Modern environmental factors

I don't think you would need to go to South America. Levels of exposure to environmental factors are likely to vary hugely nearer at home - either within regions of a Western state or maybe between states. Or there should be sudden changes with time. Covid-19 may give us just that, but nobody is doubting the likely role of microbial triggers.

 

I think both biomedical scientists and philosophers have come to the conclusion that there is no such thing as a 'root cause' in this world much. All events have vastly multifactorial origins.

 

I don't know specifics and haven't researched it myself, but as a starting point, I just asked claude.ai, and this seems like a significant influence of modern environment:

"do any of these have good evidence for being at least partly caused by modern environmental factors, like chemicals or modern diets: Crohn's disease, ulcerative colitis, ankylosing spondylitis, Hashimoto's hypothyroidism, Graves's hyperthryroidism, pernicious anaemia, type I diabetes, multiple sclerosis"

 

You can always find 'some studies suggest...' for anything.
And AI is becoming a brilliant source of scientific disinformation in this regard.
That list looks about as plumb negative as you can get to me!!
If there were know environmental factors they would go into guideline advice. We tell people not to smoke. That is about it.

 

That's if we know what environmental factors to look for. It might vary by exposure to industrial chemicals, which might not necessarily be obvious in location data. Maybe around half of most every region, every city, every neighborhood in the country by chance happens to use some specific chemicals in their cleaning products. There are so many cleaning products, so many chemicals in these cleaning products, the exposure can be so indirect, such as when people go to a grocery store that was cleaned, that it would be probably be really hard to see this data, and would require very intensive data gathering (places people shop, where they work, what cleaners they buy. and this is just one possibility - that it's in cleaning products)

With a large tribe in South America, at least we know we have a much larger advantage in relying on location data alone, since the whole population's environment is significantly different.

 

And their genes would be different and their microbial exposure different and about everything else.

I guess my view is that if there isn't a scrap of evidence for a role for environmental pollutants why go for it as a theory?

 

I don't know why you would call this disinformation. Was anything in the chatbot's reply inaccurate or even misleading? It's not a source of hard evidence, I was using it to generate hypotheses.

That's true, I couldn't find any direct evidence of medical organizations recommending to avoid chemicals.

That is true. Though if we can show that it's uncommon in all undeveloped populations and common in all developed nations, that would lower the chance that population level genes are a main risk factor.

I suppose just everything I've said in this thread up to this point. It seems almost obvious to me that it should at least have significant resources spent on its study. And while I don't know much about industrial chemicals, I have seen hundreds, possibly thousands of anecdotes of ketogenic diets improving various chronic conditions. Here's one example of a Reddit thread with dozens of people claiming keto significantly treated or cured their mental conditions.

Of course, I may be putting too much stock in anecdotes. And my reasoning in this thread might not be as strong as it feels to me.

 

I don't see how we can speculate about environmental factors without knowing anything about the history of ME.

For all we know, it could have occurred with roughly the same frequency tens of thousands of years ago. Even when we get to written sources from the Bronze Age onwards, the chances of any descriptions surviving are minuscule, let alone recognisable ones.
The introduction of the printing press still doesn't help. Could we recognise it reliably from medical descriptions that use the phraseology of the time, even when they happen to be in the same language we speak?

Diseases get recorded and discussed when they kill or disfigure lots of people. There's a preservation bias against records of conditions that don't have that impact and fear factor, even when they result in significant debility.

 

That's true, I'd love to see more research in this area as well.

 

This caught my eyes because I thought about before. Two things I came up with:

1) ME/CFS is largely a disease of the middle-aged and older who are not likely to pass on their genes anyway. So, the evolutionary pressure of ME/CFS would've been minimal. And there was no NHS in old days, so the tribes probably left these "prematurely old people" to die on their own rather than spending gobs of resources on them.

1) To me, ME/CFS is not that different than injury or other maladaptive response. Fatigue is there for a reason and its mechanisms, finely tuned and optimized the survival, got somehow broken and tilted. The evolution can't fix that without shifting resources from something else. Making bones unbreakable, for example, may cause your kidney weaker. (Yes, I made that up).

I don't think you will have an opportunity to observe ME/CFS in the wild. Life is pretty harsh for animals and anything with ME/CFS would go dead or disappear promptly. Pets, maybe. There is no concept of pet disability, so we'll never know. But I've seen plenty of sluggish cats!

ME/CFS has been around for a long time, with various different names. It could have been around since pre-historic time without name or records. We wouldn't know that one way or the other.

(Edited for clarification).

 

I live in the woods, with lots of wild animals around. Individual animals disappearing simply goes without notice, and I rarely encounter corpses (efficient scavengers here). A squirrel or hare with ME would likely get picked off by a predator pretty quickly. Prevalence in animals will have to wait until we find a biomarker.

 

All good points, thank you.

 

Plastics, and microplastics, are pretty much as old as life on this planet. Cellulose, wool, rubber, and shellac are all natural polymers. They're not different from modern plastics; shellac is polyester. So, humans evolved with microplastics in their environment. I hope someone studies ancient human (and animal ) remains for signs of natural microplastics.

One difference is that humans have had a long time to evolve to deal with natural microplastics, but haven't evolved a defense against nylon, teflon, etc.

I disagree with that. I've had numerous temporary remissions: an abrupt switch from full ME to full non-ME (and abruptly back again), so going back to baseline is possible.

I think it's most likely that at least part of the mechanism of ME will be discovered first, then figuring out which biological reactions are involved will take further research. Eventually they might have recommendations such as "if you have these genes, you should reduce your intake of these fatty acids and these other chemicals."

It may not be one environmental factor that causes a predilection to develop ME; it might be several, each contributing a small amount to the total set of changes that results in ME, and not the same set for everyone.

