Modern environmental factors

[forestglip]

Linking a person, @Cybergreen91, who argues that mold, VOCs, and/or nanoparticles, such as titanium dioxide, are likely environmental causes of ME/CFS and other chronic illnesses. No idea if his science is sound.

S4ME thread: The Role of Insoluble Nanoparticles and Other Environmental Triggers in Chronic Illness

Youtube channel

The main video explaining his theory, and his explanation in that thread, are very long, so here is an AI generated summary of just the scientific evidence in the video:

• Claim: Epithelial barrier damage leads to susceptibility to environmental toxins, causing chronic illnesses like CFS, fibromyalgia, MCS, POTS, and long COVID. Evidence: Discusses how epithelial cells form a protective barrier, and damage to this barrier from factors like chemical exposures, viral infections, or connective tissue disorders can allow toxins to enter the body.

• Claim: Inhalation of insoluble nanoparticles like titanium dioxide causes mechanical damage to tissues, leading to fatigue and pain. Evidence: Cites studies showing titanium dioxide causes separation of muscle fibers, blood vessel leakage, and a chronic fatigue-like illness in mice. Also presents personal photos he believes demonstrate skin and capillary abnormalities from nanoparticle exposure.

• Claim: Titanium dioxide exposure impairs lymphatic function and leads to metabolic disturbances. Evidence: References a study finding titanium dioxide primarily resides in lymph nodes in rats. Another rat study showed organic acid levels initially spiked then chronically declined after titanium dioxide exposure, indicating hypometabolic function.

• Claim: Amyloid fibers and microclots in long COVID/CFS may be related to titanium dioxide nanoparticles. Evidence: Discusses a study showing fibrinogen irreversibly binds to titanium dioxide, possibly leading to microclot formation. Presents personal test results showing presence of microclots despite not having long COVID.

• Claim: Transmission electron microscopy of his tissue biopsy demonstrates abnormalities in Schwann cells and keratinocytes, supporting his proposed mechanism. Evidence: TEM images show large masses and glycogen deposits in the cytoplasm of Schwann cells and keratinocytes. Also believes he sees myelin pockets and possible nanoparticles in the images.

 

[forestglip]

Potential links to cholinesterase-inhibiting chemicals in both gulf war illness and psychiatric disorders.

Acetylcholinesterase inhibitor exposures as an initiating factor in the development of Gulf War Illness, a chronic neuroimmune disorder in deployed veterans, Michalovicz et al, July 2020

Gulf War Illness (GWI) is a chronic multi-symptom disorder, characterized by symptoms such as fatigue, pain, cognitive and memory impairment, respiratory, skin and gastrointestinal problems, that is experienced by approximately one-third of 1991 Gulf War veterans. Over the nearly three decades since the end of the war, investigators have worked to elucidate the initiating factors and underlying causes of GWI. A significant portion of this research has indicated a strong correlation between GWI and exposure to a number of different acetycholinesterase inhibitors (AChEIs) in theater, such as sarin and cyclosarin nerve agents, chlorpyrifos and dichlorvos pesticides, and the anti-nerve agent prophylactic pyridostigmine bromide. Through studying these exposures and their relationship to the symptoms presented by ill veterans, it has become increasingly apparent that GWI is the likely result of an underlying neuroimmune disorder. While evidence indicates that AChEIs are a key exposure in the development of GWI, particularly organophosphate AChEIs, the mechanism(s) by which these chemicals instigate illness appears to be related to "off-target", non-cholinergic effects. In this review, we will discuss the role of AChEI exposure in the development and persistence of GWI; in particular, how these chemicals, combined with other exposures, have led to a chronic neuroimmune disorder. This article is part of the special issue entitled 'Acetylcholinesterase Inhibitors: From Bench to Bedside to Battlefield'.

Depressive symptoms and suicide attempts among farmers exposed to pesticides, Zheng et al, June 2024

Pesticides safeguard crop health but may diminish cholinesterase activity in farmers, potentially leading to psychiatric disorders like depression and suicide attempts. This study, with 453 participants (225 pesticide-exposed farmers, 228 non-farmers) in Almería, Spain, aimed to investigate the presence of depressive symptoms and suicide attempts, the decrease acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activity, and their relationship with pesticide exposure in farmers. Depressive symptoms were evaluated using the Spanish adaptation of the Beck Depression Inventory, and blood samples were analyzed for AChE and BChE activity. Farmers showed significantly increased risk of moderate/severe depression and suicide attempts compared to non-farmers (OR = 2.18; p = 0.001), with highest risks observed among mancozeb users (OR = 2.76; p = 0.001 for depression) and malathion users (OR = 3.50; p = 0.001 for suicide attempts). Findings emphasize elevated depression and suicide risks among pesticide-exposed farmers, particularly associated with chlorpyrifos, mancozeb, and malathion exposure.

 

[forestglip]

Fluoroquinolone-induced serious, persistent, multisymptom adverse effects, Golomb et al, 2015

(Fluoroquinolones are a class of antibiotics. One example is ciprofloxacin.)

This study isn't about ME/CFS, it's just talking about a variety of symptoms from taking these drugs, but the delayed fatigue is possibly related.

