Modern environmental factors

[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

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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

 

[forestglip]

Interesting commentary about the field of chemical exposomics:

Will Chemical Exposomics Be Ready for a Human Exposome Project?
Martin, Jonathan W.
Web | DOI | PDF | Environmental Science & Technology | Open Access | 2026

Snippets:

From my view, the missing piece in health research is no longer just “environment” in the abstract and hand-wavy sense; it is the chemical exposome, the complex mix of chemicals and particle-associated stressors that seep into our body’s cells daily through air, water, food, the microbiome, and commercial products.

What would surely have sounded like science fiction a decade ago, mapping and recording the complexity and dynamics of an individual’s lifetime chemical fingerprint, is now technically feasible.

For chemical exposomics specifically, an international effort involving 20 laboratories is now underway to generate an online atlas of the chemical exposome in human biofluids. (42) New international scientific constellations have developed, (43) and the Washington Declaration now gives the field a road map to establish the foundations of a Human Exposome Initiative. (44) Such an initiative was recently proposed to the European Parliament that would involve 10 million participants; (45)

Once the field emerges from its necessary but disjointed phase of early innovation, I expect the trajectory to look like that of genomics, with consolidation, method maturation, and strong commercial partnerships to follow. If the field can resist hype, invest in rigor, and stay grounded in accurately revealing exposure, chemical exposomics stands to fundamentally reshape exposure science, public health, and even medicine. (46)

 

[Murph]

Possible environmental cause, from the crazy end of the spectrum, (one I consider more interesting than probable):

Omega 6 fats . Back in the day humans ate relatively few seed oils. The unsaturated fat we got was more often from fish, I.e. Omega 3.

Three arguments in support of this idea. (All weak!)

1. The autumnal foods that prime certain mammals for hibernation and torpor are nuts, rich in omega 6. I've always imagined bear hibernation as ... snuggly...but what if instead they feel utterly debilitated?!

2. If Norway, Japan and the Celtic countries are rich in mecfs one thing they have in common is cold water. Cold water fish are the highest in omega 3. But the population of these countries are now eating more Doritos than Herring.

3. Mecfs involves lipid deregulation and possibly membrane dysfunction, suggesting perhaps a role for dietary unsaturated fats.

I don't personally find it too compelling but there's heaps out there on seed oils and their health effects.

 

[forestglip]

I sometimes search for nutrition reviews to see what the state of the science is. The field seems very hard to conclusively determine anything from, as RCTs are very difficult in nutrition, so confounding is a huge issue, and lots of the research is done using questionnaires, which is open to recall bias.

But just a quick search right now for fun, looking through the first few pages of search results for "nutrition meta-analysis risk factor" for titles that are about health conditions and talk about specific foods or food groups in the abstract. Trying not to cherry pick, but I'm also not being especially careful about making sure I don't miss anything.

Spoiler: Studies

Foods that increase risk are in red, and foods that decrease risk are in green.

Risk factors for stomach cancer: a systematic review and meta-analysis (2022, Epidemiol Health)

Results:
Of 52,916 identified studies, 232 (including 33,831,063 participants) were eligible. The OR (95% CI) of factors associated with stomach cancer were as follows: Helicobacter pylori infection, 2.56 (95% CI, 2.18 to 3.00); current smoking, 1.61 (95% CI, 1.49 to 1.75); former smoking 1.43 (95% CI, 1.29 to 1.59); current drinking, 1.19 (95% CI, 1.10 to 1.29); former drinking, 1.73 (95% CI, 1.17 to 2.56); overweight/obesity, 0.89 (95% CI, 0.74 to 1.08); sufficient physical activity, 0.83 (95% CI, 0.68 to 1.02); consumption of fruits ≥3 times/wk, 0.48 (95% CI, 0.37 to 0.63); consumption of vegetables ≥3 times/wk, 0.62 (95% CI, 0.49 to 0.79); eating pickled vegetables, 1.28 (95% CI, 1.09 to 1.51); drinking black tea, 1.00 (95% CI, 0.84 to 1.20); drinking green tea, 0.88 (95% CI, 0.80 to 0.97); drinking coffee, 0.99 (95% CI, 0.88 to 1.11); eating fish ≥1 time/wk 0.79 (95% CI, 0.61 to 1.03); eating red meat ≥4 times/wk 1.31 (95% CI, 0.87 to 1.96), and high salt intake 3.78 (95% CI, 1.74 to 5.44) and 1.34 (95% CI, 0.88 to 2.03), based on two different studies.

