This paper signals that more research is yet to come from this author.
is that a good thing?
This paper signals that more research is yet to come from this author.
This paper signals that more research is yet to come from this author.
Potentially. If somebody can point the author to this thread so he can refine his ideas about ME and our actual sleep problems. Presupposes he's genuinely prepared to learn. I like to give newcomers to the field the benefit of the doubt.is that a good thing?
Any idea of whether anything might have triggered the switch other than time?
When I investigated this twenty odd years ago there were already something like 15 or more different systems involved. This was before we even discovered the second sleep centre in the brain, in the brain stem. Most of them were suspected of involvement with ME. This needs way more research than it is getting, which is the standard ME story.
We know from African Sleeping Sickness and other findings that sleep is a complex orchestration of things, and is actively imposed on the brain in complex sequences. Its not just relaxing and lights out. Its not even like the brain turns from wake to sleep mode. Parts of the brain cycle off and on in complex patterns, and my understanding of it is not even close to adequate, its almost dismal. For example, it requires adequate synthesis and release of prostaglandin D2, which is impacted by general diet, oxidative stress (glutathione status) and dietary salicylates. Its also tied into other cycles including immune circadian patterns.
It is beyond just complex. Its something we have a bare minimal understanding of.
There are email addresses linked within the paperPotentially. If somebody can point the author to this thread so he can refine his ideas about ME and our actual sleep problems. Presupposes he's genuinely prepared to learn. I like to give newcomers to the field the benefit of the doubt.
Potentially. If somebody can point the author to this thread so he can refine his ideas about ME and our actual sleep problems. Presupposes he's genuinely prepared to learn. I like to give newcomers to the field the benefit of the doubt.
A purely brain problem is possible but it falls short on a number of things.
Jo, I'm sure you've discussed this before but I can't remember where or when. Beyond the brain, what's your take on the idea of mitochondrial dysfunction/broken ATP-cycle/etc?
Is this something that can be looked for?Nobody looks for TGF beta bound to matrix.
I contacted the author who replied. So he knows there is interest. He is doing some experiments now.
Is this something that can be looked for?
My experience has been terrible insomnia from the day I came down with EBV. I don't think I slept at all during the first few weeks of my EBV infection. Since then, I've had shocking insomnia (difficulty getting to sleep, constant waking, difficulty getting back to sleep) throughout the next 23 years.
signals painted on to matrix
what does this mean exactly?
If you cannot make ATP you find you cannot lift an arm or climb a stair but it does not make you feel ill like ME.
Sixty-two per cent of patients with mitochondrial disease reported excessive symptomatic fatigue
Mitochondrial Disease may literally cause any symptom, in any organ, with any degree of severity, at any age.”
He was clear that he did not see how these things could be explained by shortage of ATP due to mitochondrial failure.
They usually freak out when I don't sleep at all. They want to study sleep, not the lack of it.I went to a sleep lab but that experience didn't go well and my lab report was never sent to my doctor.
They usually freak out when I don't sleep at all. They want to study sleep, not the lack of it.