A random thought on contributing causes to ME/CFS

Arnie Pye

Arnie Pye

Senior Member (Voting Rights)
A lot of ME sufferers develop the condition following a virus, then for reasons that are still not understood they don't recover and instead they develop ME.

The thought crossed my mind a few days ago that perhaps the causes of ME have not been found because the triggering conditions develop before the person actually goes through the triggering event and becomes ill.

I have read that, for example, low ferritin (iron stores) is quite common in athletes.

People who have known ME sufferers from before they became ill will often be astonished because the person was so energetic before the disease struck.

Lots of people are low in vitamin D. Perhaps that is a triggering condition for ME but it requires just the right virus for it to develop.

Lots of people are low on magnesium.

Soils used for growing food are getting stripped of nutrients.

Over the last few decades lots of people (women especially) have eaten diets that are unusual in terms of human history e.g. eating very little fat and eating lots of carbs. More recently people have cut out meat.

Doctors tell people with high cholesterol that they need statins. Nature creates cholesterol for "reasons", but humans have decided they know better.

I read a few years ago that there are over 70,000 new chemicals now found in the human environment, in cleaning chemicals, food, for treatment of fabrics, for building purposes, etc that didn't exist before 1950. Perhaps one or a combination of those is a trigger for ME.

I'm not suggesting that there might one specific cause for ME to develop following a virus, but that there is a tsunami of common conditions that the body is exposed to that people can tolerate for a long time, but the body then breaks down when certain health problems (e.g. a virus) just tip the scales a bit too far.

I've never been diagnosed with ME but I think I would be if I ever told doctors all of my symptoms. I avoid doctors like the plague though, and can usually only mention one symptom at a time which is usually blamed on my mental health if it isn't visible.

I didn't have a virus that triggered what I believe is ME. Instead I had a slow decline with a problem that doctors decided I was exaggerating. I had a chronic GI bleed that went on for five years. Towards the last year or two of it I could only crawl upstairs on my hands and knees, and it would take me 20 - 30 minutes to get upstairs at home, going up one step at a time on my bum. I was losing clots the size of a golf ball or sometimes even a cricket ball. I had frequent bouts of excruciating chest pain. After the bleeding polyp that was causing the problem was finally found and removed I think I should have been given a blood transfusion but I wasn't. So I had to fix myself and it took the best part of two years to even get my ferritin up to mid-range. I should have paid privately and got an iron infusion but, for "reasons", I didn't.

Although I have improved from the days of crawling upstairs on my hands and knees and having lots of chest pain (which was, naturally, attributed to anxiety) I have never fully recovered.

So, that's my recent random thought about ME, for what it's worth.
 
I agree that environmental stresses and genetics may be involved in the likelihood of ME developing. I still believe that it's immune activation that triggers ME, but after decades of immune activations, why does a particular infection, injury, or other cause (like my type IV food sensitivity) trigger the ME state? Age (failing subsystems) probably contribute. For childhood cases, maybe the hormone changes contribute.
 
@Arnie Pye I am intrigued by the bum-first stair ascent. It makes absolute sense to sit and shuffle down each step, and it also makes sense to adapt the crawling, hands-and-knees approach to a backwards descent. But I can’t work out how one might progress from a seated position to a higher stair without one’s arms taking excessive strain.
 
Shadrach Loom said:
But I can’t work out how one might progress from a seated position to a higher stair without one’s arms taking excessive strain.
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It was my legs taking most of the strain. I hadn't (and still haven't) lost all muscle strength in my legs. I would sit with my bum on the bottom stair, feet on the floor, wait for any chest pain to stop, wait to get my breath back, then would lift myself mostly by my legs, and would use my arms just for balance and to be sure of my aim. Once I'd got my bum onto the second stair I would then repeat with getting my breath back, would wait for my chest pain to ease, then would bring my legs up to the first stair. Then I would just keep on repeating until I was at the top of the stairs, then haul myself on to my feet using the newel post at the stop of the stairs.

In the years before I became seriously ill I had walked my dog twice a day, every day, and particularly in the early days I would often walk miles once the dog was old enough, so my leg muscles were in reasonably good condition. Eventually though I could only really walk her (the dog) on the flat for short distances. And I would still have to stop and wait for bouts of chest pain to pass from time to time. I was seriously waiting for heart failure or death, I felt so ill.

I don't know what technique other people use to get upstairs when they are hobbled by illness like I was and like the people on this forum.

I should point out that I can walk upstairs like normal people now, although I still do it slowly.

