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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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This little study appears to add another layer of understanding to PEM.
So, maybe the question to ask is what do infections and high intensity physical exercise have in common? We already know that B12 is involved in the disease process. B12 is often called the energy vitamin because it helps fat and protein to metabolize in the body. It also plays a major role in the conversion of carbohydrates to glucose-your body's source of fuel. In addition, B12 enables your body to convert fatty acids into energy. It is also a promoter of normal immune function.
Intense physical exercise would deplete your body of B12. High intensity physical exercise also raises homocysteine. B12 is necessary to recycle homocysteine. So, it does impact the methylation cycle.
So, where does B12 come from? It is made by organisms in the soil. An animal that is pastured ingests B12 and we get B12 by eating proteins that come from animals that are pastured, such as eggs, meat, fish , dairy. A Tufts University study found that 40% of Americans were deficient enough in B12 to cause neurological damage. The study also found that we were consuming these proteins, but were not properly metabolizing B12. So, the problem lies in the metabolism. Is there something involved in the metabolism of B12 that would also directly impact immune function? The answer to this question could explain a great deal. It could also explain the biological findings in the disease process, such as low B12 and iron. An immune system "gone haywire" does not explain the biological findings in autoimmune disease, such as low dopamine in fibromyalgia or low acylcarnitine in the blood or muscles of people with CFS/FMS.
We agree but doesn't this paper add the concept of a possible delay between the stressor and the onset? If severe exercise in your history increases the risk of M.E. later then what was damaged/broken/worn thin during the exercise years?I believe the results of this paper are consistent with the Glutathione Depletion--Methylation Cycle Block hypothesis for ME/CFS. This hypothesis proposes that the onset of ME/CFS results from genetic predisposition together with some combination of a variety of physical, chemical, biologicial and/or psychological/emotional stressors.
One disappointment is that they tested immediately post exercise and didn't follow up over a typical PEM period of a number of days.
We agree but doesn't this paper add the concept of a possible delay between the stressor and the onset? If severe exercise in your history increases the risk of M.E. later then what was damaged/broken/worn thin during the exercise years?
If a teenager does burnouts with the family car in the local parking lot, everything may look fine but if the treadwear on the tires is severe, the odds are greater of a blowout on the highway later when mom is driving the little ones to soccer practice. What is the tire tread for the human body regarding M.E.?
After realizing the possibility that the reduced Hsp response to stressors in CFS may be further upstream than the other proposed causes of oxidative stress, I started looking for possible solutions to try. I'm currently leaning towards TEX-OE which is a Prickly Pear extract that supposedly works by stimulating heat shock factors for up to 72 hours after a single dose.