We present a case series of four previously healthy, employed adults without significant prior medical history in each of whom symptoms developed while on fluoroquinolones (FQs), with progression that continued following discontinuation evolving to a severe, disabling multisymptom profile variably involving tendinopathy, muscle weakness, peripheral neuropathy, autonomic dysfunction, sleep disorder, cognitive dysfunction and psychiatric disturbance. Physicians and patients should be alert to the potential for FQ-induced severe disabling multisymptom pathology that may persist and progress following FQ use. Known induction by FQs of delayed mitochondrial toxicity provides a compatible mechanism, with symptom profiles (and documented mechanisms of FQ toxicity) compatible with the hypothesis of an exposure-induced mitochondrial neurogastrointestinal encephalomyopathy.

A 46-year-old man in vigorous good health, employed in a physically demanding, high responsibility job, was treated with 750 mg/day levofloxacin for 21 days for an unconfirmed diagnosis of epididymitis; during treatment, low-grade muscle aches and pains newly emerged. Muscle aches continued following FQ discontinuation, with progression and emergence of symptoms including fatigue, muscle weakness and atrophy, peripheral neuropathic and autonomic disturbances (tachycardia, bradycardia), CNS manifestations (cognition and mood), vision abnormalities, with gastrointestinal manifestations and intestinal motility issues. Initially, after FQ use, he experienced what he termed an ‘autonomic storm’ comprising tachycardia, accompanied by very low energy, depression and anxiety. His symptoms evolved with tendinopathy emerging at 9 months affecting the Achilles tendons, feet and knees, and producing tendon pain with exercise in an athlete who previously ran or biked 10 miles a day. Limitations due to pain, and later fatigue, progressed, necessitating progressive curtailing of his cycling from 10 to 6, 4, 3 then 0 miles/day. He switched to walking, which then also became difficult. He purchased an exercise cycle in an effort to remain active, but discontinued use, as aerobic exercise produced delayed fatigue and pain. He stated, “I would expend energy and then pay for it later.” Bilateral patellar and foot tendon as well as knee pain with walking emerged, requiring him to stop and sit after walking 100 feet. Muscle strength seemed initially relatively preserved (compared to sustained activities—eg, he could open jars that his wife found problematic), but 15–30 min after application of effort he would experience significant fatigue, and muscle strength deteriorated with time.

Potentially similar mechanism to ME/CFS PEM?

I found this through a Google Scholar search I was trying:

"case report" exercise OR exertion "delayed fatigue" -myalgic

Hoping to find case reports or studies where they are talking about some seemingly totally unrelated condition and maybe have never heard the term PEM, but where what they describe sounds a lot like PEM. I'm seeking connections to other conditions which might give clues.

The above seems to be the only relevant result for that specific search term though.

 

[Hutan]

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.

There is the example of Long Ebola. I am certainly no expert in the living conditions of the areas where there have been Ebola epidemics, but I suspect life there for many people is different to what it is for many S4ME members. And yet, we see a substantial incidence of ME/CFS-like illness after Ebola.

I do think though that it would be useful to investigate the incidence of ME/CFS (and Long Covid) in a range of communities where there has not been a lot of genetic mixing for some time and/or there are different environmental conditions. For example, is ME/CFS more or less common at high latitudes versus the equator?

ME/CFS is largely a disease of the middle-aged and older who are not likely to pass on their genes anyway.

As others have said, this is not true. It is primarily a disease of people of reproductive age. (It may also be a disease of older people, possibly even especially a disease of old people, but there are too many other (more acceptable) things to blame the ME/CFS symptoms on.)

I don't remember the details but the most useful incidence study is from Norway and it shows peaks in late adolescence and thirties roughly. We had a discussion about it maybe around 2018. The second peak in males may be an artefact but it looked real in females.

I think I've discussed this a few times. Here's one post, although possibly not my best one:
ME Epidemiology - prevalence, peak ages of onset and gender ratioThere are things about how the paediatric and adult health systems work in Norway that probably contributed to what I believe is an artefact of that one Norwegian report that is basically responsible for the 'twin peaks' idea.

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).

As others have said, it's likely that some of the things that contribute to a vulnerability to ME/CFS are actually strengths under other conditions. A particular type of immune response might result in a greater chance of survival, but a greater chance of ME/CFS. For some disease outbreaks, that tradeoff may be an evolutionary advantage.

 

[forestglip]

From Jarred Younger's weekly YouTube update, concerning pollution:

Then we have a project of weather and pollutants in ME/CFS. And this is a project being run by Chloe Jones, one of my graduate students - medical psychology graduate student. And it's pretty interesting - it uses people - ME/CFS patients who rate their fatigue every day and then we can look at Almanac information to know what the weather was doing on those days to see if anything predicts good days and bad days. And, you know, the sneak peek is, yes, there are some weather variables that fluctuate with good and bad days of ME/CFS, including some pollutant type variables, so that's going to be very interesting and could give some clues as to what provokes ME/CFS flares potentially.

 

[Hutan]

Hopefully they will consider the obvious issue with this, that activity correlates with the weather. A sunny day, especially in winter, is likely to have someone with mild or moderate ME/CFS being more active, getting outside. Then, they have the pay back of PEM, and, because weather reverts to the mean, those PEM days are more likely to be on bad weather days.