I should also point out that I no longer live with frequent bouts of chest pain. I did develop tachycardia as a result of the chronic bleed I had, and that has never permanently gone away and I have to make use of beta blockers from time to time to slow my heart down.
 
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JemPD said:
It 'feels' instinctively like you might be right Arnie, i dunno. i dont know how we'd ever find out.

do they really do that? I've consumed so much asparteme in my life
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Hi @JemPD

Prior to ME I had lots of aspartame, but who knows if that had any affect on my health in regards to developing ME.
It seems there may be many factors.

Scientists have been looking at the artificial sweetener question for a while.

Earlier this year they said:

2022 Sep 1;185(18):3307-3328.e19.
doi: 10.1016/j.cell.2022.07.016. Epub 2022 Aug 19.
Personalized microbiome-driven effects of non-nutritive sweeteners on human glucose tolerance
Jotham Suez 1, Yotam Cohen 2, Rafael Valdés-Mas 2, Uria Mor 2, Mally Dori-Bachash 2, Sara Federici 2, Niv Zmora 3, Avner Leshem 4, Melina Heinemann 2, Raquel Linevsky 2, Maya Zur 2, Rotem Ben-Zeev Brik 2, Aurelie Bukimer 2, Shimrit Eliyahu-Miller 2, Alona Metz 2, Ruthy Fischbein 2, Olga Sharov 2, Sergey Malitsky 5, Maxim Itkin 5, Noa Stettner 6, Alon Harmelin 6, Hagit Shapiro 2, Christoph K Stein-Thoeringer 7, Eran Segal 8, Eran Elinav 9
Affiliations
Abstract


Non-nutritive sweeteners (NNS) are commonly integrated into human diet and presumed to be inert; however, animal studies suggest that they may impact the microbiome and downstream glycemic responses. We causally assessed NNS impacts in humans and their microbiomes in a randomized-controlled trial encompassing 120 healthy adults, administered saccharin, sucralose, aspartame, and stevia sachets for 2 weeks in doses lower than the acceptable daily intake, compared with controls receiving sachet-contained vehicle glucose or no supplement. As groups, each administered NNS distinctly altered stool and oral microbiome and plasma metabolome, whereas saccharin and sucralose significantly impaired glycemic responses. Importantly, gnotobiotic mice conventionalized with microbiomes from multiple top and bottom responders of each of the four NNS-supplemented groups featured glycemic responses largely reflecting those noted in respective human donors, which were preempted by distinct microbial signals, as exemplified by sucralose. Collectively, human NNS consumption may induce person-specific, microbiome-dependent glycemic alterations, necessitating future assessment of clinical implications. (my bolding)

Keywords: artificial sweeteners; hyperglycemia; metabolic syndrome; metabolomics; metagenomics; microbiome; non-nutritive sweeteners.

Copyright © 2022 Elsevier Inc. All rights reserved.


Here's the link to this study:

https://pubmed.ncbi.nlm.nih.gov/35987213/

There are some other articles I found, but they have lots of ads.

ETA: @JemPD Looks like the story is still out on this topic, as further research is needed, but if you read the bolded sentence in the abstract, it looks like the study did point to microbiome alteration from some non-nutritive sweeteners.
 
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DokaGirl said:
Hi @JemPD

Prior to ME I had lots of aspartame, but who knows if that had any affect on my health in regards to developing ME.
It seems there may be many factors.

Scientists have been looking at the artificial sweetener question for a while.

Earlier this year they said:

2022 Sep 1;185(18):3307-3328.e19.
doi: 10.1016/j.cell.2022.07.016. Epub 2022 Aug 19.
Personalized microbiome-driven effects of non-nutritive sweeteners on human glucose tolerance
Jotham Suez 1, Yotam Cohen 2, Rafael Valdés-Mas 2, Uria Mor 2, Mally Dori-Bachash 2, Sara Federici 2, Niv Zmora 3, Avner Leshem 4, Melina Heinemann 2, Raquel Linevsky 2, Maya Zur 2, Rotem Ben-Zeev Brik 2, Aurelie Bukimer 2, Shimrit Eliyahu-Miller 2, Alona Metz 2, Ruthy Fischbein 2, Olga Sharov 2, Sergey Malitsky 5, Maxim Itkin 5, Noa Stettner 6, Alon Harmelin 6, Hagit Shapiro 2, Christoph K Stein-Thoeringer 7, Eran Segal 8, Eran Elinav 9
Affiliations
Abstract


