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Losing Our Minds: How Environmental Pollution Impairs Human Intelligence and mental health

Wishful

Senior Member
Messages
5,679
Location
Alberta
I've been living in a clean, remote part of the world (cabin in the woods in Alberta. Nearest powerline is 4 miles away; nearest cell tower is 18 km away). That hasn't reduced my symptoms, which I developed in Vancouver. Travelling to a different area involves very many variables, so you can't state that it's just avoiding pollution that is responsible. It might be avoidance of a particular pollutant, but it might be difficult to isolate which one it is. When I find something that does reduce my symptoms, I do experiments to try to isolate it.
 
Messages
236
Location
Medford NJ
Definitely an art as well as a science. Sorry your symptoms have not been helped by a remote move.
My oiginal problem was Hasimoto’s thyroiditis. I wish I had known at the time about the high risk of fibromyalgia and cfs with this. Doctors schrug it off as not a big deal . It is a big deal and should not be so commonplace.
 

cigana

Senior Member
Messages
1,095
Location
UK
I think pollution is a huge part of my cfs. I left a mloldy house and we actually moved away from the city and live close to the pine barrens in NJ. My youngest son son has Aspergers ,My older son was on psyche meds his add and depression and rage attacks ( very rare but where scary out of character) totally disappeared after we moved and his psychiatrist released him. My husband has anxiety and depression I am encouraging him to go hiking with me on the weekends. Outside I can now hike ( this was impossible until very very recently. ) . I don’t. Have that cfs feeling like crap when I am in nature . Really wish I could move to a remote area.

I am currently spending as much time in the forest as possible and sleeping outside on a sleeping potrch, This sounds crazy but it is really helping I am much more functional. If I am in Clear Air ( did terrific in Death Valley) I do much better.
Same for me. In a remote pine forest I can walk for hours and suffer no PEM or pain.
Back in the city I can't even get out of the chair.

It's not as simple as avoiding mold. Mold is just one component, you have to avoid all environmental toxins.
 

cigana

Senior Member
Messages
1,095
Location
UK
I've been living in a clean, remote part of the world (cabin in the woods in Alberta. Nearest powerline is 4 miles away; nearest cell tower is 18 km away). That hasn't reduced my symptoms, which I developed in Vancouver. Travelling to a different area involves very many variables, so you can't state that it's just avoiding pollution that is responsible. It might be avoidance of a particular pollutant, but it might be difficult to isolate which one it is. When I find something that does reduce my symptoms, I do experiments to try to isolate it.
That must be tough, do you have chemical sensitivities?

I have been in some clean places where I expected to feel better and haven't. Conversely I've been in some places where I didn't expect to feel better and have. One thing I've noticed in common is that the places I felt good in did not contain any new furnishings etc indoors - they were all old building with old interiors. Don't know how important this is.
 

pattismith

Senior Member
Messages
3,930
That must be tough, do you have chemical sensitivities?

I have been in some clean places where I expected to feel better and haven't. Conversely I've been in some places where I didn't expect to feel better and have. One thing I've noticed in common is that the places I felt good in did not contain any new furnishings etc indoors - they were all old building with old interiors. Don't know how important this is.

formaldehyde is a common toxic in new buildings and furniture...
 

HowToEscape?

Senior Member
Messages
626
formaldehyde is a common toxic in new buildings and furniture...
...And sometimes in significant quantities.

Your body naturally produces tiny amounts of formaldehyde, but we’re not accustomed to breathing it.

I will hazard guess that a building with new carpet, new wall coverings, a new foam covered furniture as well as an airtight building envelope and very little outside air is elevating your formaldehyde level well above what naturally occurs
 
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Wishful

Senior Member
Messages
5,679
Location
Alberta
I don't have chemical sensitivities that I know of. My home is pretty low in those chemical-emitting items that are common in modern dwellings. I don't notice any difference in symptoms seasonally, which greatly changes my fresh air/stale air time. I can't think of any environmental factors that are significant for me.
 