 

[Sean]

For me the big indisputable weather correlation is humid heat. Dry heat, within reason, is manageable. But when it gets humid (above ≈50%) as well as hot, the going gets very rough. Tropical summer, especially the pre-monsoon build-up, is bad enough for healthy people, but it is a lot tougher for any patient with thermo-regulation or -sensitivity issues.

Hence I live in air-con for 6 months of the year (Oct-Apr).

Best time of year for me is now, our southern tropical dry 'winter', especially the first half before its also gets dusty. The temps regularly still get into the low 30s C, but the humidity drops right down (currently about 30%, at 11am, and will fall further into the afternoon).

 

[forestglip]

If it turns out risk of ME or some other chronic illness is increased by chemicals which circulate in the blood, then maybe some modern day bloodletting is in order:

Effect of Plasma and Blood Donations on Levels of Perfluoroalkyl and Polyfluoroalkyl Substances in Firefighters in Australia: A Randomized Clinical Trial
Gasiorowski et al
8 April 2022

Abstract

Importance Elevated levels of blood perfluoroalkyl and polyfluoroalkyl substances (PFASs) have been associated with a range of adverse health outcomes. Firefighters have been exposed to PFASs in firefighting foams and have previously been shown to have higher PFAS levels in blood samples than the general population. No interventions have been shown to reduce PFAS levels.

Objective To examine the effect of blood or plasma donations on PFAS levels in firefighters in Australia.

Design, Setting, and Participants This 52-week, open-label, randomized clinical trial enrolled participants from May 23 to August 23, 2019. Participants were 285 Fire Rescue Victoria staff or contractors with serum levels of perfluorooctane sulfonate (PFOS) of 5 ng/mL or more who were eligible to donate blood, had not donated blood in the 3 months prior to randomization, and were able to provide written informed consent. Analysis was performed on an intention-to-treat basis from May to July 2021.

Interventions Firefighters with baseline PFOS levels of 5 ng/mL or more were randomly assigned to donate plasma every 6 weeks for 12 months, donate blood every 12 weeks for 12 months, or be observed only.

Main Outcomes and Measures The primary end points were changes in the serum PFOS and perfluorohexane sulfonic acid (PFHxS) levels after 12 months of plasma or blood donations or after observation only. Secondary end points included changes in serum PFAS levels from week 52 to week 64, changes in other PFASs, and changes in complete blood count, biochemistry, thyroid function, and lipid profile from screening to week 52.

Results A total of 285 firefighters (279 men [97.9%]; mean [SD] age, 53.0 [8.4] years) were enrolled; 95 were randomly assigned to donate plasma, 95 were randomly assigned to donate blood, and 95 were randomly assigned to be observed. The mean level of PFOS at 12 months was significantly reduced by plasma donation (–2.9 ng/mL; 95% CI, –3.6 to –2.3 ng/mL; P < .001) and blood donation (–1.1 ng/mL; 95% CI, –1.5 to –0.7 ng/mL; P < .001) but was unchanged in the observation group. The mean level of PFHxS was significantly reduced by plasma donation (–1.1 ng/mL; 95% CI, –1.6 to –0.7 ng/mL; P < .001), but no significant change was observed in the blood donation or observation groups. Analysis between groups indicated that plasma donation had a larger treatment effect than blood donation, but both were significantly more efficacious than observation in reducing PFAS levels.

Conclusions and Relevance Plasma and blood donations caused greater reductions in serum PFAS levels than observation alone over a 12-month period. Further research is needed to evaluate the clinical implications of these findings.



------

• After a year, levels of perfluorooctane sulfonate (PFOS) decreased by about 30% (eyeballing values from chart for this) with plasma donations every six weeks, and 10% with blood donation.
• Perfluorohexane sulfonic acid (PFHxS) decreased by about 28% with plasma donation, but did not decrease with blood donation.
• Perfluorooctanoic acid (PFOA) decreased by about 45% with plasma donation, but did not decrease with blood donation.

 

[forestglip]

Four Cases of Pesticide Poisoning, Presenting as “ME,” Treated with a Choline and Ascorbic Acid Mixture
John Richardson

Journal Of Chronic Fatigue Syndrome Volume 6, 2000 - Issue 2

Abstract
Objectives: 1. To demonstrate in four patients, in whom the correct diagnosis of pesticide poisoning had been missed, the injustices inflicted on them when they are told ME does not exist. 2. To show how closely the features of such poisoning, especially by organochlorines, resemble those of the much more classic ME which is usually due, at least in the author's practice in the northern region of the UK, to persistent enteroviral infection. 3. To draw attention to a new and apparently successful form of treatment with an oral mixture of choline and ascorbic acid. 4. To suggest reasons why this treatment merits further scientific investigation.

Setting: A charity based private practice involved in the investigation of viral mediated disease.

Subjects: Four patients, two male and two female, each referred with a diagnosis of ME.

Intervention: a. Samples of blood were sent to Biolab Medical Unit where a variety of pesticide residues, including the very persistent organochlorines, were identified and progress in detoxification was monitored, b. All four cases were treated orally with a choline and ascorbic acid mixture.

Results: After a variable number of months, during the early phase of which the blood levels of some of the toxins rose, possibly due to mobilization from fatty stores, all symptoms cleared as blood levels fell.

