Can the autoimmunity hypothesis explain the sporadic nature of ME symptoms?

[Bob]

My current view about the delay in PEM, at least in my case, is that PEM is largely due to mineral/electrolyte depletion and possibly dehydration. My reasoning is that overexertion appears to be a cause of my polyuria (excessive urination). Having found that I am prone to salt deficiency - which seems to be common in ME - and having an extremely-high urine sodium level in 2010, whilst blood sodium was low, I presume that this polyuria is the cause of mineral deficiency. The fact that others here gain great relief from IV saline also supports this theory.

My PEM bears an uncanny resemblance to a hangover. These too are largely due to electrolyte depletion and dehydration.

What I haven't yet figured out is why we get electrolyte depletion after exertion, but I think I am fumbling my way towards it. We seem to get an increase in blood acidity (a fall in pH) as a result of exertion. It looks as though this can promote electrolyte loss in urine, but I have already forgotten how! I had been thinking that it must be lactic acid/lactate that was involved, but now wonder whether other sources of acidity could do the same.

It seems that we have different experiences of PEM, and so perhaps we each have a different basis for our PEM. I know I'm just stating what we all know, but this demonstrates why we're not going to get anywhere, in terms of gaining insight into ME, without large biomedical research trials that attempt to determine subgroups.

 

[alex3619]

Do you mean there is no such thing in ME?

http://www.ncbi.nlm.nih.gov/pubmed/10659341

This is what happens in disseminated Yersinia Enterocolitica infection: the bacteria moves from the gut lumen to the mesenteric lymph nodes, spleen, liver, etc.

There is no such thing because without urgent intervention such bacterial infection, usually following disintegration of the gut mucosal barrier (which we do not have) almost invariably results in rapid death. Even with antibiotics and high level medical care the death rate is high. If it occurred in ME on any scale then we would be dying like flies.

Bacterial translocation has never, I mean never, been demonstrated in ME. Its been speculated about. What has been demonstrated is bacterial product translocation, such as lipopolysaccharide. Indeed at one point it was mooted that LPS levels might match symptom severity but I do not recall reading a proper study on this. LPS translocation does not require very much in the way of loss of gut integrity. It also induces major changes in liver function, and a host of sudden cytokine and other immune modulator changes, as well as mass migration of certain types of immune cells.

The risk of gut bacteria infecting the body means that gut surgery requires massive antibiotics to kill the gut bacteria, and dosing the patient with even more antibiotics.

The notion of bacterial translocation in ME has been around for a very long time. So far nobody has provided any evidence of this occurring.

 

[Scarecrow]

My PEM bears an uncanny resemblance to a hangover. These too are largely due to electrolyte depletion and dehydration.

I know what you mean.

Not a reliable source by any means but did you happen to catch that programme that was on BBC maybe about two months ago featuring the twins who are both doctors? They both drank 21 units of alcohol over a week. One had to drank 21 units in a single night, the other 3 units a day. The night that the both drank they both consumed the same amount of liquid overall, the moderate drinker making up the volume with water or soft drinks. They both measured volume of urine and there was little between them but the moderate drinker actually peed more.

I think the conclusion was that it was to do with the vasodilatory effects of alcohol (or was that my conclusion? I forget). Anyway, obvious connection to ME / OI.

 

[msf]

Disseminated Yersiniosis does not always cause sepsis.

 

[Marco]

I know what you mean.

Not a reliable source by any means but did you happen to catch that programme that was on BBC maybe about two months ago featuring the twins who are both doctors? They both drank 21 units of alcohol over a week. One had to drank 21 units in a single night, the other 3 units a day. The night that the both drank they both consumed the same amount of liquid overall, the moderate drinker making up the volume with water or soft drinks. They both measured volume of urine and there was little between them but the moderate drinker actually peed more.

I think the conclusion was that it was to do with the vasodilatory effects of alcohol (or was that my conclusion? I forget). Anyway, obvious connection to ME / OI.

The most interesting result for me from that experiment was that both the moderate and binge patterns produced similar levels of pro-inflammatory cytokines but the binge drinker only had significant levels of gut derived endotoxins.

 

[lansbergen]

My PEM bears an uncanny resemblance to a hangover.

When I sometimes forgot to take the immune modulator I got a huge hangover the next day.

 

[MeSci]

I know what you mean.

Not a reliable source by any means but did you happen to catch that programme that was on BBC maybe about two months ago featuring the twins who are both doctors? They both drank 21 units of alcohol over a week. One had to drank 21 units in a single night, the other 3 units a day. The night that the both drank they both consumed the same amount of liquid overall, the moderate drinker making up the volume with water or soft drinks. They both measured volume of urine and there was little between them but the moderate drinker actually peed more.

I think the conclusion was that it was to do with the vasodilatory effects of alcohol (or was that my conclusion? I forget). Anyway, obvious connection to ME / OI.

No, I didn't see it. I rarely watch live TV nowadays but I could probably watch it on iPlayer...if I run out of good comedy.

Were they identical twins?

 

[Scarecrow]

Were they identical twins?

 

[MeSci]

The most interesting result for me from that experiment was that both the moderate and binge patterns produced similar levels of pro-inflammatory cytokines but the binge drinker only had significant levels of gut derived endotoxins.

I don't seem to get changes in urine production from alcohol consumption. One thing that seems to reduce output is eating, perhaps because it draws fluid into the gut to assist digestion.

Polyuria is a damn*d nuisance. I can stop the type that appears to be due to a lack of vasopressin, by taking desmopressin, but the other type is apparently unstoppable, and loves to afflict me when I am out shopping so that I have to either rush home or use public loos. The state of the latter means that I almost always choose to rush home. E.g. today.

I WILL find a solution one day.

 

[MeSci]

I guess that means yes. There are subtle differences, and not just the hair partings, but those could be environmental.

They are monozygotic twins anyway.

 

[duncan]

The moderate drinker clearly looks less hungover than his brother.

 

[MeSci]

The moderate drinker clearly looks less hungover than his brother.

Oh yes. To me the one on the right looks hungover. Eyes more squinty, bags more prominent, not smiling, fist clenched...

 

[duncan]

The one on the right??

Yes, that's the one.