Non-nutritive sweeteners (NNS) are commonly integrated into human diet and presumed to be inert; however, animal studies suggest that they may impact the microbiome and downstream glycemic responses. We causally assessed NNS impacts in humans and their microbiomes in a randomized-controlled trial encompassing 120 healthy adults, administered saccharin, sucralose, aspartame, and stevia sachets for 2 weeks in doses lower than the acceptable daily intake, compared with controls receiving sachet-contained vehicle glucose or no supplement. As groups, each administered NNS distinctly altered stool and oral microbiome and plasma metabolome, whereas saccharin and sucralose significantly impaired glycemic responses. Importantly, gnotobiotic mice conventionalized with microbiomes from multiple top and bottom responders of each of the four NNS-supplemented groups featured glycemic responses largely reflecting those noted in respective human donors, which were preempted by distinct microbial signals, as exemplified by sucralose. Collectively, human NNS consumption may induce person-specific, microbiome-dependent glycemic alterations, necessitating future assessment of clinical implications. (my bolding)

Keywords: artificial sweeteners; hyperglycemia; metabolic syndrome; metabolomics; metagenomics; microbiome; non-nutritive sweeteners.

Copyright © 2022 Elsevier Inc. All rights reserved.


Here's the link to this study:

https://pubmed.ncbi.nlm.nih.gov/35987213/

There are some other articles I found, but they have lots of ads.

ETA: @JemPD Looks like the story is still out on this topic, as further research is needed, but if you read the bolded sentence in the abstract, it looks like the study did point to microbiome alteration from some non-nutritive sweeteners.
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I lived off of squash basically my whole life because I have an icky thing about water (neurodivergence?) Which has aspartame. I stopped about six months ago by buying bottled water, and have graduated to tolerating britta filtered water (bottled being the gateway drug, I suppose!).

But then, so many people just drink diet coke 3-4 x a day or more and don't have ME.
 
Shadrach Loom said:
@Arnie Pye I am intrigued by the bum-first stair ascent. It makes absolute sense to sit and shuffle down each step, and it also makes sense to adapt the crawling, hands-and-knees approach to a backwards descent. But I can’t work out how one might progress from a seated position to a higher stair without one’s arms taking excessive strain.
Click to expand...
I struggled with stairs when I wasn't pacing myself enough, but my problem was being vertical and stepping upwards so I bear crawled a lot and kneeled to rest or rested on the wall a bit
 
Haveyoutriedyoga said:
I lived off of squash basically my whole life because I have an icky thing about water (neurodivergence?) Which has aspartame. I stopped about six months ago by buying bottled water, and have graduated to tolerating britta filtered water (bottled being the gateway drug, I suppose!).

But then, so many people just drink diet coke 3-4 x a day or more and don't have ME.
Click to expand...
Water with aspartame?

I'm not a fan of artificial sweeteners, I feel the potential issues (microbiome alterations, change in taste/hunger stimuli etc) are difficult to measure and so won't be picked up in general testing.
 
Pre ME I avoided any artificial sweeteners (have always disliked the taste), though during the week I did eat a lot of processed carbohydrates ( bread and pasta ) and did use chocolate or coke a cola (full fat) as a stimulant (I have never liked tea or coffee), however at weekends and in holidays I cooked from scratch with fresh ingredients.

I am now intolerant of gluten, caffeine and too much sugar, so wonder if that has any relationship to my previous overconsumption. However I can see such as aspartame being a predisposing factor for me in relation to my ME.

[added - just realised I’m missing a significant n’t from the last sentence, which should read “ … I can’t see such as aspartame being a predisposing factor …”
 
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Sadly, though, in the fight for "healthier" foods it's becoming increasingly difficult to avoid squashes without artificial sweeteners. I'm down to about Waitrose High Juice Orange squash and little else - most other things have succumbed :( And I originally started on high juice squashes decades ago because they didn't contain any nasty artificial ingredients ...

Sorry, getting a little off-topic here.
 
Peter Trewhitt said:
Pre ME I avoided any artificial sweeteners (have always disliked the taste), though during the week I did eat a lot of processed carbohydrates ( bread and pasta ) and did use chocolate or coke a cola (full fat) as a stimulant (I have never liked tea or coffee), however at weekends and in holidays I cooked from scratch with fresh ingredients.

I am now intolerant of gluten, caffeine and too much sugar, so wonder if that has any relationship to my previous overconsumption. However I can see such as aspartame being a predisposing factor for me in relation to my ME.
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I also used coffee and chocolate as stimulants for years, now am on medical stimulants for recent dx of ADHD (they help my overall wellbeing enormously, especially brain fog). But again, so many people also live on chocolate and coffee and are fine...which brings it back to the theory that its just a straw breaking the camels back?
 