Key Messages: The term ME comprises a number of clinical features, characterizing a patient who is ill. To refuse to recognize their existence does the patient much injustice.

Some cases of ME may be found to have pesticide poisoning. The possibility of it should always be borne in mind. The source may be either in the UK or abroad. A positive enquiry and a single blood test will provide a diagnosis.

Organochlorines may persist in the body for many years, as may the symptoms derived from them.

A detoxification program based on oral administration of a choline and ascorbic acid mixture has shown much promise and deserves verification of its value.

Conclusions: Amongst the group of clinical features known as ME, the possibility of pesticide poisoning should always be borne in mind. Treatment with choline and ascorbic acid mixture is worth trying, pending its more formal investigation.

In my experience over 40 years before and since retirement from general practice, a persistent enteroviral infection is far more often the aetiological agent in ME/CFS in this region and the virus is usually of the Coxsackie group. Normally, most viral infections initiate antibody responses which quickly cut the illness short, whereas many pesticides are notoriously very persistent. In my experience of enteroviral infections, a small but important proportion of such infections do not clear up quickly but lead to months or years of illness, the classical ME/CFS. The clinical features of this are not usually exactly the same as those of pesticide poisoning but, as in Cases 1, 3 and 4, they can be remarkably similar. The best precaution against error is to insist on identifying the initiating virus by serological tests and always to bear in mind the possibility of pesticide intoxication. The four cases show the variety of pesticides used in different countries, including some that have been banned elsewhere. Proprietary preparations often contain a mixture of several. With increasing amounts of foreign travel and the increasing and proper attention to personal hygiene both here and abroad, it does not seem likely that cases of pesticide poisoning will become rare. Meanwhile it is easy to understand why, if the symptoms of some of the ‘‘Gulf War’’ and ‘‘Sheep Dip’’ cases are due to pesticide intoxication, they may persist for many years. It is certainly strange that, in the latest study (14) of the Gulf War Syndrome, although 69% of the men had been exposed to pesticides, no attempt seams to have been made to perform blood tests for evidence of persistent intoxication.

The four cases, summarized by AI:

• Case 1: 43-year-old male welder became acutely ill after work trip to South Korea where streets were sprayed at night to control vermin. Diagnosed with viral illness and anxiety but did not improve over 5 years. Blood tests showed elevated levels of polychlorinated biphenyls (PCBs). Treated with oral choline and ascorbic acid mixture, leading to 80% recovery within 7 months as PCB levels fell.

• Case 2: 38-year-old male carpenter developed ME-like symptoms after holiday in Turkey with heavy exposure to anti-mosquito spray. Blood tests showed variety of organochlorine pesticides. Treated with choline/ascorbic acid mixture, leading to complete recovery over 28 months as pesticide levels declined.

• Case 3: 35-year-old female diagnosed with post-viral fatigue. Later admitted spraying bedroom furniture with pesticides. Blood tests showed dieldrin, p-dichlorobenzene and mevin-phos. Cessation of exposure plus choline/ascorbic acid treatment led to symptom resolution over 8 months.

• Case 4: 33-year-old female developed ME-like illness after vacation in Turkey using anti-mosquito cream extensively. Blood showed high organochlorine and lindane levels. Improved over 4.5 months on choline/ascorbic acid as pesticide levels fell.

Study (Paywall)

-------------------

Book by the above author, John Richardson, available to borrow on Internet Archive:

Enteroviral and toxin mediated myalgic encephalomyelitis/chronic fatigue syndrome and other organ pathologies, 2001

This valuable book covers varied organ pathology in a wide range of syndromes induced by viral infection and toxin exposure. Enteroviral and Toxin Mediated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Other Organ Pathologies discusses such lethal problems as cardiomyopathy, liver failure, pancreatic cancer, brain tumors, and renal disease, as well as the debilitating disorders of myalgic encephalomyelitis/chronic fatigue syndrome and other post-viral syndromes. This essential text is profusely illustrated with photographs, photomicrographs, charts, EKGs, X-rays, and graphic depictions of other medical test results.

With case studies of individual patients and whole families, Enteroviral and Toxin Mediated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Other Organ Pathologies brings you the benefit of seeing the patients and their illnesses in the context of their lifestyles, work histories, and family medical history. Not a retrospective survey using medical records alone, this unique book is the result of Dr. Richardson's more than 45 years doing research with the prestigious Newcastle Research Group while engaged in General Family Practice.

The scope of this book includes:

• the complex relationship between host and virus
• the aftereffects of viral illnesses on various systems, including the cardiovascular, nervous, and endocrine
• discussions of varied effects of viral syndromes on different family members
• consideration of viral effects on mother and fetus during pregnancy
• ideas for treatment and further research

Enteroviral and Toxin Mediated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Other Organ Pathologies provides both powerful case studies and exciting theoretical considerations based on research. It is an essential tool for family physicians as well as researchers into post-viral syndromes and the effects of toxin exposure.

 

[forestglip]

MEpedia has some good information on Pesticide exposure link to ME/CFS.

