Modern environmental factors

[forestglip]

One of the talks at IIMEC 2024 was from a clinician, Irina R. Rozenfeld, and was about how her clinic focuses on environmental toxins in relation to ME/CFS.



Quoting an interesting case. Screenshots of the slides have a bit more detail:

"This gentleman was our patient for many years with a history of myalgic encephalomyelitis and at one visit, he presented with severe cognitive decline. His neurologist put him on Alzheimer's medication.

We did some evaluation and this gentleman practically retains everything that he possibly can retain. Arsenic was a thousand times more than he should have, and he also had mercury and he had water damaged building exposure - mold and micro toxin. We got very excited with his treatment and he responded to treatment very well.

When he came with cognitive decline in Florida, he was 66 years old he was already taking his driver license off. He practically was given homebound assessment. He could not live without his wife.

After treatment, he got his driver's license back. He started traveling, and he has fully recovered his cognitive function. And it affected his myalgic encephalomyelitis. He started traveling, he started being more active."

 

[forestglip]

Wired: 'Scientists Thought Parkinson’s Was in Our Genes. It Might Be in the Water'

All told, more than half of Parkinson’s research dollars in the past two decades have flowed toward genetics.

But Parkinson’s rates in the US have doubled in the past 30 years. And studies suggest they will climb another 15 to 35 percent in each coming decade. This is not how an inherited genetic disease is supposed to behave.

“We thought we were going to solve it,” Langston told me. Researchers affiliated with the institute created the first animal model for Parkinson’s, identified a pesticide called Paraquat as a near chemical match to MPTP, and proved that farm workers who sprayed Paraquat developed Parkinson’s at exceedingly high rates. Then they showed that identical twins developed Parkinson’s at the same rate as fraternal twins—something that wouldn’t make sense if the disease were purely genetic, since identical twins share DNA and fraternal twins do not. They even noted TCE as a potential cause of the disease, Langston says.

Human Genome Project

But for Langston and his colleagues, the Human Genome Project sucked the air out of the environmental health space. Genetics became the “800-pound gorilla,” as one scientist put it. “All the research dollars went toward genetics,” says Sam Goldman, who worked with Langston on the twin study. “It’s just a lot sexier than epidemiology. It’s the latest gadget, the bigger rocket.”

“The Human Genome Project was a $3 billion investment, and what did we find out?” says Thomas Hartung, a toxicologist at Johns Hopkins. “Five percent of all disease is purely genetic. Less than 40 percent of diseases even have a genetic component.”

Trichlorethylene (TCE)

For approximately 35 years, Marines and sailors who lived at Lejeune unknowingly breathed in vaporized TCE whenever they turned on their tap. The Navy, which oversees the Marine Corps, first denied the toxic plume’s existence, then refused to admit it could affect Marines’ health.

But as Lejeune’s vets aged, cancers and unexplained illness began stalking them at staggering rates. Marines stationed on base had a 35 percent higher risk of developing kidney cancer, a 47 percent higher risk of Hodgkin’s lymphoma, a 68 percent higher risk of multiple myeloma. At the local cemetery, the section reserved for infants had to be expanded.

When Goldman compared both populations, the results were shocking: Marines exposed to TCE at Lejeune were 70 percent more likely to have Parkinson’s than those stationed at Pendleton. And in a follow-up study last year, he showed that disease progression in Lejeune vets with the highest exposure to TCE was faster than those with low or no exposure, too.

Briana De Miranda has re-created Camp Lejeune in her lab, but for mice. [...] De Miranda’s studies, the first ever on inhaled TCE toxicity and Parkinson’s, are compelling, her colleagues agree, and well designed.

“I think TCE is the most important cause of Parkinson’s in the US,” says Ray Dorsey, the Parkinson’s expert at the University of Rochester.

No one knows exactly how much of the world’s drinking water is laced with TCE. The US Centers for Disease Control and Prevention reckons that the water supply of between 4 and 18 percent of Americans is contaminated, although not always at dangerous concentrations; the Environmental Working Group figures 17 million Americans drink the stuff.

Yet only 1 percent of the roughly 350,000 chemicals in use in the United States have ever been tested for safety. In its 55-year history, the EPA has banned or restricted about a dozen (by contrast, the EU has banned more than 2,000).

Human Exposome Project

[Miller] grew tired of the “whack-a-mole approach” of modern toxicology: identifying one of the 350,000 chemicals on the market as a potential toxicant

He wanted a shotgun approach, an answer to the way genome sequencing identifies all the genes in the body. What Miller wants is a Human Exposome Project. “We realized that this wasn’t just about Parkinson’s,” he says. “There were so many disease states we could look at.” Quantify our exposomes, Miller hopes, and we can know what ails us.

