Periodic Paralysis, myotonia, channelopathy and ME

@duncan @Jenny TipsforME

Thanks for the information. I wonder would having great difficulty holding my arms at or above shoulder height (aged early teens -ten years prior to ME/CFS) fit the pattern?

 

But the only study citing that hypothesis paper which measures stuff in CFS is:

Exercise responsive genes measured in peripheral blood of women with Chronic Fatigue Syndrome and matched control subjects Toni Whistler, James F Jones, Elizabeth R Unger and Suzanne D Vernon*

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1079885/pdf/1472-6793-5-5.pdf

 

What's ATS?

 

Great find, @Jenny TipsforME . I see the authors focused on sodium imbalances in the first study. The second study with Unger and Vernon seems to suggest in the abstract that some ion channelopathy (or at least ion irregularities?) might be inferred?

I wonder why these were not followed up.

@Inara , one specific type of Periodic Paralysis is called Andersen-Tawil Syndrome - ATS.

 

I might just message Suzanne Vernon and ask her opinion.

 

@Jenny TipsforME, would you say Periodic Paralyses and ATS might be found via genome testing? I suppose there are also cases where no gene changes are found but the illness is present?

 

It might. Every PP patient is different, just like pwME. Most - but not all - episodes are triggered by something. For my wife, the trigger is sleep or prolonged rest - how's that for irony?

 

Sorry, @Jenny TipsforME , I am on line at the moment, so I hope you don't mind me answering a question directed at you. Yes, @Inara , some forms of PP can be determined through genetic testing, while others cannot. Some of those that cannot be uncovered thru genetic testing can be figured out thru potassium or sodium imbalances.

Some are probably out there with no means of being formally diagnosed yet.

 

Thank you, @duncan!

If a person with PP would supplement potassium (or sodium in any form), what would happen?

 

Do you know how many % are detected via genetic tests?

 

70-80% can be picked up through genetic testing. So can be a false negative.

 

For many there would be a need to first determine if you are hypo vs hyperkalemic. Not everyone can do this, though. My wife cannot, so we do not know which side she should be erring on, ie, supplementing potassium, or avoiding it.

But for many, knowing whether to supplement or avoid becomes a lifelong commitment to scrutinizing your diet.

 

I understand it this way: a positive genetic test doesn't necessarily mean an illness will break out. But if there are symptoms, the test would ensure the diagnosis. Did I understand you correctly?

 

I don't know how you can avoid potassium...

But still, I don't understand what would happen if potassium is supplemented. Let's assume someone doesn't know he has PP and takes potassium/sodium - what could happen?

 

@Inara it is complicated because there are several types. Hypokalemic and hyperkalemic have opposite responses. Potassium is generally a potentially dangerous thing to mess with even if you don’t have PP.

Re the false negative I meant if you don’t have a currently known mutation that doesn’t necessarily mean you don’t have this. There are other tests too.

 

Thank you, Jenny.

I take ca. 3g potassium-citrate daily (ca. 1g potassium), and for me it helps, I think. (WHO's recommendation is 6-7g daily if I remember correctly, and I don't eat that with my food, I am certain.) I had no problems with it. I know it is said potassium is dangerous - and it can be - but normally (fresh) food contains a lot of potassium (and phosphorous).

I was just wondering...

 

I found this Phoenix Rising paper written in 2012. In that year I was moving house and then having a bedbound relapse so I wasn’t following research debate. It could be there’s some reason people aren’t talking about this anymore? Eg @JaimeS @alicec @Valentijn does anyone remember?

A Neurological Channelopathy in Chronic Fatigue Syndrome (ME/CFS)?
MARCH 4, 2012
(This paper is based on ‘Chronic Fatigue Syndrome is an Acquired Neurological Channelopathy’ by Chaudhuri and Behan)

Background
http://phoenixrising.me/research-2/...annelopathy-in-chronic-fatigue-syndrome-mecfs

This post/essay is good at explaining channelopathy.
Says also

Myotonia is a similar, overlapping condition to Periodic Paralysis

So what happened to this as a general idea?

 

I’ve changed the title of this thread

 

It's an article, not a paper. I'm not sure which studies you want to discuss ... a lot are cited, but some are just hypotheses (not research), and others are not regarding CFS.

 

@Valentijn it describes itself as a paper I don’t know who wrote it? I’m interested more in the general hypothesis rather than a specific paper. It seemed like it was discussed quite a bit at one point then hasn’t been for a few years. Was this because evidence was found to refute the idea of channelopathy in ME, or was it simply lack of funding?