New Hypothesis for why our ME is so individualistic

Wishful

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The thread about ME causing nightmares or weird dreams triggered this idea. I think ME's core dysfunction is in the brain, and many of the symptoms people experience are downstream effects of dysfunction in the brain, and the variety of responses to various environmental factors are upstream of that core dysfunction.

When a fetus develops, it's not directly following a detailed blueprint. Just how and when each cell develops depends on its chemical environment. How many AA transporters develop in the membrane, how many mitochondria or extracellular vesicles it produces in response to some stimulus: these depend on what the mother ate for breakfast, what her mood (hormones, etc) was, what activities she did, etc. Those variations are in addition to the individual DNA of the person. These developmental variations could be part of what makes us likely to develop ME, and how our ME responds to various factors and what symptoms we develop. On top of that are epignetic factors post-birth and other variations such as toxin exposure, allergen exposure, stress, trauma, etc.

These various developmental factors determine brain cell responses to stimuli, capillary function (and how far each cell is from the blood supply), etc. Thus one person will have their ME affect the part of the brain involved in dreaming (with further variations in the effects on the 'happy dream' or 'vivid weird dream' cells vs the 'nightmare' cells), while another person gets double-vision, and a third gets sound sensitivity. Other variations might affect gut function or the muscle control system or the pain processing system.

I suppose this hypothesis isn't of much use, but it does reduce the worth of genetic testing. The existence or non-existence of a specific gene is not the only factor that determines how your body is now.
 
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Its also tied to the vagaries of simply what tissue is swollen, inflamed, compressed, and sending out misguided instructions as a result. Lower brain stem issues.

I wish I had a weird dream.
 
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I’m big fan of Cortene theory. Different neurons with upregulated CRFR2 receptor explains why we have different symptoms. What neurons are affected depends on ANS injury we had in the first place (trigger).
There are scientific papers about CRFR and how it controls the homeostasis of cardiovascular system. Upregulated CRFR explains orthostatic intolerance and sympathetic predominance. I don’t know how this theory fits ME cases when there is no orthostatic intolerance/sympathetic overactivation.
Genetics predisposes person to acquire ME, and genetics can also dictate how illness will progress (or stop progression)
Moreover, I believe it’s possible to damage other CRFR receptors when you already have ME. That’s the case when disease progresses abruptly at some period of time. Or, upregulated receptors can upregulate further, leading to slow disease progression. (That’s the case when the same stressor/trigger is repeated)
Other, downstream symptoms are coming from inability of our body to compensate the problem. I think the most disabling ME symptoms are downstream, they are not primary. But everyone is different, so in some cases this isn’t true.
Sorry for being too pushy about Cortene. Lot of my messages is about their theory :)
 
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I was just looking at diagrams of the brain stem, with labels. None of them wanted to be copied here.

All kinds exist. As soon as you read the labels examine the many many things which are supposed to flow in and out of this area.

This illness I call: No Flow...

Go with the flow, it aint; flowing. My lymph, blood and cerebral spinal fluid. My calcium ion channels. My Qi.

So when 2020, in 1994 ran the Surgeon opened up the skull, so the brain stem was not squeezed, this person's CFS was cured.

And I said: THAT...THATS WHAT IS WRONG HERE.