Modern environmental factors

[forestglip]

I wanted to make a thread for environmental causes of ME because I have very high certainty (Edit: changing to "fairly high certainty") that the answer will ultimately lie in the modern environment - for ME, and likely for most chronic conditions. Traditional treatments like medications will be band-aids, useful to mask or slow our modern environment relentlessly destroying our bodies. At best, they will give us clues about where to look in the environment. But drugs likely won't fix the root cause.

Why is ME not just genetic? Because it doesn't make sense in terms of evolution. At least 1 in 200 people have ME. Living in the harsh conditions that humans would have faced for the hundreds of thousands of years before the abundance we now enjoy, any human with ME would have had a massive survival and reproductive disadvantage, and would have been unlikely to pass those genes on. Their whole tribe would be at a disadvantage. Imagine a prehistoric tribe needing to feed, care for, and protect a severe ME sufferer for a lifetime. The tribes that don't have a massive drain on their time, resources, and ability to travel would have had a massive advantage and outcompeted them.

It is possible there were sporadic ME sufferers back then. But those people likely did not often pass their genes very far through the generations.

Is it possible there's some wonkiness with genetics and evolution that could explain this? Sure. Maybe the ME gene was present in people in every tribe and could not be removed from our genetics for some reason. Maybe bonding over helping a sick person increased social connections and did provide a weird advantage. So I'm not 100% sure about any of this, but my intuition says the gene being selected against is more plausible.

Another argument against pure genetic cause: do we know of any other species that have anything like ME in the wild? Of course the wild is enormous and we can't be certain. But have we found any evidence at all of a species of bird, or groundhog, or chimp, where it is common that a significant fraction of the population never leaves their nest or burrow? Where they always act sluggish? If so, I'd love to hear about it. If not, what's the chance that humans were the only species blessed with this seemingly pointless mutation?

Although, I'm not so sure many people are arguing for pure genetics being the root cause. I just wanted to cover all my bases.

What many do seem to be predicting though is that the cause is an infectious pathogen - a virus, bacteria, or fungus.

Do I think the root cause could be one of these? Sure. It counts as a modern environmental factor. A recent mutation could have turned a strain into an ME causing strain.

Do I think there could be multiple pathogen root causes - completely different species - that could bring about ME totally separately? Going back to evolution, this seems too unlikely.

Viruses, bacteria, and fungi have been a part of the human environment for all of our species' history.

Suppose it's common for multiple pathogens to cause ME. In this case, those humans who couldn't fight the infection wouldn't have survived and passed on their susceptibility. We know there are humans today that don't get ME. In the past, these are the ones that would have passed on their genes, until ME was rarely seen.

Either that, or in recent history, multiple - completely different - pathogens suddenly started separately mutating to cause this condition. This seems very statistically unlikely.

If it's a pathogen, it will likely be one species or family. Maybe two if we got really unlikely. Not EBV and mold and HSV2 and SARS-CoV-2 and poliovirus and all the other suspects.

What (I'm pretty sure) it will be: genetics and a modern environmental trigger. Our environment is extremely different from that of our prehistoric ancestors. Thousands of chemicals never before seen in the history of the Earth have been created and put into our air, water, and food, whether purposely or not. Every person on Earth is now part microplastic. The average modern human's diet is very different from our ancestors diets.

The body exists in a delicate homeostasis, and we're throwing the kitchen sink filled with all sorts of toxic sludge at it constantly, and the sink is getting more ingredients added every day. Plenty of industrial chemicals cause fast onset disease and death. We notice and take them off the market or stick a warning on the safety data sheet. Maybe we'll even eventually notice a few that cause some long term disease, like asbestos causing lung cancer. But how many haven't we noticed yet? How many are so slow and insidious in their destruction of the body that they easily fly under the radar?

