11 replies to this topic

[Destiny's Equation]

Thanks to my aromatherapy direct inhalation addiction I have effectively destroyed my own brain.

(I primarily (ab)used Herb Pharm tea tree oil and Olbas inhaler.)

I do not wish to discuss my hellish cognitive decline symptoms on the public forum. It is far too personal of a horror story. But I will assure you that I now barely even recognize myself.

Why didn't I bother to extensively research this before doing it, you ask? I was an addict. I found breathing the cool fresh tingly vapor to feel absolutely wonderful. (Being an Aspie I am wired differently than your average bear when it comes to sensory stimuli.) Because of this instead of thinking "I want to be absolutely sure this is 100% safe and will take everything I read with a healthy dose of critical thought", my mentality was "I love what I am doing, and will find any way possible to justify it!" So I came up with numerous ways to assure myself that it was a relatively safe activity: the temporary short-lived surge in brainpower allowed me to convince myself that it couldn't be that all that bad for my brain. Several books written by doctors recommend it to soothe irritated airways. A physicist wrote on his site about how it completely cured the emphysema his doctors were powerless to treat. And the fact that it put an end to my treatment-resistant chronic bronchitis made justifying it terribly convenient.

I would vape at every chance: while reading books, while using the computer, while talking on the phone...I even found a way to inhale vapor in my sleep.

During that time period I gradually descended into darkness. Finally going into a building with extremely low levels of disinfectant fumes was the straw that broke the camel's back: it all went to hell in a handbasket. I was suddenly a drooling vegetable with "brain fog" as thick as pea soup.

Phone conversation with prospective doctor:

"I am baffled as to how being exposed to disinfectant fumes in such a minute amount could induce the shocking mental decline you are complaining of. This is all very strange. Anyway, if you came in here I would start you off with some IV vitamins..."

"I would prefer to take my vitamins orally. I already have PVC poisoning, so I am not a fan of getting more PVC from IV bags."

"So you have PVC poisoning from IV bags?"

"Not from IV bags. PVC lung disease from fumes."

I then told him the story of how my doctors had a crack at it, failed, gave up, and sent me on my way. Finally I took matters into my own hands and completely cured it with generous amounts of aromatherapy direct inhalation.

"Aha! Aromatherapy has been suspected to cause MCS syndrome. That could explain it."

"CRAP!!!"

From an aromatherapy site: "direct inhalation regenerates damaged lung tissue, greatly improving the absorption of oxygen."

Perhaps it also greatly increases the absorption of CHEMICALS?!!

(And I suspect that my lungs were overly permeable. They became ridiculously flexible, far more so than when I was a young child. I remember lying on my back doing full inhales...I could just keep expanding bigger and bigger for what seemed like an eternity. At times they were so intensely alive that I could actually feel the random movement of the air swirling around.)

A Life Extension Foundation doctor said on the phone "The aromatherapy is probably what messed you up. It has been suspected to effect the liver..." I personally doubt that I have liver problems (no symptoms of that), but however it happened, he suspected that what I did was not good.

I recently watched a youtube video of a lady making and using an aromatherapy inhaler. Her bizarre mannerisms looked just like mine did during the beginning of my downsliding period. I know a brain problem when I see one.

I will be seeing a cutting-edge doctor to figure out the how's and why's of what happened (at the moment she is busy looking into ways to make the bloodwork more affordable for me). But until then, unless you want a Flowers For Algernon experience...

STAY AWAY FROM THIS STUFF.

[aaron_e]

MCS means your body is having issues processing chemicals and is usually liver related. I believe high Phase 1 detox with low Phase 2 detox is usually indicated in MCS. Try supplements that lower Phase 1 and raise Phase 2 liver function, like curcumin. N-acetyl-cysteine could also be helpful. Niacinamide and Grapefruit juice (Naringenin) can also lower Phase 1 detox.

[Destiny's Equation]

Thank you much appreciated.

I started drinking the grapefruit juice. Will try the other stuff as soon as I am able to get a hold of it.

is usually liver related

Haven't been having any liver symptoms...weird.

[aaron_e]

Haven't been having any liver symptoms...weird.

there are many different detox pathways in the liver, and if they get out of balance in relation to each other then problems arise.

[Destiny's Equation]

there are many different detox pathways in the liver, and if they get out of balance in relation to each other then problems arise.

That would explain it.

My friends said that my eyes were pink and I had a strange chemical smell coming from me...

[aaron_e]

there are some nice charts here about liver function: http://www.genovadia...on_AppGuide.pdf

i am not sure if they still offer that liver function test, you might ask your doctor about it. the supplement recommendations i made above were best guesses without any hard data available and lab tests are always preferable.

Edited by aaron_e, 15 March 2011 - 01:00 AM.

[Dorian Grey]

Your case is interesting to me as I developed MCS a few years back working with glycols and disinfectants at work (medical profession). Propylene Glycol is often used as a carrier/solvent in aroma therapy agents.