In one study, Scottish sheep farmers using organophosphate-based sheep dip to protect their sheep against parasites were found to suffer much higher rates of myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS): the prevalence of ME/CFS in these farmers was 4 times the national UK average, implicating organophosphates as a probable causal factor in ME/CFS.[1][2] Farmers who used organophosphate-based sheep dip were also found to be 10,000 times more likely to suffer from mental health disorders.[3]

 

[forestglip]

American ME and CFS Society: What Causes ME/CFS?

"ENVIRONMENTAL CAUSES

• Organophosphates and other pesticides can trigger symptoms similar to ME/CFS
• Radiation exposure may be a catalyst for ME/CFS
• Toxins can cause mitochondrial impairment

Environmental toxins have frequently been implicated as possible causes of ME/CFS, particularly in patients with gradual onset. Dr. Majid Ali, a physician who believes that ME/CFS is caused by toxic overload, writes in his book, The Canary and Chronic Fatigue, that “chronic fatigue sufferers are human canaries—unique people who tolerate poorly the biologic stressors of the late 20th century.”

Dr. Martin Pall has noted that the symptoms of post-radiation syndrome are identical to those of ME/CFS. Alan Cocchetto, Medical Director of the National CFIDS Foundation, has identified some unique mitochondrial characteristics in his research that implicate low level radiation as the catalyst for some patients. As Dr. Pall’s NO/ONOO‾ model can also lead to mitochondrial defects, the two models may eventually prove to be similar, if not the same.

Pesticides are the primary focus of researchers investigating environmental causes of ME/CFS. A retrospective study conducted in Scotland, found that sheep farmers who had been exposed to organophosphates in sheep dips showed high prevalence of chronic fatigue and that higher chronic fatigue scores were associated with higher exposure to organophosphate pesticides.

Dunstan and colleagues found that serum levels of organochlorine (a chemical found in pesticides) was higher in ME/CFS than in controls. There were no significant differences in organochlorine levels between those ME/CFS patients with a history of toxic chemical exposure, and those without. The researchers concluded that the exclusion of patients from the CDC definition of ME/CFS on the basis of a history of exposure to toxic chemicals was not valid, and that low level organochlorine bioaccumulation might lead to the development of ME/CFS.

A third group of Scottish researchers led by Dr. Faisel Khan, found a link between ME/CFS, Gulf War Illness (GWI) and agricultural workers exposed to organophosphate pesticides. All three exhibited cholinergic abnormalities, however only the ME/CFS group showed abnormalities in the vascular system. They concluded that ME/CFS had a different etiology from either GWI or pesticide exposure.

Two later studies by the authors found that sensitivity to acetylcholine was restricted to those patients who fit descriptions for ME and post-viral fatigue syndromes, but not those for Gulf War Illness or for those exposed to organophosphate compounds, or those with fibromyalgia. (For recent developments see: Gulf War Illness: New Report Lauds Treatment Research, Confirms Toxic Causes.)

The authors were confident that the finding of increased sensitivity to acetylcholine in ME/CFS patients was “robust and unusual,” but did not conclude that pesticide exposure was causal.

Vaccinations have also been reported as triggers. In 1997, Doris M Jones MSc reported that among the 225 ME/CFS patients in her study group, 13% had received one or more vaccines in the month before ME problems developed. In a separate group of 55 subject, 16% had received one or more vaccines in the month before ME/CFS problems developed. There have been a number of studies implicating aluminum adjuvants (substances which are added to vaccines to increase their effectiveness) in the development of long-term neurological impairments. A particular concern is that even small amounts of adjuvant have the capacity to pass the blood-brain barrier."

 

[forestglip]

The Canary and Chronic Fatigue
by Majid Ali, published 1994

Full scanned book available to borrow on Internet Archive.

 

[Milo]

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.

Thank you for keeping it real @Jonathan Edwards
The last thing we need for this field is telling our doctors that pollution and environment is the cause of ME or suggesting to researchers that it is a good research lead. It would set us back yet again.

There is some humility in saying ‘we don’t know what causes you to not recover’ and yet please stop there and do not suggest that if you are less meat, no wheat, and avoided toxic products that everyone uses, you would have had a different outcome. We still don’t know what causes ME and we are even not sure yet whether it is one disease or several diseases.

 

[forestglip]

Thank you for keeping it real @Jonathan Edwards
The last thing we need for this field is telling our doctors that pollution and environment is the cause of ME or suggesting to researchers that it is a good research lead. It would set us back yet again.

There is some humility in saying ‘we don’t know what causes you to not recover’ and yet please stop there and do not suggest that if you are less meat, no wheat, and avoided toxic products that everyone uses, you would have had a different outcome. We still don’t know what causes ME and we are even not sure yet whether it is one disease or several diseases.

I don't have an issue saying "we don’t know what causes you to not recover".

But I will largely have to disagree with the rest. Researchers are barely even looking at this, and for those that are, it is inherently extremely hard to study.

I don't know if the issue is that there's a sentiment that reducing environmental toxins is some new age mumbo jumbo akin to healing cancer with crystals and positive affirmations. Maybe it gets associated with influencers selling grass smoothies to reduce toxins in the body based on no science. We're breathing and eating low doses of thousands of different newly created chemicals for our entire lives, almost none of which have been thouroughly studied for long term effects like ME or many of the other chronic conditions that plague the world.

