low adenosine in general?
Does anyone know how to find this gene? Is there a place to look up the mutation?
Has anyone ever tried treatment with adenosine or a medication that breaks it down like the asthma med theophylline?
Thanks for your input!
Ema
http://www.legerepharm.com/uploads/CFS_6-1-12_PP.pdf
I'm really interested in adenosine since it seems like it can cause almost all the problems most of experience in ME/CFS.
I originally thought that my adenosine was too high - it was over range on the methylation panel - and not degrading properly into uric acid. My uric acid levels are below range.
When I take inosine (an intermediary), my uric acid levels rise so that part seems to work OK.
I think that my adenosine is not breaking down by adenosine deaminase into inosine possibly due to a genetic defect. When people are homozygous recessive for that gene, they can develop severe combined immune deficiency (ie bubble boy).
I'm wondering if being heterozygous is not simply being a nonsymptomatic carrier as is commonly thought, but actually can produce symptoms.
High adenosine produces fatigue, vasodilation, migraines, orthostatic intolerance, increased neurotransmitters and there are a lot of adenosine receptors in the hypothalamus which might explain why so many of us have endocrine abnormalities.
Adenosine is also displaced by caffeine temporarily which may explain why caffeine helps some of us. It blocks the adenosine which makes us feel more alert.
There is also a relationship with nicotine - but it seems to be the opposite one. Nicotine enhances the circulatory effects of adenosine apparently.
But these two thoughts don't seem to work together - is it high adenosine failing to break down into uric acid? Or just low adenosine in general?
Does anyone know how to find this gene? Is there a place to look up the mutation?
Has anyone ever tried treatment with adenosine or a medication that breaks it down like the asthma med theophylline?
Thanks for your input!
Ema