Glycol metabolism burns through thiamine, and guess what... "In rodent TD (thiamine deficiency), the earliest region-specific pathological change is breakdown of the blood-brain barrier (BBB)"

http://www.ncbi.nlm..../pubmed/9708819

Induction of nitric oxide synthase and microglial responses precede selective cell death induced by chronic impairment of oxidative metabolism.
Calingasan NY, Park LC, Calo LL, Trifiletti RR, Gandy SE, Gibson GE.

Cornell University Medical College at Burke Medical Research Institute, White Plains, New York 10605, USA.
Abstract
Abnormal oxidative processes including a reduction in thiamine-dependent enzymes accompany many neurodegenerative diseases. Thiamine deficiency (TD) models the cellular and molecular mechanisms by which chronic oxidative aberrations associated with thiamine-dependent enzyme deficits cause selective neurodegeneration. The mechanisms underlying selective cell death in TD are unknown. In rodent TD, the earliest region-specific pathological change is breakdown of the blood-brain barrier (BBB). The current studies tested whether nitric oxide and microglia are important in the initial events that couple BBB breakdown to selective neuronal loss. Enhanced expression of endothelial nitric oxide synthase and nicotinamide adenine dinucleotide phosphate diaphorase reactivity in microvessels, as well as the presence of numerous inducible nitric oxide synthase-immunoreactive microglia, accompanied the increases in BBB permeability. Nitric oxide synthase induction appears critical to TD pathology, because immunoreactivity for nitrotyrosine, a specific nitration product of peroxynitrite, also increased in axons of susceptible regions. In addition, TD elevated iron and the antioxidant protein ferritin in microvessels and in activated microglia, suggesting that these cells are responding to an oxidative challenge. All of these changes occurred in selectively vulnerable regions, preceding neuronal death. These findings are consistent with the hypothesis that the free radical-mediated BBB alterations permit entry of iron and extraneuronal proteins that set in motion a cascade of inflammatory responses culminating in selective neuronal loss. Thus, the TD model should help elucidate the relationship between oxidative deficits, BBB abnormalities, the inflammatory response, ferritin and iron elevation, and selective neurodegeneration.

PMID: 9708819 [PubMed - indexed for MEDLINE]PMCID: PMC1852979

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

I was drinking a lot of tea during this time, and the tannin in tea is also an antithiamine/thiaminase.

Thiamine is absorbed only in small quantities in a short portion of the small intestine, which can only take 1mg or so at a time. Any damage to this portion of the intestine (which often occurs with alcohol consumption) means even less thiamine is being utilized.

Thiamine supplements may state they provide 3,333 times the MDR of thiamine, but very little of this is actually absorbed!

I cured my MCS with frequent small doses of thiamine (taken with every meal), combined with a phospholipid supplement (PPC / polyenylphosphatidylcholine) that heals damaged epithelial tissue which is the tissue in the small intestine that absorbs thiamine.

Phospholipid supplements are also good at fixing mitochondrial and cell membranes... The astrocyte cells that make up the blood brain barrier are highly reliant on good mitochondrial function to maintain the "tight junctions" that keep chemicals out of the CSF/brain.

Please look into: astrocyte cells of the blood brain barrier and the effect of thiamine deficiency on them; polyenylphosphatidylcholine (AKA "essential phospholipids" or EPL) and mitochondrial membranes; and thiamine uptake in the gut for more info on MCS.

It took me three years and many doctors to find out the hows and whys of MCS, but once I got on the right track, I was well again in a few short months.

Good Luck and GodSpeed to you.

Edited by synesthesia, 15 March 2011 - 05:24 PM.

[Destiny's Equation]

Your case is interesting to me as I developed MCS a few years back working with glycols and disinfectants at work (medical profession). Propylene Glycol is often used as a carrier/solvent in aroma therapy agents.

Glycol metabolism burns through thiamine, and guess what... "In rodent TD (thiamine deficiency), the earliest region-specific pathological change is breakdown of the blood-brain barrier (BBB)"

http://www.ncbi.nlm..../pubmed/9708819

Induction of nitric oxide synthase and microglial responses precede selective cell death induced by chronic impairment of oxidative metabolism.
Calingasan NY, Park LC, Calo LL, Trifiletti RR, Gandy SE, Gibson GE.