Just looking at the one description of the Scottish study above. You think it would be best to not pursue any more research even though they've shown a significant link between pesticides and something like ME and a 10,000 (!) times higher risk of depression? Or the two others linking pesticides with depression or GWI? Just stop there and don't even look at other populations or other pesticides to try to see if the above link is sound and if more cases of ME-like illness are caused by pesticides?

Is it not obvious that if a high dose of pesticides, or some other industrial chemical, is highly dangerous to the people that work with it, a low dose spreading to the entire world may also be dangerous to a large number of people? It's just incredibly hard, in comparison, to make the connection to a single chemical out of the thousands in our environment being inhaled/ingested for our entire lives, and there is no dramatic onset, like with acute exposure, to make it easy to point to anything.

I mean, plenty of people with ME have sensitivity and obviously increased symptoms to even tiny amounts of fragrances in laundry detergent, connections that likely were not easy for them to find, and researchers weren't exactly falling over themselves to prove it for them. How are they going to know whether or not they're also sensitive to some pollutant wafting into their bedroom 24/7? Or sensitive to something that takes years to build up in the body to cause symptoms? Researchers and clinicians are barely considering even just the chemicals that patients are saying they are sure make their ME symptoms worse.

Researchers should be exploring all available avenues, including genetics, immune dysfunction, viral persistence, microbiome, etc. But for environmental toxicity to virtually not even be mentioned in relation to ME or other chronic illness research is incredible.

 

[forestglip]

HYPOTESIS: We underestimate the risk of chemicals in water and food in ME/CFS

Henrik Nielsen

EUROMENE Book of Abstracts, p. 10, March 2020

"When conventional organisations of farmers and industry inform that the use of pesticides, chemicals and heavy metal are safe, they make an error. It is a statement that pesticides, chemicals as well heavy metals enter nerve tissue and gut and no doubt interfere with health negatively. What we need is to show the exact mechanism/relationships between specific diseases and “poison” involved. This statement may not be an excuse for politicians not to handle now. Data collected over the past many years shows a growing support that healthcare problems are growing secondary to exposure worldwide to these elements. The Seveso disaster close to Milan in 1976 was one of the first accidents in industry which resulted in research in health risk secondary to chemicals. As a result, 2.5 kg dioxin was spread out in an area where many people lived, the understanding of this was not obvious, as information about chemicals used was not given prior to the two weeks had passed – after that the area was evacuated. A year later, 122 children were born with deformities, 450 children with chronic dermal diseases, and an increased occurrence of type 2 diabetes especially in women was observed. Dioxin is only one example how damage can involve living organisms – Danes are daily exposed to drinking water and food. In 2019, it was found that two in three tests in water to drink were positive for smaller cocktails of pesticides. Dependent on how the cocktails are mixed – they invade the human organs. A lab-study from 2017 illustrates the example of 338 pesticides’ penetration over membranes in the boiled egg model [1]. Today it is clearer that several diseases can result as a consequence of exposure to environmental factors – named trigger points. One factor of pesticides includes phthalate and chemicals in dress coats. Industrial air emission and proximity to emitters are associated with anti-citrullinated protein antibodies (ACPA) in a sample of 1586 unselected subjects [2]. In a controlled clinical study based on exposure to pesticides in tobacco field workers (n = 40) versus a control group in an office (n = 40), the groups were followed 360 hours in a period from June to September. All 80 tested subjects were non-smokers. In the exposed group blood concentration of aluminum, arsenic, chromium, copper, nickel, potassium, selenium and zinc were increased. Blood levels of antioxidants (e.g. B12–C vitamins) were increased but not sufficient to counterbalance the damage – mitochondrial damage/DNA damage [3]. From other designs GWI (Gulf War Veterans) [4], Alzheimer and Parkinson diseases [5], the evidence of pre- and post- natal exposures to environmental factors that predispose to the onset of neurodegenerative diseases later in life highlights the necessity to expand the research on identifying environmental risk factors to the development of neurodegenerative diseases (ME/CFS) – see reprogramming cells from Veterans [4].

References:
1. L. Chedik, D.Mias-Lucquin A. Bruyere, O. Fardel, Int. J. Environ. Res. Public Health, 14 (2017) 708.
2. S. Bernatsky, A. Smargiassy, L. Joseph, P. Awadalla, I. Colmegna, M. Hudson, M. J. Fritzler, Environ Res, 157
(2017) 60-63.
3 V. F. S. Kahl, V. Dhillon, M. Fenech, M. R. de Souza, F. N. da Silva, N. A. P. Marroni, E. A. Nunes, G.
Cerchiaro, T. Pedron, B. L. Batista, M. Cappetta, W. Mártinez-López, D. Simon, J. da Silva, Oxid Med Cell
Longev, 2018 Jun 3;2018:7017423.
4. L. Qiang, A.N.Rao, G. Mostoslavsky, M. F. James, N. Comfort, K. Sullivan, P. W. Baas, Neurology, 88
(2017)1968-1975.
5. M. Chin-Chan, J. Navarro-Yepes, B. Quintanilla-Vega, Front Cell Neurosci, 9 (2015) 124"

Link

 

[forestglip]

Links between air pollution and COVID-19 in England
Marco Travaglio, Yizhou Yu, Rebeka Popovic, Liza Selley, Nuno Santos Leal, Luis Miguel Martins

