Pain isn't helping. I can't get on top of that either with the tiny amount of oxycodone I am on (in combo with naloxone) so my mood is pretty dead pan and no doubt I would be cranky if there was someone here trying to push me into "trying harder", "going for a walk just to the end of the street, or simply not understanding. But I will say it again......I feel like I have got the flu and it is so hard to push through that when you know you might end up worse off because you didn't rest. I'm wondering if I get enough rest even though I don't do anything much except potter around because I still resist going to bed and just doing nothing. I am always working on something even when my brain isn't working efficiently enough to do it properly, I have to keep engaged or else the pain will overwhelm me and it is only when it does that I lie down. The horrible part is that when I wake up again I am usually in too much pain because the pain killers have worn off while I've been asleep although there are still times that sleeping will help reduce pain levels in the long run even if I wake up sore and wrecked for the first 2 hours. It's also because my body creaks and groans into the new position of lying down and I can feel things either click into a different place as gravity seems to contract me into myself and things hurt. I've always had pain from moving - that is easier to accept but I am also still feeling like I am putting things out in my back and neck and hearing things click in and out or just click whatever way and I know I have grainy knees and similar crackles in my neck just when I turn my head even when I am not attempting to lift my arms. Just taking a top off the right way by crossing my arms before lifting the garment over my head, is enough to ruin the whole day. If I get a migraine then it can often mean the end of my plans for the day and it seems like I have been planning to get out of this house since last year but can't get further than Golden Beach. I have not even had a swim this entire Summer which is soon over.
I am glad I managed to talk Ange into getting out for her swim before Summer was over but she is confined for different reasons. The thing is that she did it thinking that I was going to do the same thing down here but I didn't. "Good idea woman" she typed. I tried but by the time I was feeling half alright for it, it was cool and after dark and all I managed was another "look" at the water with a paddle for me and Milo thrown in after midnight so it wasn't even the same day that Ange went.
The Gold Coast team are moving along in leaps and bounds with regards to research into Chronic fatigue syndrome as defined by Canadian Consensus Criteria which means that at least post-exertion relapse is required for being defined as having CFS aka ME more correctly when using those criteria. Anyway they are discovering lots of things about people with ME/CFS (which is now more commonly known as CFS/ME - huge contribution to our understanding thank you researchers) thanks to grants from the Queensland Government and Fox I think the other main one is.
Here is an excerpt explaining a bit of it but I am not at all familiar with calcium ion transport in the body so it does not mean enough to me other than my genes should be able to confirm it if I knew which ones to look up on my genetic testing but I don't. I think they are still picking out the best genes to look at. Here is the excerpt anyway:
The breakthrough came after researchers from Griffith University identified that patients with CFS/ME were far more likely to have single nucleotide polymorphisms - DNA typos - in the genetic code for certain cell receptor.
This cell receptor is known as transient receptor potential melastatin 3 (TRPM3), and in healthy cells it plays a crucial role - transferring calcium from outside the cell to the inside, where it helps regulate gene expression and protein production.
But in several peer-reviewed papers published by the Griffith team last year, they showed that in CFS/ME patients, something seemed to be going wrong with TRPM3.
In the latest study, the team looked at blood samples 15 CFS/ME patients and 25 healthy controls, and found that immune cells in chronic fatigue patients had far fewer functioning TRPM3 receptors than those of healthy participants.
As a result, calcium ions weren't making it inside the cell like they should be, meaning cell function was impaired.
What makes matters worse is that TRPM3 isn't just found in immune cells. The team tested its presence on immune cells as they're easy to access in blood samples, but the receptor is found on every single cell in the body, which not only explains why CFS/ME has been so difficult to diagnose, but also why it's so severe.
"This is why it's such a devastating illness, and why it's been so difficult to understand," one of the researchers, Don Staines, co-director of Griffith University's National Centre for Neuroimmunology and Emerging Diseases, told ScienceAlert.
"This dysfunction affects the brain, the spinal cord, the pancreas, which is why there are so many different manifestations of the illness - sometimes patients will suffer from cardiac symptoms, sometimes it will be symptoms in the gut."
It's something that's confused doctors for decades, and has lead to much of the misdiagnosis of the condition - but the new research suggests that all of the common CFS/ME symptoms can be explained by these faulty calcium ion channels.
"We now know that this is a dysfunction of a very critical receptor and the critical role that this has, which causes severe problems to cells in the body," said Staines.
To be clear, the research is still in its early phases - all we know for now is that these dysfunctional TRMP3 receptors are involved in the disease, and there's a lot more work to be done.
But Staines suggests that the involvement of TRPM3 receptors could explain why so many patients appear to experience CFS/ME following a traumatic event or serious infection.
The class of receptors TRPM3 belongs to are also known as 'threat receptors', because they're upregulated when the body is under any kind of threat, such as infection, trauma, or even childbirth.
Staines and his colleagues predict that it's this upregulation that causes the the faulty genetic receptors to get over-expressed and then take over, messing up the calcium transfer in a range of cells.
For now, that's just a hypothesis. But it's a much-needed starting point for researchers to look into further.