As opposed to pathogens, I think more than one new chemical can be a root cause. With pathogens, it would seem strange for multiple organisms we've lived alongside for all of prehistory to simultaneously mutate to cause ME at the same time that a much more convenient, plausible target appears on the scene - the colossal change from the prehistoric environment to the modern environment. And when there are thousands, maybe millions, of new chemicals in this new environment, I don't doubt that many different chemicals are shaped just right to jam up the works.

And genetics is involved because most everyone experiences the same new chemical environment, but only some are susceptible. These genes are around now because they weren't an issue in the prehistoric environment.

Personally, mostly based on intuition, I think one of the main, if not the only root cause is diet, with a high likelihood that high carbohydrate intake plays a large part. This is based on a large number of anecdotes I've read of ketogenic diets helping with chronic conditions. And it is also based on evolutionary diets often being theorized to be basically ketogenic - mostly meat, almost no sugar.

But I'm far from certain about this and am not equipped to debate the science of ketogenic diets. Just wanted to add this as my gut says diet is where a lot of the focus should be.

Now if we can pinpoint the environmental trigger, this would potentially lead to the easiest, safest, and most effective treatment for ME we could hope for.

Easiest - It might be simply banning a chemical from being produced.

Safest - Virtually all drugs have side effects. Avoiding ingesting poison does not have side effects.

Most effective - Drugs will most likely only be masking the symptoms, hoping they don't find a way to get through our almost certainly imperfect mask. Removing the environmental trigger will pull the disease out at the base, preventing any downstream harms from slipping through.

I'll add the caveat that the environment might have messed people up permanently after exposure, and removing the initial cause doesn't bring the sick back to baseline. In this case, drugs or alternative treatments will be necessary.

But this doesn't negate placing huge importance on figuring out what the environmental factor is. We don't know if it's permanent, and even if it is, finding it would inform design of the treatment. And the knowledge would prevent the next generation from falling victim to it.

Anyway, given all of the above, what do we do? How do we find the environmental triggers that might be causing ME months or years after exposure? Or causing it due to constant, almost undetectably low, exposure?

I don't know. But that's what researchers should be using a lot of resources on.

I would love for people here to suggest avenues for doing this. Maybe the most effective types of observational/interventional studies to get answers. Or the researchers/organizations best poised to find the answer. Or the researchers who already *have* found the answer, but the world isn't listening.

 

[Jonathan Edwards]

These are all relevant questions to ask, but the causation of disease is more complex than just bad genes and environment. A major third class of factor is internal stochastic - random events generated from within. These are important in most autoimmune diseases and of course cancer. We are all exposed to the sun but developing melanoma also involves random internal events. In the immune system random events are self-generating, not even responses to environment.

Genes that predispose to disease are well recognised and are retained in populations despite evolution. The best example is HLA-B27. The immune system has evolved so that within a population different individuals have different strategies for coping with infections - the MHC HLA genes are polymorphic so that we all have a different selection of these 'tissue type' genes. It is assumed that this means that for any new infection at least some members of the community will form strong immunity and e.g. evade tricks by viruses to mimic host receptors. HLA-B27 is very good at protecting people against, for instance, the development of AIDS following HIV infection, but the downside is that it can lead to an overreactive process producing ankylosing spondylitis or Reiter's disease. Reiter's disease can be triggered by a range of organisms so we have a model for that situation well known.

If polluting chemicals were responsible for ME/CFS I would expect to see clear differences in prevalence in different countries and regions of a sort that as far as I know we do not. Similarly for diet - diets vary greatly between communities within a country and there is no evidence for ME/CFS being specific to any such community.

I do agree that prevention makes a lot more sense than treatment. We could have prevented the Covid pandemic. It would never have started if safety measures in the Wuhan lab had been adequate, very likely. And in January 2020 it was perfectly possible to close the pandemic down. The Chinese did it and in many Western countries we showed you could eradicate it and then stupidly decided not to bother after all. The irony is that the resistance to taking the virus seriously seemed to be driven by exactly the same popular anecdotes as drive fashions in diet and objections to radio masts!!