Environmental Pollution
January 2021

"Abstract
In December 2019, a novel disease, coronavirus disease 19 (COVID-19), emerged in Wuhan, People’s Republic of China. COVID-19 is caused by a novel coronavirus (SARS-CoV-2) presumed to have jumped species from another mammal to humans. This virus has caused a rapidly spreading global pandemic. To date, over 300,000 cases of COVID-19 have been reported in England and over 40,000 patients have died. While progress has been achieved in managing this disease, the factors in addition to age that affect the severity and mortality of COVID-19 have not been clearly identified. Recent studies of COVID-19 in several countries identified links between air pollution and death rates. Here, we explored potential links between major fossil fuel-related air pollutants and SARS-CoV-2 mortality in England. We compared current SARS-CoV-2 cases and deaths from public databases to both regional and subregional air pollution data monitored at multiple sites across England. After controlling for population density, age and median income, we show positive relationships between air pollutant concentrations, particularly nitrogen oxides, and COVID-19 mortality and infectivity. Using detailed UK Biobank data, we further show that PM2.5 was a major contributor to COVID-19 cases in England, as an increase of 1 m3 in the long-term average of PM2.5 was associated with a 12% increase in COVID-19 cases. The relationship between air pollution and COVID-19 withstands variations in the temporal scale of assessments (single-year vs 5-year average) and remains significant after adjusting for socioeconomic, demographic and health-related variables. We conclude that a small increase in air pollution leads to a large increase in the COVID-19 infectivity and mortality rate in England. This study provides a framework to guide both health and emissions policies in countries affected by this pandemic."

Full text

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It seems premature for them to say they show that PM2.5 particles were a "major contributor to COVID" based on this study, although I've only skimmed the full text. Just with all the potential confounders, like maybe jobs in the more polluted areas tend to have people in closer contact. Or maybe there's more public transportation squeezing people together in those areas.

 

[Hutan]

Researchers should be exploring all available avenues, including genetics, immune dysfunction, viral persistence, microbiome, etc. But for environmental toxicity to virtually not even be mentioned in relation to ME or other chronic illness research is incredible.

I think anyone with a curious outlook and a life-limiting unexplained chronic disease will think about all sorts of possible factors that might have caused them to become unwell. Certainly I have, and some of them I have put in a 'maybe' box and every now and then I try pulling one out (e.g. impact of sulphides on acetylcholine pathways...) and investigating it. I do think, in time, we will find that exposure to certain chemicals does increase the risk of ME/CFS, even if it just slightly tips the balance in the direction of disease. On pesticides - there are plenty of reasons other than a contested link with ME/CFS symptoms for people to avoid exposure.

But, the problems with ideas about environmental causes is that we lack really good data and it is so easy to come across as, well, not scientific, luddite even. Many of these chemicals are everywhere; to avoid them would require major lifestyle changes and/or lots of money. Very few people want to hear that the chemicals that are almost impossible to separate from their modern comfortable life might be causing harm. Research funders don't really want to entertain that idea, certainly not when the evidence to support it is tenuous. At this point, pushing the idea of an environmental cause of ME/CFS can easily be counter-productive.

Progress appears to have finally been made on GWI, I guess mostly because it was possible to quantify exposure to a seriously bad toxin in a well defined group of people, at a well defined point in time.

I think we need to take advantage of phenomena like that. And right now, Covid-19 is our sarin gas equivalent. There are a lot of people with similar symptoms, probably as a result of a well defined pathogen. Long covid is getting harder to ignore and harder to disbelieve even though it is inconvenient to governments who really just want to get on with life as normal.

I think too, we need better epidemiology and more patient registries. Is there an occupation that seems to have a much higher incidence of ME/CFS? Is there a community somewhere in the world where there is no ME/CFS, or one where there is lots? If we had a really solid clue rather than anecdotes and hypotheses, then it would become a lot easier to support an investigation of environmental factors.

 

[tornandfrayed]

I think anyone with a curious outlook and a life-limiting unexplained chronic disease will think about all sorts of possible factors that might have caused them to become unwell. Certainly I have, and some of them I have put in a 'maybe' box and every now and then I try pulling one out (e.g. impact of sulphides on acetylcholine pathways...) and investigating it. I do think, in time, we will find that exposure to certain chemicals does increase the risk of ME/CFS, even if it just slightly tips the balance in the direction of disease. On pesticides - there are plenty of reasons other than a contested link with ME/CFS symptoms for people to avoid exposure.

But, the problems with ideas about environmental causes is that we lack really good data and it is so easy to come across as, well, not scientific, luddite even. Many of these chemicals are everywhere; to avoid them would require major lifestyle changes and/or lots of money. Very few people want to hear that the chemicals that are almost impossible to separate from their modern comfortable life might be causing harm. Research funders don't really want to entertain that idea, certainly not when the evidence to support it is tenuous. At this point, pushing the idea of an environmental cause of ME/CFS can easily be counter-productive.

Progress appears to have finally been made on GWI, I guess mostly because it was possible to quantify exposure to a seriously bad toxin in a well defined group of people, at a well defined point in time.