Low-fat foods were first sold in substantial amounts in the 1970s (in my experience) and more and more foods started to appear in altered forms as common fats, eaten for centuries, were removed and replaced by artificial fats, vegetable oils, sugars and sweeteners.

Throughout the 20th century vegetable oils (which are mostly produced with the help of laboratory processes) became more and more common, while lard, dripping, butter, and other animal-sourced fats became stigmatised. Read this snippet from a book about Crisco.

If people ate a low-fat diet did they also start to suffer from deficiencies or low levels of fat-soluble vitamins?

Don't forget trans-fats. They may have been largely removed from most processed foods now, but for decades they were probably in practically everything that was processed.

Saturated fats, which would probably have been a major component of many diets before the industrial revolution, were also stigmatised and people were encouraged to use unsaturated fats for cooking. Saturated fats are now assumed to be a major cause of cardiovascular disease. But what often happened when saturated fats were removed from foods is that it became tasteless, and one of the ways used to try and overcome this was to add sugar in various forms, as well as artificial flavourings.

All of these things will have had effects on people's health, and I consider it unlikely that all these changes were perfectly safe and healthy. (We know that introducing trans-fats wasn't a good idea.)
 
Mithriel said:
The problem with this is that epidemics started in the 1930s, if not before. There has been a continuity and overlap of patients since then so it is not a different disease.
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There were many epidemics before the 1930s.

https://en.wikipedia.org/wiki/List_of_epidemics#Chronology

I wonder what the rate of long-term post-viral illness is now compared to the 20s and 30s, or after the Spanish Flu epidemic at the end of World War One. Were people allowed to convalesce in those days? What proportion eventually recovered?

If (using made up numbers) 20% of people who got Covid developed Long Covid, and of those 20%, one-tenth developed ME, how does that compare to the rates of these problems in historical epidemics?

Suppose a severe viral infection hit people in London in the late 18th century, there would already have been immense numbers of people who were starving and living in overcrowded conditions before an epidemic hit, so they would have died in greater numbers compared to the the wealthier classes. Very poor people who developed severe viral infections would not only die in greater numbers than the wealthy, but if they survived an epidemic and developed post-viral problems, they would not have been able to earn money and would then have died of starvation - and nobody would ever have known they were suffering from a post-viral condition because death from starvation would already have been so common. I think it would be impossible to compare people today to those who suffered similar epidemics in the past.
 
Arnie Pye said:
A lot of ME sufferers develop the condition following a virus, then for reasons that are still not understood they don't recover and instead they develop ME.
Click to expand...
Stripping it down to the most parsimonious statement, all we can say is that: "in those patients with a diagnosis of ME/CFS, a high percentage report that they became permanently unwell following a viral like illness". This isn't to say that viral or other infections play no role in ME/CFS it's just that there isn't population level evidence to show that infection prior to onset is other than correlation.

Post infection/post viral syndromes certainly seem to exist but there's no current evidence to support ME/CFS being a perpetual PIS/PVS in contrast to self limiting PIS/PVS.

Arnie Pye said:
The thought crossed my mind a few days ago that perhaps the causes of ME have not been found because the triggering conditions develop before the person actually goes through the triggering event and becomes ill.
Click to expand...
To quote from post I made earlier:

"This indication of absence might also require questioning of the assumption that a single recognisable infection is foundational and causative in ME. As noted in the first post in this thread, a majority of patients report that they become long term ill after (in their recollection) a virus like infection, however these remembered events may not link to actual pathology." https://www.s4me.info/threads/possi...ong-covid-discussion.20766/page-3#post-350415

The heterogeneity of ME/CFS could be explained by a single pathological process expressed differently in different people but at this point multiple processes in individuals with multiple variations between individuals may be as likely. And within that complexity, disease processes may very well be happening long before the disabling symptoms of ME/CFS emerge, with or without an external trigger.
 
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Viral infections may be a common trigger for ME, but I believe that it's not the virus that's important, but the activation of the immune cells. T-cell activation may be a stronger trigger for ME than IG cells, since there are fewer reports of triggering on Type I allergies, but maybe people are less likely to notice a correlation between developing ME and having an allergy attack. If you've been having hayfever or food reactions weekly (or daily), you're not likely to connect one event with developing ME.

My guess is that at least some of the reports of "I had a viral infection before 'getting sick' (that turned out to be ME)" are false memories of an infection then, caused by reading that ME is caused by viral infections.
 
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