 

[tornandfrayed]

I don't think there's a case that the genes predisposing towards ME would have been likely to be mostly eradicated. Since the prime age for onset starts in the mid-twenties, in the past and in many societies today, the majority would have started a family before becoming ill.

 

[FMMM1]

I don't think there's a case that the genes predisposing towards ME would have been likely to be mostly eradicated. Since the prime age for onset starts in the mid-twenties, in the past and in many societies today, the majority would have started a family before becoming ill.

I recall MEAction’s Jaime Seltzer using the term "menarche"* i.e. to describe age of onset. The only data I recall was the (fairly) famous Norwegian study**
Also, I wonder if the age of onset was a factor in Jonas Bergquist doing a hormone study -- looking for hormone dysregulation?

I guess the age of onset of schizophrenia is roughly the same as the earlier "peak"** suggested by the Norwegian study - even if it is though, may not be that helpful i.e. since schizophrenia is also poorly understood!

*"The major landmark of puberty for females is menarche, the onset of menstruation, which occurs on average between ages 12 and 13."
**"The incidence rate varied strongly with age for both sexes, with a first peak in the age group 10 to 19 years and a second peak in the age group 30 to 39 years." - Bakken - https://link.springer.com/article/10.1186/s12916-014-0167-5

 

[forestglip]

These are all relevant questions to ask, but the causation of disease is more complex than just bad genes and environment. A major third class of factor is internal stochastic - random events generated from within. These are important in most autoimmune diseases and of course cancer. We are all exposed to the sun but developing melanoma also involves random internal events. In the immune system random events are self-generating, not even responses to environment.

I don't discount random internal events, and would be happy to say "genes + environment + random internal events" is the cause. Though, I don't think these random events by themselves would be the main or only cause, except in rare circumstances. I haven't extensively studied paleolithic humans, or even more recent humans we have records for, but it's hard to imagine this many individuals becoming sick for the rest of their lives. And why don't we see this same disease state in any wild animals? (Although, again, correct me if we do.)

As far as I know, genetics can protect against random internal events as well, and should have selected against those more susceptible. At least to a level much lower than 1 in 200, I think.

I posit that the environment can decrease tolerance to these random events. For example, many internal events can be dealt with by the body, like randomly occuring cancer cells. Toxic chemicals can impair the immune system that seeks out and destroys these cells.

If polluting chemicals were responsible for ME/CFS I would expect to see clear differences in prevalence in different countries and regions of a sort that as far as I know we do not. Similarly for diet - diets vary greatly between communities within a country and there is no evidence for ME/CFS being specific to any such community.

This is true, and I don't have a satisfactory answer. Maybe it's a superlight chemical that has been uniformly distributed around the world. (Though why aren't animals getting sick then.) Maybe it only takes a tiny bit of exposure that most people get at least once, like a chemical involved in sugar processing.

I haven't looked into many studies on prevalence of ME around the world, but it'd be interesting to see if there are any hotspots or places devoid of ME.

I don't think there's a case that the genes predisposing towards ME would have been likely to be mostly eradicated. Since the prime age for onset starts in the mid-twenties, in the past and in many societies today, the majority would have started a family before becoming ill.

For those where onset is after having children, it's true they've passed on their genes for the moment. But then they get sick, and their whole tribe is worse off. Everyone in the tribe needs to do more work to secure enough food for the perpetually tired person, to protect against threats, to make accomodations for travel to new hunting/gathering grounds. If they are competing with a nearby tribe that does not have people getting ME, the other tribes would likely have a significant survival advantage in the long term, passing more genes down the generations.

 

[FMMM1]

Derek Pheby [Professor of Epidemiology?] comes to mind - if there was any clear evidence, re environmental factors, then I guess Derek would have spotted the opportunity!

One thing that's struck me re the "discovery" [they were testing the hypothesis] that roughly 29 out of 30 cases of MS follow EBV infection was how did they predict the link given that roughly:

• 90%+ of the general population have had EBV; and
• 100%+ of people with MS have had EBV;

not that much difference but perhaps enough?
Just Googled & there's an article on this*!

