David Bell about "slow sepsis" in ME

Inara said:
But are we absolutely sure there isn't a state which one could call 'slow sepsis', something where some processes are known, and maybe some are not? Something that actually is new to us? Something that doesn't lead to death, but to a slow progression of degeneration?
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No. Slow sepsis is just a silly term that only someone who does not understand pathology would use. Sepsis is not fast or slow. It is defined as a state where there are gross biochemical disturbances triggered by infection that may either be due to direct toxins from the microbe or to host responses.

A milder version of this is perfectly well known and is just called bacterial infection. If that goes on for a long time it is called chronic infection. There is nothing new or unknown here, just a confusion of concepts.

If there was chronic infection it is highly unlikely that the bacterium would not be found at least in a minority of people. And for it to cause symptoms one would expect to see at least a low level of the biochemical changes of sepsis - otherwise how can one even call it 'slight sepsis'. And those changes are not found in ME/CFS.

And I think this has absolutely nothing to do with the fact that cut-offs between normality and disease on tests are arbitrary. That can become an issue when considering individual cases but it cannot be relevant when considering data on mean levels for ME/CFS. If sepsis is a deranged biochemical state defined by tests then a mild version would have to be at least slightly different from the normal test values on average - and it isn't.


Inara said:
And why is it more plausible that some infection starts a certain cascade, and then there is a 'slow/low-level starvation mode'? Which - at first glance - doesn't sound more plausible. WHY is that cascade started? The infection alone can't be the answer. Wouldn't that have been found up til now, maybe?
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I think that account in Health Rising is pretty garbled. My information on Chris Armstrong's ideas comes via Jo Cambridge who collaborates with him. My understanding is that he does not think that there is continuing infection but that an acute episode triggers some shift in metabolic control that continues abnormalities that you might see with infection. If there is no infection then calling it sepsis is just confusing. There is some shift in a regulatory mechanism. We are familiar with things like that. As an example, after a major surgical operation and anaesthetic the body often continues to destroy protein, as it does after trauma, ('negative nitrogen balance') sometimes for weeks.
 
Jonathan Edwards said:
No. Slow sepsis is just a silly term that only someone who does not understand pathology would use. Sepsis is not fast or slow. It is defined as a state where there are gross biochemical disturbances triggered by infection that may either be due to direct toxins from the microbe or to host responses.

A milder version of this is perfectly well known and is just called bacterial infection. If that goes on for a long time it is called chronic infection. There is nothing new or unknown here, just a confusion of concepts.

If there was chronic infection it is highly unlikely that the bacterium would not be found at least in a minority of people. And for it to cause symptoms one would expect to see at least a low level of the biochemical changes of sepsis - otherwise how can one even call it 'slight sepsis'. And those changes are not found in ME/CFS.

And I think this has absolutely nothing to do with the fact that cut-offs between normality and disease on tests are arbitrary. That can become an issue when considering individual cases but it cannot be relevant when considering data on mean levels for ME/CFS. If sepsis is a deranged biochemical state defined by tests then a mild version would have to be at least slightly different from the normal test values on average - and it isn't.




I think that account in Health Rising is pretty garbled. My information on Chris Armstrong's ideas comes via Jo Cambridge who collaborates with him. My understanding is that he does not think that there is continuing infection but that an acute episode triggers some shift in metabolic control that continues abnormalities that you might see with infection. If there is no infection then calling it sepsis is just confusing. There is some shift in a regulatory mechanism. We are familiar with things like that. As an example, after a major surgical operation and anaesthetic the body often continues to destroy protein, as it does after trauma, ('negative nitrogen balance') sometimes for weeks.
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If that thesis is that an acute episode triggers some shift in metabolic control, then the question is: can this metabolic control be localised, or repaired? And this is sounding like cell danger response to me.
 
Perrier said:
If that thesis is that an acute episode triggers some shift in metabolic control, then the question is: can this metabolic control be localised, or repaired? And this is sounding like cell danger response to me.
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I think cell danger response is too vague a term to be useful for working out a disease mechanism. For the diseases we understand the abnormal pathways are very specific. I am not sure what localised would mean either. Certainly, if the hypothesis is on the right track one would want to try to identify the faulty signal pathway and reverse it.

I don't think degenerative is a useful word here either. It is largely a word used by doctors to sound knowledgeable when they have no real idea. It tends to imply irreversible structural change with loss of function. At the moment we have no evidence of structural change in ME/CFS.
 
Perrier said:
What do you mean by degenerative? Do you mean the severity of symptoms increases?
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Existing symptoms get worse, new symptoms appear, problems with organs arise etc. (in my family's case: the heart, arteriosclerosis, brain strokes...but also rheumatism, cataract, Carpal tunnel syndrome, diabetes, whatever...).

I have to say my impression is this is due to overdoing. I am maybe the only one who sticks to pacing in my family. The others either overdo it always (and ignore worsening) or crash, then rest, then overdo it again, crash, rest...and ignore the (slower) worsening, too.
 
Jonathan Edwards said:
I don't think degenerative is a useful word here either. It is largely a word used by doctors to sound knowledgeable when they have no real idea. It tends to imply irreversible structural change with loss of function. At the moment we have no evidence of structural change in ME/CFS.
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It's a word I use to explain what I see in my family. (No doctor would tell me my illness might be degenerative, quite the contrary.) It doesn't have to be correct, particularly in general. But it fits my personal observation.

I see structural change and loss of function of organs in my family. Sometimes it's scary. One of my ("older") family members is very bad off.
 
Jonathan Edwards said:
I think cell danger response is too vague a term to be useful for working out a disease mechanism. For the diseases we understand the abnormal pathways are very specific. I am not sure what localised would mean either. Certainly, if the hypothesis is on the right track one would want to try to identify the faulty signal pathway and reverse it.

I don't think degenerative is a useful word here either. It is largely a word used by doctors to sound knowledgeable when they have no real idea. It tends to imply irreversible structural change with loss of function. At the moment we have no evidence of structural change in ME/CFS.
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Dear Dr Edwards
You say: If the hypotheses is on the right rack one would want to try to identify the faulty signal pathway and reverse it. Who is investigating these potentially faulty pathways. Who is involved in this kind of research?

And do you think that this is an old illness or something contemporary?

The symptoms are unsustainable in many patients, who have non stop flu feeling, malaise, sick feeling, dying feeling, etc. and are just crying out for relief or death.
 
Perrier said:
Dear Dr Edwards
You say: If the hypotheses is on the right rack one would want to try to identify the faulty signal pathway and reverse it. Who is investigating these potentially faulty pathways. Who is involved in this kind of research?

And do you think that this is an old illness or something contemporary?

The symptoms are unsustainable in many patients, who have non stop flu feeling, malaise, sick feeling, dying feeling, etc. and are just crying out for relief or death.
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Lots of people are investigating potentially faulty pathways: Chris Armstrong, Jo Cambridge, the CureMe group at London School of Hygiene, Oystein Fluge, Mady Hornig, Ron Davis, you name it.

I have no information on whether or not this is an old illness or new. I doubt anybody else has anything reliable.
 
Perhaps worth considering from OMF data presentation - last speaker. In severely affected gene expression study matched sepsis
Have a sceenshot but don't ' t know how to upload it
 
Amw66 said:
At around 16.50 mins in
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Are you referring to the 100% identity of the ME/CFS gene expression signature with that of Systemic Inflammatory Response Syndrome referenced at about 14:10? Until recently (2016), the SIRS criteria were being used to diagnose probable sepsis.
 
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