Link to Human Exposome Project

 

[Hutan]

I found this Facebook post:

I noticed some chat about using Genklene... Have put together some research around this stuff and if you were a user of it as I was... Trichloroethylene... (inhibited) [Genklene]. Still approved for use in NZ and sold freely as a useful solvent cleaner in electronics and metal fabrication... It is safe to use with correct protection in place. My Foreman was pretty strict in this aspect so it was well known back then, but maybe not well communicated in some areas.... Approved for use by EPA NZ is classified as several levels of toxicity depending on exposure routes, importantly as a "known carcinogen"... CAS 71-55-6. UN #1710. EPA approval #HSR001555

Suggest next time former users of Genklene visit their GP, they ask to be logged in the Ministry of Health HSDIRT database... see this link to explain this database. http://www.bestpractice.net.nz/feat_mod_HSDIRT.php. Every Medical Practice has access to this database, to log potential chronic low level or high level acute chemical exposures... You will need dates, chemical name (Trade Name 'Genklene' / Proper Shipping Name 'Trichlorethylene), activity, and define as routine inhalation and skin absorption exposure. The HSDIRT database is run by Massey University, paid for by our very own Ministry of Health... but very poorly communicated and GPs are expected to use but not paid to do so. As such it's poorly used by GPs, more by specialists and EDs. This is how MoH gather chemical exposure stats and why they are so inaccurate in real world NZ.

It refers to a database for recording exposures to chemicals that New Zealand doctors have access to. People can ask their GP to record their exposure to a particular chemical - high level acute exposure or lower level chronic exposure. Obviously there are issues with a nocebo effect, but if databases like that could identify high rates of very specific diseases, that could create interest.

Probably other countries have similar databases.

As a person with ME/CFS, I don't fancy asking my GP to log my exposure to agrichemicals on the database - I can't imagine the request would be met well. But if someone had a documented high exposure to TCE - and clearly some people have had major exposures - it sounds as though it would be worth looking for a good place to record it.

 

[Creekside]

I remember hearing about a "toxic blob" in I think it was the St. Lawrence river. It was drycleaning solvent and whatever else in a big blob on the riverbed, which of course supplied drinking water to cities downstream. How many such blobs still exist, hiding in mud? Which toxins aren't tested for in domestic water?

 

[nataliezzz]

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.

I just figured I would weigh in with how a UARS etiology could fit in with this. Our jaws have shrunk in modern times since the agricultural revolution (smaller jaws predispose to obstructive sleep-disordered breathing); hunter-gatherers generally did not experience dental crowding, impacted wisdom teeth, etc. "Despite claims that the cause of this jaw epidemic is somehow genetic, the speed with which human jaws have changed, especially in the last few centuries, is much too fast to be evolutionary. Correlation in time and space strongly suggests the symptoms are phenotypic responses to a vast natural experiment—rapid and dramatic modifications of human physical and cultural environments" - from this article, which discusses some of the potential reasons why: The Jaw Epidemic: Recognition, Origins, Cures, and Prevention

Comparisons of Medieval and modern skulls demonstrate this dramatically, with tooth crowding considerably less frequent in the Middle Ages (Moore et al. 1968, Helm and Prydsö 1979, Luther 1993), and there has been rapid change in jaw morphology in that brief period (Goose 1981). With very rare exceptions, hunter-gatherers had roomy jaws. Malocclusion and noneruption of third molars (wisdom teeth) and crowding of the tongue were close to nonexistent; preindustrial jaws were simply roomier than those of people exposed to modern lifestyles (e.g., Price 1939, Proffit 1975, Helm and Prydsö 1979, Gibson and Calcagno 1993, Luther 1993, Kaifu 1997, 2000, Evensen and Øgaard 2007, Rose and Roblee 2009, Lieberman DE 2013, Kahn and Ehrlich 2018). The jaw epidemic is therefore a recent phenomenon and temporal and geographic correlation strongly suggests that it can be traced to changes in environmental factors due to agriculture and industrialization, but exactly what those factors are and how they operate remain uncertain.

See the thread Sleep-disordered Breathing and Hypotension, 2001, Guilleminault et al. for some of the anatomical factors associated with UARS (all of the UARS patients in the study - of whom 15/15 with "low BP" [<105/65 here] who underwent tilt table testing had orthostatic hypotension - had an abnormally small oral cavity):

All of the UARS patients in the study had an abnormally small oral cavity based on objective measurements:

Subjects with UARS were also examined by an otolaryngologist. A craniofacial evaluation performed by a specialist indicated the presence of at least one of the following: crossbite, long face, high-arched hard palate with narrow maxilla, and small mandible with either decreased anteroposterior length or decreased intermolar distance (20, 23). The anatomic findings always resulted in a small oral cavity impacting on the resting position of a normal-size tongue.

The index calculated on the basis of oral cavity measurements was abnormal in all subjects (20). Only three subjects had wisdom teeth (23). Cephalometric radiographs demonstrated an abnormally small airway space behind the base of the tongue (in 87 of 89 subjects).

Personally, I feel like once you are aware of these anatomical factors, it's kind of hard to unsee. I feel like there are way too many people with ME/CFS who look like me (UARS poster child, I have all of the above minus a crossbite) to be a coincidence; however, the anatomical factors can be subtle in some individuals (e.g. in the UARS Facebook group, there are plenty of people who look pretty "normal" from the front - i.e. they don't have narrow dental arches, but a profile view will reveal some degree of recession of the jaws). And of course, other factors that aren't visible like having a larger tongue, nasal obstruction/rhinitis, connective tissue laxity (causing increased upper airway collapsibility) can all contribute too.

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?

Most animals do not experience obstructive sleep-disordered breathing, I believe, with the exception of brachycephalic dog breeds like pugs, bulldogs, boston terriers, etc. (other animals like pigs/rodents/etc. can develop it when they become obese).