Luckily there are hypothesis free ways to try to identify the cause of ME/CFS i.e.:

• common variant genetic studies (GWAS - like DecodeME) & potentially rare variant studies whole genome sequence studies;
• metabolomics - check out Dr Li's [Jackson Laboratory] presentation in the NIH metabolism webinar.

If there were biomarkers for ME/CFS then perhaps the environmental factors (if any) would be more obvious - as per MS/EBV link!


*[https://med.stanford.edu/news/all-news/2022/01/epstein-barr-virus-multiple-sclerosis.html#:~:text=MS and viruses: an elusive connection&text=In fact, more than 99,with 94% of healthy individuals.]

 

[forestglip]

If there were biomarkers for ME/CFS then perhaps the environmental factors (if any) would be more obvious - as per MS/EBV link!

That's true, and I think the work should continue. But I think we should hedge our bets in case it is significantly environmental because trying to play detective with genes and blood feels like a much more roundabout, murky way of pinpointing an environmental cause, versus trying to see the connection directly (e.g. epidemiology). Maybe I'm wrong and the biomarker way will be easier, but I think the direct search for an environmental factor should at least get a pretty significant chunk of resources.

Derek Pheby [Professor of Epidemiology?] comes to mind - if there was any clear evidence, re environmental factors, then I guess Derek would have spotted the opportunity!

Thanks, I'll look into this person!

 

[Jonathan Edwards]

As far as I know, genetics can protect against random internal events as well, and should have selected against those more susceptible. At least to a level much lower than 1 in 200, I think.

I think a lot of these arguments could be applied equally to the autoimmune and auto inflammatory diseases. Interestingly, it seems that most of these indicate a tolerance of somewhere around 1/100-1/1000 (e.g. RA and lupus). That includes Crohn's disease, ulcerative colitis, ankylosing spondylitis, Hashimoto's hypothyroidism, Graves's hyperthryroidism, pernicious anaemia, type I diabetes, multiple sclerosis and so on.

 

[Jonathan Edwards]

I posit that the environment can decrease tolerance to these random events. For example, many internal events can be dealt with by the body, like randomly occuring cancer cells. Toxic chemicals can impair the immune system that seeks out and destroys these cells.

Except that we don't have any epidemiological patterns to fit with that as far as I can see. There ought to be hot spots.

 

[FMMM1]

That's true, and I think the work should continue. But I think we should hedge our bets in case it is significantly environmental because trying to play detective with genes and blood feels like a much more roundabout, murky way of pinpointing an environmental cause, versus trying to see the connection directly (e.g. epidemiology). Maybe I'm wrong and the biomarker way will be easier, but I think the direct search for an environmental factor should at least get a pretty significant chunk of resources.

As per Jonathan above - we don't have anything environmental to investigate! OMF looked at (toxic) heavy metals (small study - nothing) incidence of prior infections (small study - nothing) --- think Ian Lipkin looked at exposure to pathogens (larger study but still nothing). Only thing I can think of is the pathogen associated with goats in Holland - Q Fever - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322078/
I'd be interested to know what the genetic signals for Q Fever are i.e. via a large genetic study [like DecodeME] then comparing that to ME/CFS.

Thanks, I'll look into this person [Derek Pheby]!

Sadly Derek Pheby died a few years ago but perhaps check out his work e.g. as part of EUROMENE.

 

[forestglip]

I think a lot of these arguments could be applied equally to the autoimmune and auto inflammatory diseases.

Yes, I don't think there's anything special about ME in this regard. Different genetics among the population could let the environment mess us up in different ways.

Except that we don't have any epidemiological patterns to fit with that as far as I can see. There ought to be hot spots.

That's unfortunate and would be the first place I'd look if I was pursuing an environmental factor. Though do we have any data on the incidence of ME in any of the few remaining primitive/semi-primitive populations, like the 35,000 Yonomami people of South America?