I agree with Jonathan Edwards in that there's no evidence supporting localized variations in prevalence of ME. Even ubiquitous modern chemicals have different concentrations in different parts of the world, but I'm unaware of any "hotspots" for ME. This also applies to EMFs, staring at computer screens, certain types of clothing, etc. I'll wait for statistical evidence of environmental factors before supporting that hypothesis.

We simply don't know whether the prevalence of ME has increased in modern times. The symptoms aren't distinct enough to be identified in historical records. Also, the lack of widespread networking meant that people might rarely meet another person who "feels worse the day after exertion", so PEM was assumed to be a personal failing, and not recorded.

 

This all makes sense and I'm pretty much out of energy to comment on anything, but thank you for your input.

Though just to reply to the "temporary remission" part: I've also had "temporary remission" from adderall. Relatedly, anyone with depression can get temporary remission with MDMA. Can you be sure the symptoms weren't just temporarily masked? I'm not arguing remission isn't possible in this case, potentially with much better drugs than adderall. I'm just suggesting a root anatomical "switch" that can't be "unswitched". Not even saying it's likely, just possible. I'm hopeful it’s not the case!

 

I think for this it's important to mention that ME/CFS is a "young people disease", at least compared to more common health problems, in the sense that onset typically occurs early in life https://www.frontiersin.org/articles/10.3389/fped.2018.00412/full. From what I've seen the age of onset appears to be similar to that of MS and other autoimmune diseases with a similar age of onset, however none of these have stopped existing due to evolutionary pressure, which is probably a far to simplified view of the problem at hand as evolution seems to be far more complex than a simple and easy selection processes. There's certainly animals where "sluggishness" has been the reason for successful survival, many of these are almost constantly sluggish. Does that have anything to do with ME/CFS? I have no reason to think so. I don’t think we can say anything sensible about the role of ME/CFS in animals. It’s assumed that the only species we know of that develops MS are humans and we know that risk genes for MS exist and similar that EBV seems to play some role, which would probably be a solid counterargument for “genes can’t play a role because we haven’t seen animals with ME/CFS”.

Similarly most other arguments in this "modern enviromental hypothesis" can probably be "debunked" by looking at MS. I don't think anybody believes that ME/CFS is purely genetic in the sense that one gene or a combination of genes completely determines whether you develop ME/CFS or not. Similarly I don't think anybody believes in such a thing as "one cause" in the sense of a logical relationship between "Event A" occuring implies that "Event B" occurs and that, that is the end of the story.

I think unless studies, hopefully DecodeME will show first clues, reveal better evidence we have to accept that the only thing we know is that there might be risk factors for certain people, such as glandular fever, that possibly there's a genetic component, but that for the largest majority everything for now appears to be and might be random, similar to how things look like for better studies diseases such as the largest majority of autoimmune diseases.

This thread reminded me of the recent thread The causes that aren't genetic or pathogenic where similar arguments had been discussed.

 

I don’t know either, but I think it will might an awfully long-lasting task that requires a tremendous amount of funding. From what I recall Ascherios highly cited EBV-MS study spanned across a timeframe of roughly 35 years https://www.science.org/doi/10.1126/science.abj8222 with the protocol being published 20 years before the results https://jamanetwork.com/journals/jama/article-abstract/194503. I feel something similar would probably be needed for ME/CFS and given such large efforts required I see little reason why one should focus on "modern environmental factors" instead of just running a study that looks whether it can identify any factors at all and that simultaneously collects a lot of other data we are currently missing for ME/CFS.

I hope that studies such as DecodeME can unveil evidence that than helps us further and similarly that we are able to ensure that studies that are already collecting this kind of data by looking at other diseases look at ME/CFS as well (for example it seems Ascherio was considering looking at ME/CFS as well but decided against it due to the additional effort and resources required).

 

Yes, that does make sense, thanks.

 

All 3 charts seem to show the majority of diagnoses are past the age of 40. What am I supposed to look at? Maybe we have different definition of "young"?

That's different though. They evolved to be sluggish; they are adapted. Animals that didn't evolve to be sluggish but are because of disease or injury are not going to survive long.

 

Upps then I posted the wrong study, I thought it also contained something about age of onset, I agree that onsets past the age of 40 isn't young (to see what the data of study means in terms of ME/CFS ages one probably would have to compare it to same data of the average population and see if they are younger since ME/CFS is a non-deadly disease). I recall different studies looking at onset age that had found 2 peaks of onset age, one somewhere around teenhood and another around 30 years of age but can't find it now (I only found https://www.ncbi.nlm.nih.gov/books/NBK284897/# stating that average age of onset is 33), with the largest majority of onsets occuring before the age of 40 and hardly any onsets occuring past the age of 55.

That seems right to me and that's why I also said "I have no reason to think it has anything to with ME/CFS". Perhaps as you better put it my argument is entirely pointless as its entirely different things. I don't know anything about evolution, but does that automatically mean that we can assume all of them evolved to become sluggish (in my head I was thinking something along the lines of it may be that sometimes sluggishness could be favoured for other reasons, for example an ME/CFS genetic disposition yielding "a sluggishness state" might be favourable to remain present in some animals if the same genes offer protection against cancer or something of that sort)?

 

Also evolution is not always about single issues. Often things are tied together, getting rid of one apparently undesirable trait might have a knock on effect on a desirable trait. A good example might be the cost of giving birth to children with such large heads, not great for mothers, but presumably the associated increase in brain size is presumably good for humanity as a whole.

Alternatively evolution can select for some very foolish things such as the peacock’s tail that is presumably a result of run away mate selection, certainly it does not give the individual peacock any added survival chances, just better chances of reproducing.