Messages
236
Location
Medford NJ
I think I have chemical sensitivities but don’t fully realize it yet. I have been able to sleep inside more recently.

Sometimes I get into an awful anxiety state which sometimes starts with small discomfort and build to an intolerable level especially if I remain indoors and there is stormy weather outside. My cure is to go into the forest or go outside to my enclosed porch even in winter snowy weather . If I do this the anxiety disapppears within 10 - 15
minutes. I usually do much better in the warmer months.
 

BadBadBear

Senior Member
Messages
571
Location
Rocky Mountains
Same for me. In a remote pine forest I can walk for hours and suffer no PEM or pain.
Back in the city I can't even get out of the chair.

It's not as simple as avoiding mold. Mold is just one component, you have to avoid all environmental toxins.

Me, three. Even though I live in the country, I feel much better up in the pine and spruce and aspen forests. I am able to do more, and generally feel good.

I try to forest bathe in the summer as much as possible. Hoping this year I can take my camper up and stay for a while.
 

cigana

Senior Member
Messages
1,095
Location
UK
Me, three. Even though I live in the country, I feel much better up in the pine and spruce and aspen forests. I am able to do more, and generally feel good.

I try to forest bathe in the summer as much as possible. Hoping this year I can take my camper up and stay for a while.
Did you ever try any of the chemicals trees emit, like limonene?
 

pattismith

Senior Member
Messages
3,930
Association between exposure to organochlorine compounds and maternal thyroid status: Role of the iodothyronine deiodinase 1 gene
2017
Highlights

Exposure to HCB and b-HCH was significantly associated with lower TT3 during pregnancy.


The magnitude of the association between exposure to some OCs and THs depended on the genotype for the DIO1 rs2235544 SNP.


The DIO2 rs12885300 SNP did not modify the association between any of the OCs and thyroid hormones.

Abstract
Introduction: Exposure to organochlorine compounds (OCs) may interfere with thyroid hormone (TH) homeostasis. The disruption of the deiodinase (DIO) enzymes has been proposed as a mechanism of action.

Aim: To evaluate the association between exposure to OCs and TH status in pregnant women, as well as to explore the role of genetic variations in the DIO1 and DIO2 genes.

Methods: The study population (n = 1128) was composed of pregnant women who participated in the INMA Project (Spain, 2003–2006). Hexachlorobenzene (HCB), 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (4,4´-DDE), b-hexachlorocyclohexane (b-HCH), polychlorobiphenyl (PCB) congeners 138, 153 and 180, thyroid stimulating hormone (TSH), total triiodothyronine (TT3) and free thyroxine (FT4) were measured in serum samples taken during the first trimester of pregnancy (mean [standard deviation (SD)]: 13.5 [2] weeks of gestation). Polymorphisms in DIO1 (rs2235544) and DIO2 (rs12885300) were genotyped in maternal DNA. Sociodemographic and dietary characteristics were obtained by questionnaire.

Results: A 2-fold increase in HCB was associated with lower TT3 (% change = − 1.48; 95%CI: − 2.36, − 0.60). Women in the third tertile for b-HCH had lower TT3 (% change = − 3.19; 95%CI: − 5.64, − 0.67). The interactions between DIO1 rs2235544 and PCB153 and b-HCH were statistically significant. The inverse association between PCB153 and TT3 was the strongest among women with AA genotype. Women with CC genotype presented the strongest inverse association between b-HCH and FT4.

Conclusion: Exposure to HCB and b-HCH was associated to a disruption in maternal TT3. The DIO1 rs2235544 SNP modified the association between exposure to some of the OCs (specifically b-HCH and PCB153) and maternal thyroid hormone levels. These results strengthen the hypothesis that DIO enzymes play a role in explaining the disruption of thyroid hormones in relation to exposure to OCs.
 

pattismith

Senior Member
Messages
3,930
"The existence of acquired partial thyroid hormone resistance has been postulated [241, 242], but this condition may be rare or underrecognised.