I cheated and bolded fish since it was just barely not significant.

Risk factors for postpartum depression: An evidence-based systematic review of systematic reviews and meta-analyses (2020, Asian J Psychiatr)

The risk factors are mainly concentrated in the following aspects: [...] vitamin D deficiency, [...], traditional dietary pattern (Japanese, Indian, United Kingdom, and Brazilian dietary pattern) [...]

higher concentrations of DHA in mothers' milk, greater seafood consumption, healthy dietary patterns, multivitamin supplementation, fish and PUFA intake, calcium, Vitamin D, zinc and possibly selenium are protective factors.

Investigation on factors associated with ovarian cancer: an umbrella review of systematic review and meta-analyses (2021, J Ovarian Res)

Among nutritional factors, coffee, egg, and fat intake significantly increase the risk of ovarian cancer.

Role of Diet in Colorectal Cancer Incidence: Umbrella Review of Meta-analyses of Prospective Observational Studies (2021, JAMA Network Open)

There was convincing evidence of an association of intake of red meat (high vs low) and alcohol (≥4 drinks/d vs 0 or occasional drinks) with the incidence of CRC and an inverse association of higher vs lower intakes of dietary fiber, calcium, and yogurt with CRC risk.

Umbrella Review of Systematic Reviews and Meta-Analyses on the Consumption of Different Food Groups and the Risk of Overweight and Obesity (2025, Nutrients)

High intakes of whole grains, legumes, nuts, and fruits are associated with a reduced risk of overweight and obesity. In contrast, high intakes of red meat and sugar-sweetened beverages are associated with increased risk of overweight and obesity. No significant results were found for the remaining food groups, and no meta-analysis was found for fish, eggs, white meat, and added sugars.

Umbrella Review of Systematic Reviews and Meta-Analyses on Consumption of Different Food Groups and Risk of Type 2 Diabetes Mellitus and Metabolic Syndrome (2025, J Nutr)

Our results showed that a high intake of whole grains was associated with a lower risk of type 2 diabetes (metaevidence: moderate) and metabolic syndrome (metaevidence: low), with a similar tendency also for a high intake of fruits and vegetables (metaevidence: moderate). In contrast, the high intakes of processed meat (metaevidence: high), red meat (metaevidence: moderate), and sugar-sweetened beverages (metaevidence: moderate) were associated with a higher risk of type 2 diabetes.

Nutrient and food intakes in early life and risk of childhood fractures: a systematic review and meta-analysis (2015, Am J Clin Nutr)

Overall, fracture risk seemed to be associated with milk avoidance, high energy intake, high cheese intake, high intake of sugar-sweetened beverages, and no breastfeeding.

Landscape of dietary factors associated with risk of gastric cancer: A systematic review and dose-response meta-analysis of prospective cohort studies (2015, Eur J Cancer)

consumption of total fruit and white vegetables, but not total vegetables, was inversely associated with gastric cancer risk. [...] Furthermore, we found concordant positive associations between high-salt foods and gastric cancer risk. In addition, a strong effect of alcohol consumption, particularly beer and liquor but not wine, on gastric cancer risk was observed compared with nondrinkers.

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Here's a little state of the science on seed oils from a blogger/epidemiologist who seems to write intelligent posts: What’s the deal with seed oils?

As she says, it kind of seems to be more of an "influencer"-type topic to talk about negative effects of seed oils, though I can't say I've dug into the science much.

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I was looking at the Scientific Report of the 2025 Dietary Guidelines Advisory Committee recently. This is a report which provided recommendations to the US government for the 2025-2030 dietary guidelines. I assume this would be some of the most rigorous analysis of the current state of the science.

Compelling evidence was noted in the systematic reviews in which dietary patterns that had higher levels of beans, peas, and lentils (often presented in the literature as “legumes”) were associated with beneficial health outcomes

Systematic review evidence also consistently indicated that dietary patterns with higher intakes of red and processed meats were related to detrimental health consequences, whereas dietary patterns with higher intakes of fish and seafood were related to beneficial health outcomes

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It'd be great if there was also an S4ME-type website that tackled the field of nutrition. I'd love to read more about nutrition science, but I barely even have the energy for reading about ME/CFS research.