Modern environmental factors

[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).

 

[nafione]

New member here. Has anyone drawn the connection between gulf war illness (GWI) and me/cfs, since GWI presents practically the same?

This researcher claims to have proven the environmental and genetic trigger of GWI: https://www.utsouthwestern.edu/newsroom/articles/year-2022/sarin-nerve-gas-gulf-war-illness.html

It's clear that governments (US particularly) are slow walking any outright admission to this effect. The US govt initiated a media campaign prior to the end of the war that many soldiers had PTSD, which was false. This is no surprise as it would harm the reputation of the military, plus our conditions have been historically stigmatized and neglected. Unfortunately it has left those affected without treatment or commensurate research for 35 years.

I had a suspected exposure to an organophosphate pesticide which pre-dated the beginning of my chronic symptoms by 18 months. Currently I'm attempting to find out whether I have the vulnerable gene.

 

[forestglip]

Hi @nafione, welcome.

This researcher claims to have proven the environmental and genetic trigger of GWI: https://www.utsouthwestern.edu/newsroom/articles/year-2022/sarin-nerve-gas-gulf-war-illness.html

We have a thread for that study: Evaluation of a Gene–Environment Interaction of PON1 and Low-Level Nerve Agent Exposure with Gulf War Illness..., 2022, Haley et al

But it looks like most of the discussion for that study was on the general gulf war illness thread: Gulf war illness - causes

 

[ScoutB]

Great to have you nafione

Has anyone drawn the connection between gulf war illness (GWI) and me/cfs

Yes, we definitely are interested in GWI given their similarities. You can find more of our threads about it with the gulf war illness and gwi tags.

The US govt initiated a media campaign prior to the end of the war that many soldiers had PTSD, which was false.

Right, exactly. In fact, that's another similarity -- the same people tend to turn up discrediting both GWI and ME/CFS. Eg. this fellow.

I had a suspected exposure to an organophosphate pesticide which pre-dated the beginning of my chronic symptoms by 18 months. Currently I'm attempting to find out whether I have the vulnerable gene.

Hope you are able to get some clarity.

 

[forestglip]

Neuroscience News: "Home Drinking Water May Impact Parkinson’s Risk"

People whose drinking water came from newer groundwater had a higher risk of developing Parkinson’s disease than those whose drinking water came from older groundwater, according to a preliminary study released March 2, 2026, that will be presented at the American Academy of Neurology’s 78th Annual Meeting taking place April 18-22, 2026, in Chicago and online.

The study included 12,370 people with Parkinson’s disease and more than 1.2 million people without the disease who were matched for factors like age, sex and race and ethnicity. All participants lived within three miles of 1,279 groundwater sampling sites across 21 major U.S. aquifers.

“In these aquifers, newly recharged groundwater is more vulnerable to surface contamination, while older groundwater can remain cleaner if it is separated from recent inputs by a confining layer.”

Link

---

Younger Groundwater Associated with Greater Risk of Parkinson’s Disease in Nationwide Medicare Study: Implications of Aquifer Type
Renee Tessman, Michelle Uher

Spoiler: Abstract

Objective
To assess the relationship between groundwater age and risk of Parkinson disease (PD).

Background
Older groundwater typically contains fewer anthropogenic contaminants because it is generally deeper and better shielded from surface contaminants than newer groundwater. Although environmental neurotoxicants are linked to PD, the contribution of groundwater exposures remains poorly understood.

Design/Methods
We performed a population-based, case-control study of 12,370 incident PD patients and 1,224,174 matched controls in the Medicare population in the 3 miles surrounding 1,279 groundwater sample sites across 21 principal aquifers.

Groundwater age, aquifer type, and drinking water source (municipal vs private well) were evaluated as a proxy for neurotoxicant exposure. All models adjusted for age, sex, race, smoking, use of care, income, urban/rural residence, and air pollution in the form of average annual PM2.5. ore rapid.

Results
After adjusting for covariates, beneficiaries living in regions sourcing drinking water from municipal groundwater systems or private wells on carbonate aquifers exhibited the highest overall risk of PD—24% higher compared to all other aquifer types (OR = 1.24, 95% CI: 1.18–1.30) and 62% higher when compared to glacial aquifer types (OR = 1.62, 95% CI: 1.45–1.81).

Additionally, we observed an interaction between groundwater age and aquifer type, with the protective effect of older groundwater observed only within carbonate systems. In carbonate aquifers, for each one–standard-deviation increase in groundwater age, the risk of Parkinson's disease declined by approximately 6.5%.

When modeled categorically, individuals sourcing Anthropocene-aged groundwater in carbonate systems had a greater risk of PD (OR = 1.11, 95% CI: 1.02–1.20) compared with those using Pleistocene-aged water.

Conclusions
These findings suggest that groundwater age and aquifer type contribute independently to PD risk, with newer groundwater posing greater risk particularly in carbonate systems where contaminant infiltration is more rapid

PDF | American Academy of Neurology | Abstract Only