I think we need to take advantage of phenomenon like that. And right now, Covid-19 is our sarin gas equivalent. There are a lot of people with similar symptoms, probably as a result of a well defined pathogen. Long covid is getting harder to ignore and harder to disbelieve even though it is inconvenient to governments who really just want to get on with life as normal.

I think too, we need better epidemiology and more patient registries. Is there an occupation that seems to have a much higher incidence of ME/CFS? Is there a community somewhere in the world where there is no ME/CFS, or one where there is lots? If we had a really solid clue rather than anecdotes and hypotheses, then it would become a lot easier to support an investigation of environmental factors.

I think that, as you'd expect, there's a higher prevalence in health care and education. The (late) ME nurse Keith Anderson told me there was higher prevalence around estuaries, but I don't know what his source was.

You are right @Hutan, we know so little about the patient population.

 

[forestglip]

I think anyone with a curious outlook and a life-limiting unexplained chronic disease will think about all sorts of possible factors that might have caused them to become unwell. Certainly I have, and some of them I have put in a 'maybe' box and every now and then I try pulling one out (e.g. impact of sulphides on acetylcholine pathways...) and investigating it. I do think, in time, we will find that exposure to certain chemicals does increase the risk of ME/CFS, even if it just slightly tips the balance in the direction of disease. On pesticides - there are plenty of reasons other than a contested link with ME/CFS symptoms for people to avoid exposure.

But, the problems with ideas about environmental causes is that we lack really good data and it is so easy to come across as, well, not scientific, luddite even. Many of these chemicals are everywhere; to avoid them would require major lifestyle changes and/or lots of money. Very few people want to hear that the chemicals that are almost impossible to separate from their modern comfortable life might be causing harm. Research funders don't really want to entertain that idea, certainly not when the evidence to support it is tenuous. At this point, pushing the idea of an environmental cause of ME/CFS can easily be counter-productive.

I hear that. I'm not confident it is the case that spreading awareness and sharing research about this field is counter-productive, but I can maybe see an argument for that.

I'm too tired for trying to navigate the politics of research, though I get that it's a big factor in things like this. But I'm just frustrated because it's like there's a building with water all over the floor all the time and everyone is focusing on making clever systems to clean up the water or work around it, but no one cares to check if there's a leak somewhere.

I think too, we need better epidemiology and more patient registries. Is there an occupation that seems to have a much higher incidence of ME/CFS? Is there a community somewhere in the world where there is no ME/CFS, or one where there is lots?

Sure, those would be great, as would a biomarker. I can imagine researchers trying to compare rates of ME between the US and a tribal population in the Amazon rainforest would be extremely difficult with all the language, cultural, and practical challenges that would surely arise. If they could just draw some blood and send it to a lab, that'd make things much easier.

If we had a really solid clue rather than anecdotes and hypotheses, then it would become a lot easier to support an investigation of environmental factors.

It's not just anecdotes though. There's one example of a solid lead in a post above, with the sheep dip causing ME. The next step should surely be to try to confirm or deny this study, right? Look for correlations with the same or similar chemicals in other populations. [Edit: Though looking more into that, even though news articles and the study refer to ME or CFS, the study says "It should be noted that the questionnaire provided an assessment of CF and not CFS". But even if the link is to CF instead, then pesticide links to CF should be further investigated.]

And I'm not just advocating for this for ME, but for all chronic illnesses - this research is lagging everywhere. We even have perfect examples of environmental toxins flying under the radar for years, causing illness in millions of people: things like lead, asbestos, mercury, radium, PCBs. It is not unscientific to think "I wonder if there are more examples of this clear issue that we haven't found yet. Maybe we should try harder to find them before a million more people have cancer or brain damage, and try to limit the suffering that will happen." It's unscientific to look at that and think we're now perfect and industry is only pumping out the safest of chemicals after learning its lessons. (I know/think you personally aren't calling me a Luddite, but that'd be my response to someone that does think that.)

Maybe that's the price we pay as society to have modern technology, where the powers that be know they can't possibly thoroughly test everything their population demands and some or many people will be harmed, but the risks and benefits are carefully weighed by government and industry (which I doubt). Even in that case, the risk should be part of public consciousness so that people are free to protect themselves or demand change. It seems like the majority of people don't even know or think about the possibility that the next lead or asbestos could be happening right now, in a thousand different ways.

But I get that people want a relatively easy fix. If the majority of the population only experiences mild health issues, yeah, why would they, for example, like being told they should upend their life and move to a rural town to avoid air pollution to calm their asthma if they have the alternative of pills and inhalers with minimal side effects, and science promising them ever-better medications.

 

[tornandfrayed]

I think anyone with a curious outlook and a life-limiting unexplained chronic disease will think about all sorts of possible factors that might have caused them to become unwell.

I was recently thinking about a cat I had who was diagnosed with cat leukemia and eventually had to be put down. I'm very bad at remembering timelines, so I don't know if I adopted him before or after my precipitating infection (I inherited him from a friend), but it was around the same time. I also don't remember if he had a blood test to confirm the diagnosis.

When he became ill he stopped eating and spent all his time on lying on a shelf away from the light. At the end he was struggling to breathe.

I've become much more aware of transmission of infections between species because of Covid-19 and H5N1, so that's why I'm thinking about this, although it's probably most likely that his and my illnesses are unrelated.

(I miss him)