 

[forestglip]

Sadly Derek Pheby died a few years ago but perhaps check out his work e.g. as part of EUROMENE.

Systematic Review of the Epidemiological Burden of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Across Europe: Current Evidence and EUROMENE Research Recommendations for Epidemiology, 2020

Only three papers on ME/CFS prevalence in Europe were included in this review. Two of these studies were conducted in the United Kingdom. [Iceland was the third.] The prevalence estimates from Europe appear to be in the same range as those from other continents. The current review shows that in Europe only two studies have aimed at estimating the incidence of ME/CFS, one in adults and the other in adolescents. [Both in the UK] ... Overall, as expected, studies on prevalence and incidence of ME/CFS in Europe were scarce.

It seems they weren't able to get much high quality data for Europe in 2020.

 

[FMMM1]

Systematic Review of the Epidemiological Burden of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Across Europe: Current Evidence and EUROMENE Research Recommendations for Epidemiology, 2020



It seems they weren't able to get much high quality data for Europe in 2020.

Thanks - could you send a link to this?

 

[forestglip]

Thanks - could you send a link to this?

You should be able to click the title in my last message. But here's the URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7290765/

 

[Mij]

When I saw a virologist years ago and all my lymphocytes (CD4, CD8 et) were way below normal range, he told me that I was born with it.
I don't know if there's any truth to that or he just wanted me out of his clinic because I was asking too many questions.

I was a perfectly healthy person before M.E and never caught a cold or flu. I don't recall either of my parents ever having a cold or flu either.

 

[forestglip]

To add a bit, if my reasoning for it being unlikely that multiple different pathogens can be the root cause has some merit, then COVID would almost certainly not be a root cause, and is only exploiting a weakness opened up by previous insults to the body. Therefore, it may be highly valuable to look at epidemiological data on Long COVID specifically, because there are so many simultaneous, new cases of ME. Even if there is current epidemiological data on regions around the world, a lot of the developed world is pretty environmentally homogenous, in terms of industrial chemicals in their foods and other goods, and even diet, at least compared to ancestral diets, and these are probably the regions most likely to be in a position to provide data on incidence. The important information might be hidden in the regions not intertwined as much in global commerce, and that lack the infrastructure needed for the study of incidence.

Even if I'm wrong, and environment+genetics is not the primary cause in developing ME and other chronic illnesses, there is still a very good chance that environment at least plays a role and increases risk, even slightly, from other possible causes, like pure genetics or random internal processes. Pinpointing which exact environmental causes make things worse, if there are any, can help to find solutions to these other possible causes.

 

[forestglip]

CDC: Notes from the Field: Long COVID Prevalence Among Adults — United States, 2022

Investigation and Outcomes
CDC analyzed data from noninstitutionalized U.S. adults aged ≥18 years participating in the 2022 Behavioral Risk Factor Surveillance System (BRFSS), a population-based cross-sectional survey (4). Respondents were sampled using random digit dialing of both landline and cellular telephones. Self-reported age, sex, previous COVID-19 diagnosis,† and ever having experienced Long COVID were ascertained via telephone interview. Long COVID was defined as the self-report of any symptoms lasting ≥3 months that were not present before having COVID-19. CDC estimated weighted age- and sex-standardized prevalence with a 95% CI of ever having experienced Long COVID among all adults nationally, irrespective of COVID-19 history, in the 50 states, the District of Columbia, Guam, Puerto Rico, and the U.S. Virgin Islands. Estimates were standardized to the 2020 U.S. Census Bureau population of noninstitutionalized, civilian adults. Sex-specific weights by age group were applied for persons aged 18–44, 45–64, and ≥65 years. Analyses were conducted using SAS-callable SUDAAN (version 9.4; RTI International) and account for complex survey design. Prevalence estimates were divided into quintiles. This activity was reviewed by CDC, deemed not research, and was conducted consistent with applicable federal law and CDC policy.