In NTIS, however, disruption of thyroid hormone signalling by cytokines, metabolites, toxins or drugs may contribute substantially to the clinical phenotype of affected patients [242].

Possible mechanisms of acquired thyroid hormone resistance include impairments of transmembrane transport [15, 16, 243], deiodination [19, 227, 228, 244], entry into nucleus [245, 246], receptor binding [243, 247253], and nongenomic effects of iodothyronines [28, 254264].

Similar effects may ensue from exposure to endocrine disruptors [265] like phthalates [266268], brominated flame retardants [266, 267, 269], perfluorinated compound [266, 267, 270], polychlorinated biphenyls [271276], bisphenol A [254, 266269, 274], or bisphenol F [277].

Some environmental toxins may also act as thyroid hormone agonists, as demonstrated for certain polychlorinated biphenyls [278, 279]."

Dietrich 2012
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3544290/
 
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Wishful

Senior Member
Messages
5,679
Location
Alberta
It sounds like we need our medical system to do more complete testing of the thyroid system, and more education of physicians about why it's important and how to interpret results. Add it to the already long list that includes gut function, immune function, etc.

My hope is that someday all these tests will become cheap and easy to do (microtesting devices), maybe with do-at-home-or-via-phone disposable devices, and an expert system will do the diagnosing. Diagnosing is easier if you have a long history of tests results showing what is normal for an individual. Doctors will do stuff that needs hands-on training (that nurses don't do better already), and specialists will try to deal with what the expert system can't.
 

pattismith

Senior Member
Messages
3,930
Disruption of Type 2 Iodothyronine Deiodinase Activity in Cultured Human Glial Cells by Polybrominated Diphenyl Ethers
Simon C Roberts,1 Antonio C Bianco,2 and Heather M Stapleton1,*


Abstract
Polybrominated diphenyl ether (PBDE) flame retardants are endocrine disruptors and suspected neurodevelopmental toxicants. While the direct mechanisms of neurodevelopmental toxicity have not been fully elucidated, it is conceivable that alterations in thyroid hormone levels in the developing brain may contribute to these effects. Cells within the brain locally convert thyroxine (T4) to the biologically active triiodothyronine (T3) through the action of the selenodeiodinase Type 2 iodothyronine deiodinase (DIO2). Previous studies have demonstrated that PBDEs can alter hepatic deiodinase activity both in vitro and in vivo; however, the effects of PBDEs on the deiodinase isoforms expressed in the brain are not well understood. Here, we studied the effects of several individual PBDEs and hydroxylated metabolites (OH-BDEs) on DIO2 activity in astrocytes, a specialized glial cell responsible for production of more than 50% of the T3 required by the brain. Primary human astrocytes and H4 glioma cells were exposed to individual PBDEs or OH-BDEs at concentrations up to 5 µM. BDE-99 decreased DIO2 activity by 50% in primary astrocyte cells and by up to 80% in the H4 cells at doses of 500 nM or greater. 3-OH-BDE-47, 6-OH-BDE-47, and 5’-OH-BDE-99 also decreased DIO2 activity in cultured H4 glioma cells by 45–80% at doses of approximately 1–5 µM. Multiple mechanisms appear to contribute to the decreased DIO2 activity, including decreased expression of DIO2 mRNA, competitive inhibition of DIO2, and increased posttranslational degradation of DIO2.
We conclude that reductions in DIO2 activity caused by exposure to PBDEs may play a role in the neurodevelopmental deficits caused by these toxicants.

tileshop.fcgi
 

Wishful

Senior Member
Messages
5,679
Location
Alberta
If the conversion of T4 to T3 in the brain is inhibited, so too would be the conversion of T3 to T2. That could explain why I need to boost serum T2, either directly or through increasing production in the thyroid gland.