Cornell University Medical College at Burke Medical Research Institute, White Plains, New York 10605, USA.
Abstract
Abnormal oxidative processes including a reduction in thiamine-dependent enzymes accompany many neurodegenerative diseases. Thiamine deficiency (TD) models the cellular and molecular mechanisms by which chronic oxidative aberrations associated with thiamine-dependent enzyme deficits cause selective neurodegeneration. The mechanisms underlying selective cell death in TD are unknown. In rodent TD, the earliest region-specific pathological change is breakdown of the blood-brain barrier (BBB). The current studies tested whether nitric oxide and microglia are important in the initial events that couple BBB breakdown to selective neuronal loss. Enhanced expression of endothelial nitric oxide synthase and nicotinamide adenine dinucleotide phosphate diaphorase reactivity in microvessels, as well as the presence of numerous inducible nitric oxide synthase-immunoreactive microglia, accompanied the increases in BBB permeability. Nitric oxide synthase induction appears critical to TD pathology, because immunoreactivity for nitrotyrosine, a specific nitration product of peroxynitrite, also increased in axons of susceptible regions. In addition, TD elevated iron and the antioxidant protein ferritin in microvessels and in activated microglia, suggesting that these cells are responding to an oxidative challenge. All of these changes occurred in selectively vulnerable regions, preceding neuronal death. These findings are consistent with the hypothesis that the free radical-mediated BBB alterations permit entry of iron and extraneuronal proteins that set in motion a cascade of inflammatory responses culminating in selective neuronal loss. Thus, the TD model should help elucidate the relationship between oxidative deficits, BBB abnormalities, the inflammatory response, ferritin and iron elevation, and selective neurodegeneration.

PMID: 9708819 [PubMed - indexed for MEDLINE]PMCID: PMC1852979

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

I was drinking a lot of tea during this time, and the tannin in tea is also an antithiamine/thiaminase.

Thiamine is absorbed only in small quantities in a short portion of the small intestine, which can only take 1mg or so at a time. Any damage to this portion of the intestine (which often occurs with alcohol consumption) means even less thiamine is being utilized.

Thiamine supplements may state they provide 3,333 times the MDR of thiamine, but very little of this is actually absorbed!

I cured my MCS with frequent small doses of thiamine (taken with every meal), combined with a phospholipid supplement (PPC / polyenylphosphatidylcholine) that heals damaged epithelial tissue which is the tissue in the small intestine that absorbs thiamine.

Phospholipid supplements are also good at fixing mitochondrial and cell membranes... The astrocyte cells that make up the blood brain barrier are highly reliant on good mitochondrial function to maintain the "tight junctions" that keep chemicals out of the CSF/brain.

Please look into: astrocyte cells of the blood brain barrier and the effect of thiamine deficiency on them; polyenylphosphatidylcholine (AKA "essential phospholipids" or EPL) and mitochondrial membranes; and thiamine uptake in the gut for more info on MCS.

It took me three years and many doctors to find out the hows and whys of MCS, but once I got on the right track, I was well again in a few short months.

Good Luck and GodSpeed to you.

THANK YOU so much for your post!!! I really appreciate it!

When I went to the neurologist today I asked him to send me in for a B1 test.

"No I won't do that, B1 deficiency doesn't cause cognitive dysfunction, B12 deficiency does..."

"Can I please have it anyway, just to err on the side of caution?" (knowing that launching a discussion of astrocyte cells, mitochondrial dysfunction, and the BBB would only result in getting shipped off to the psychiatrist)

"There are no B1 tests."

So I will buy LEF's B1 test on my own.

Both Herb Pharm and Olbas claim that their aromatherapy products are solvent-free, but they might not be telling the truth. I've heard horror stories of people getting sick from taking supplements that weren't exactly what they claimed to be, regulation is an issue.

(Plus a picture I took of my face a few months ago SCREAMS beriberi.)

It took a while for me to get back to you because I wanted to give you a follow-up.

[Destiny's Equation]

MCS means your body is having issues processing chemicals and is usually liver related. I believe high Phase 1 detox with low Phase 2 detox is usually indicated in MCS. Try supplements that lower Phase 1 and raise Phase 2 liver function, like curcumin. N-acetyl-cysteine could also be helpful. Niacinamide and Grapefruit juice (Naringenin) can also lower Phase 1 detox.

Tried NAC it made me feel less rotten!

Combined with the grapefruit juice it's even better. I can tell when it's been too long since my last glass of grapefruit juice, because my brain starts to "fog up"...

Will try to get my hands on some curcumin next.

Thanks again for the tips

[rwac]

I was drinking a lot of tea during this time, and the tannin in tea is also an antithiamine/thiaminase.

Thiamine is absorbed only in small quantities in a short portion of the small intestine, which can only take 1mg or so at a time. Any damage to this portion of the intestine (which often occurs with alcohol consumption) means even less thiamine is being utilized.

Thiamine supplements may state they provide 3,333 times the MDR of thiamine, but very little of this is actually absorbed!

Hey, you got a reference for thiamine not being absorbed very well ?
I'm also pretty interested in thiamine.
I find that ttfd (aka allithiamine) is great for increasing thiamine levels.

[triplecrown]

What about benfotiamine for increasing thiamine levels?

[rwac]

What about benfotiamine for increasing thiamine levels?

I believe benfotiamine doesn't perform all the functions of thiamine.