Fibromyalgia and Chronic Fatigue Fibromyalgia syndrome is a widespread musculoskeletal pain and fatigue disorder which generally occurs in the muscles, ligaments, and tendons – the soft fibrous tissues in the body. This forum is for fibromyalgia and Chronic Fatigue Immune Deficiency Syndrome (CFS/CFIDS).


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Old 10-22-2012, 07:37 PM #12
anon20160311
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anon20160311
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[I think fibromyalgia is a combination of three things:
1. Shortage of digestive adenosine
2. Shortage of choline
3. Inflammation

Inflammation can be triggered by any number of things. Its most prominent trigger is ingested antigen-like proteins. The damage from these proteins starts in the digestive tract as an immune reaction. The reaction releases interluken 15, an inflammatory cytokine. The reaction also releases zonulin. Zonulin cuts digestion short by making the intestine walls porous. The porosity passes the intestinal lumen into the bloodstream before DPPIV, a digestive enzyme, can digest carb proteins into adenosine. The result is a shortage of adenosine.

Adenosine fulfills two major functions. 1. Adenosine is the body primary queller of inflammation. 2. Adenosine is the base molecule of adenosine triphosphate (ATP). ATP is the energy currency of all human cells. Without adenosine, we have no energy.

So what happens when ingestion of antigenic carb proteins deprives us of adenosine? The liver produces two chemicals important to digestion 1) bile acid, and 2) choline (including cholinesterase).

When we eat the liver releases bile acid. In the stomach bile acid dissolves fat, and triggers the enzymes which digest meat proteins. Cholinesterase is the substance responsible for absorbing and neutralizing bile acid. W hen digestion is complete the liver is supposed to stop producing bile and start producing cholinesterase. How does the liver tell when digestion is complete? It monitors its own metabolic rate. As I said, adenosine is the base molecule of ATP, and ATP is responsible for metabolism. So the liver monitors when to stop releasing bile acid and start releasing cholinesterase by monitoring the concentration of digestion-produced adenosine.

When we digest antigenic carb proteins, and cut digestion short, the shortage of adenosine makes the liver fill the digestive tract with excess bile acid. It also creates a shortage of choline and cholinesterase. The digestive results would be bad enough, except for one thing. Choline is a squelch-er of nerve impulses. Choline and acetylcholine sit at the junctures of all nerve neurons. Acetylcholine is a neurotransmitter. It facilitates impulse transmission. After transmission choline squelches the transmission. When antigenic carb proteins suppress choline production, they cause pain nerves to continue firing long past when they should stop.

This condition is exacerbated by inflammation. The inflammation exists because there is not enough adenosine present to quell the inflammation.
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