Preliminary Conclusions and Analysis
Nationally, 6.4% of noninstitutionalized U.S. adults reported ever having experienced Long COVID (95% CI = 6.2%–6.5%) (Supplementary Table, https://stacks.cdc.gov/view/cdc/147385). The weighted age- and sex-standardized prevalence ranged from 1.9% (95% CI = 0.9%–4.1%) for the U.S. Virgin Islands to 10.6% (95% CI = 9.5%–11.8%) for West Virginia (Figure) and exceeded 8.8% (the highest prevalence quintile cutoff) in seven states. Prevalences tended to be lower in New England and the Pacific and higher in the South, Midwest, and West.¶

This study was subject to some limitations. BRFSS did not capture treatment during acute COVID infection, time since COVID-19 illness, or duration or severity of symptoms, which could influence the reported prevalence of Long COVID. In addition, information about COVID-19 vaccination was only available for a subset of jurisdictions and is not included in this report.

The findings in this report address an important data gap in knowledge about the prevalence of Long COVID. Given the increased health care needs among persons experiencing Long COVID (5), ongoing assessment of state- and territory-level prevalence data could guide policy, planning, or programming. State-level estimates might also help identify geographic disparities in Long COVID across the United States that could guide interventions to promote health equity.

Prevalence of reported experience of Long COVID among adults aged ≥18 years, by jurisdiction — Behavioral Risk Factor Surveillance System, United States, 2022

Abbreviations: DC = District of Columbia; GU = Guam; PR = Puerto Rico; USVI = U.S. Virgin Islands.

Very small samples for the three that showed a very low prevalence, though.

 

[rvallee]

Living in the harsh conditions that humans would have faced for the hundreds of thousands of years before the abundance we now enjoy, any human with ME would have had a massive survival and reproductive disadvantage, and would have been unlikely to pass those genes on. Their whole tribe would be at a disadvantage. Imagine a prehistoric tribe needing to feed, care for, and protect a severe ME sufferer for a lifetime. The tribes that don't have a massive drain on their time, resources, and ability to travel would have had a massive advantage and outcompeted them.

I'm not sure about that. ME data is unreliable, but although there is a bit of a peak in teenage years, recovery odds are higher. It's really around mid-20s that prolonged disability starts increasing. In those days, that's plenty of time to be, hell, grandparent. In the LC community I often see people's ages, and although there are some below 20, it's pretty rare. Or maybe they're not as vocal about it.

That teenage peak is at a time when help is more likely to be motivated, whereas in adulthood, when it becomes unlikely, plenty of children can be had by that time.

As for disadvantaging the tribe, seeing how modern society treats us, I have no doubt that sick people back then were abandoned most of the time. 'Used to it' probably doesn't really give it justice, but mortality rates back then were atrocious. If it's short enough, and we know from LC that most recover within 3 months, that probably still works out, people are willing to help short term.

So there is an evolutionary pressure here, but it's probably not enough to be more than a slight one. Most humans born in that time died before they reached puberty. There were simply too many other forms of evolutionary pressures for this to matter much.

Ironically, that pressure is probably far higher in modern times, but it hasn't been long enough for it to have an impact.

 

[forestglip]

I'm not sure about that. ME data is unreliable, but although there is a bit of a peak in teenage years, recovery odds are higher. It's really around mid-20s that prolonged disability starts increasing. In those days, that's plenty of time to be, hell, grandparent. In the LC community I often see people's ages, and although there are some below 20, it's pretty rare. Or maybe they're not as vocal about it.

That teenage peak is at a time when help is more likely to be motivated, whereas in adulthood, when it becomes unlikely, plenty of children can be had by that time.

As for disadvantaging the tribe, seeing how modern society treats us, I have no doubt that sick people back then were abandoned most of the time. 'Used to it' probably doesn't really give it justice, but mortality rates back then were atrocious. If it's short enough, and we know from LC that most recover within 3 months, that probably still works out, people are willing to help short term.

So there is an evolutionary pressure here, but it's probably not enough to be more than a slight one. Most humans born in that time died before they reached puberty. There were simply too many other forms of evolutionary pressures for this to matter much.

That's totally possible, thanks for the perspective.

One of my main objections would be that it as far as I can tell, there is no evidence of significant prevalence of any ME/CFS-like disease in any wild animals. I asked a chatbot if they knew of anything similar:

"are there any example of ME/CFS like diseases in wild animals, with significant prevalence?"

Claude.ai:

There are no well-documented examples of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)-like illnesses in wild animal populations with significant prevalence. ME/CFS is a complex, multisystem disorder that is not fully understood, and its potential occurrence in animals is not well-studied.

However, there are a few examples of conditions in certain animal species that share some similarities with ME/CFS, but they are not considered direct equivalents:

1. Post-viral fatigue syndrome in horses: Some horses have been observed to develop a prolonged state of lethargy, weakness, and exercise intolerance after a viral infection, similar to the post-viral onset seen in some ME/CFS cases. However, this condition is not well-characterized, and its prevalence is unknown.
2. Sickness behavior in various animal species: Sickness behavior is a coordinated set of behavioral changes that occurs in animals during the course of an infection or illness, including lethargy, fatigue, and reduced activity levels. This is thought to be an adaptive response to conserve energy for fighting the infection. While not identical to ME/CFS, some researchers have drawn parallels between the two conditions.
3. Chronic wasting disease in cervids (deer, elk, and moose): Chronic wasting disease is a prion disease that affects cervids and causes progressive weight loss, behavioral changes, and eventual death. Some researchers have suggested that the fatigue and behavioral changes observed in these animals could be considered analogous to ME/CFS, but the underlying mechanisms are different.

It is important to note that these examples are not perfect analogues of ME/CFS, and the prevalence of such conditions in wild animal populations is not well-documented. ME/CFS is a complex disorder with multiple potential triggers and a range of symptoms, making it difficult to establish clear equivalents in animal models.

Furthermore, the diagnosis of ME/CFS in humans relies heavily on self-reported symptoms and subjective experiences, which are challenging to assess in non-human animals. As such, the lack of well-documented cases of ME/CFS-like illnesses in wild animals could be due to the difficulty in recognizing and diagnosing such conditions in these populations.

I bolded the last part, which is an important objection, but there are external signs of ME, like barely leaving home, which we should be able to witness in animals. Although it's very possible we haven't looked hard enough.

For post-viral conditions in horses, I assume it's referring to domesticated horses, which are often being fed industrial chemicals and unnatural diets.

What's the chance that humans are completely unique of all the animals we see?

Apart from that, sure maybe they just kicked out the permanently severe ME sufferers from the tribe. But, I'm not so confident that it's only a slight pressure. Grandparents theoretically played an important role for the tribe (or they probably wouldn't live for so long after reproducing), helping with non-physically intensive tasks, babysitting during hunts, etc. If they were kicking members out, or people were too sick to help at all, that could have significantly hampered their survival chances. Yes, maybe it paled in comparison to total mortality, but this disability/mortality seems wholly unnecessary, and should have been selected against, and it's likely some people's genes today protect them from ME (I think there are studies showing increased risk in family members of ME patients), so it shouldn't have been impossible to remove from the gene pool.

I think the main forms of mortality would have been injuries and acute disease. Both of these are also common in wild animals, and at least injuries were arguably an unavoidable risk of necessary survival activities.

And if encompassing chronic disease as a whole, instead of just ME, then how much more significant is the survival disadvantage? It's hard to imagine that left and right people were getting ME, Parkinson's, Alzheimer's, arthritis, cancer, etc. Without modern medicine, the total burden from these conditions could possibly have rivaled or exceeded that of more "normal" mortality.

 

[Jonathan Edwards]

Yes, I don't think there's anything special about ME in this regard. Different genetics among the population could let the environment mess us up in different ways.

But none of those conditions has anything much to do with environmental factors as far as we know. Smoking predisposes to RA but the others seem to be largely genes + stochastic.