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The cause of Patulous Eustachian Tube (Hypothesis)

patulous eustachian tube acetylcholine acetylcholinesterase

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#1 Caravaggio

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Posted 25 January 2018 - 07:07 PM


I have this condition for over 17 years. 
 
My hypothesis is that PET is caused by excess Acetylcholine (ACh) either bei overproduction (Choline acetyltransferase) or by inhibition of Acetylcholinesterase (which breaks down ACh).
 
The Eustachian tube (aka auditory tube or pharyngotympanic tube) has 4 muscles:
 
Levator veli palatini (innervated by the vagus nerve)
Salpingopharyngeus (innervated by the vagus nerve)
Tensor tympani (innervated by the mandibular nerve of CN V)
Tensor veli palatini (innervated by the mandibular nerve of CN V)
 
The vagus nerver has its oirgin in the medulla oblongata of the brainstem.
The mandibular nerve has its origin in the pons of the brainstem.
 
 
Acetylcholine is the neurotransmitter which causes the muscle to contract (calcium and magnesium do the electric part of contraction and relaxation).
 
Pesticides like e.g. glyphosate cause irreversible inbition of acetylcholinesterase, which causes a rise in ACh.
 
 
 
Substances that worsen PET (cholinergic):
 
Caffeine
 
Ginkgo
 
 
 
Substances/methods that improve PET (anticholinergic):
 
Alcohol/Nicotine
 
By binding to the Nicotinic acetylcholine receptors (nAChRs) the ethanol probably blocks the Acetylcholine to bind to the receptors and therefore relaxes the muscle that is in a permanent spasm.
 
 
 
Anectodal evidence:
 
 
Nicotine attenuates the PET but the pesticides in the cigarettes probaly caused irreversible acetylcholinesterase inhibition.
 
 
 
Creatine
 
 
 
Vertical position
 
Laying vertical seems to improve PET, I suppose that while laying vertical the body produces less peripheral ACh for relaxed muscles while sleeping (although ACh raises in the brain during REM sleep).
 
There is an idopathic condition called Postural orthostatic tachycardia syndrome (POTS) where the heartbeat increases while changing position from laying to upright (test done on a tilt table).
 
Unlike the contracting effect of ACh on the Nicotinic acetylcholine receptors (nAChRs) of the skeletal muscles, ACh has an inhibitory effect on the Muscarinic acetylcholine receptor M2 of the heart.
 
The paradox effect of the higher heartbeat could be due to acetylcholine receptor antibodies.
 
 
Botox (Botulinum toxin)
 
Prevents the release of ACh, therefore the muscles relaxes.
 
 
 
 
 
 
 
 
 
 
 
 


#2 Caravaggio

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Posted 03 February 2018 - 04:54 PM

A quote from the book Caffeine and Activation Theory: Effects on Health and Behavior by Barry D. Smith, Uma Gupta, B.S. Gupta

 

Interactive effects of caffeine, oestrogen and acetylcholine

 

Arnold et al., (1987) first suggested that an additional confound for female samples is a
possible caffeine-oestrogen interaction. This suggestion was based on the fact that their
female sample, who showed positive caffeine-related performance effects, were in fact tested
only during the menstrual cycle, to standardise hormonal influences. This is a particularly
interesting result, then, in the light of the increased evidence for changes in cognitive
competence as a consequence in oestrogen depletion in older female populations (e.g.
Paganinihill & Henderson, 1994; Williams, 1998; Gibbs & Aggarwal, 1998). If oestrogen depletion
is associated with memory impairment, that young women only show benefits of caffeine at that
point in their cycle when oestrogen levels take a substantive dip is entirely consistent with the view
that, for the most part, healthy adults are working with optimized systems whose efficiency, in
terms of cognitive processes at least, can not be boosted significantly by stimulants.
In fact, such potential interactions on memory measures between oestrogen and caffeine do
not appear to have been systematically considered in the published literature. As summarised
earlier, there appear to be no age x caffeine interactions on subjective assessments of mood
change, despite a main effect of caffeine on mood. Many of these studies, however, were run
on male only samples; where mixed sex samples were used, sex differences were not
anticipated, and sex was rarely incorporated as a factor in the analyses. Similarly, on
measures of memory, sex differences have rarely been systematically explored as a possible
source of differential effects. Rees et al., (1999) tested a mixed older age sample of 24 males
and 24 females, and reported no significant effects of caffeine on digit span (a measure of
working memory) or on immediate or delayed free recall of a 20 -item word list. Rogers &
Derncourt, (1998) tested 11 women and 7 male volunteers aged between 55 and 84 years on
an immediate free recall task; there were no significant effects of caffeine on recall scores. Yu
et al., (1991) tested 20 elderly volunteers on a paired associate learning task. They did not
specify the sex ratio of their sample, but again found no significant effects of caffeine on
cognitive performance levels. It remains possible that these null results may mask sex
differences in caffeine-related performance effects, and the interesting possibility that women
may be substantially more sensitive to caffeine-induced performance benefits during the
menstrual cycle.
 
Oestrogen-related effects on memory have been associated with the modulatory effects of this
hormone on the cholinergic neurotransmitter system, this being the neurotransmitter system
most closely associated with effective acquisition and storage of new memories (see Everitt
and Robbins, 1997, for an excellent review). One study, Riedel, et al. (1995) explored the
pharmacological basis of caffeine's cognitive-enhancing effects by testing its ability to reverse
the robust impairments induced by the drug scopolamine. Scopolamine is a cholinergic
antagonist which produces transient dose dependent impairments in both memory and
attention when administered to healthy volunteers. It is commonly used as a model of ageand
dementia-related changes in cognitive performance, since changes in efficiency of the
cholinergic system are robustly associated with both age- and dementia- related cognitive
decline. (Riedel, et al. 1995) reported that moderate doses of caffeine (250 mg) reversed the
scopolamine-induced deficit in immediate and delayed recall of unrelated word lists, while
having no effect on memory scanning times, visual search, simple, choice or incompatible
choice RT measures. In a control condition, co-administration of nicotine (a cholinergic
agonist) with scopolamine reversed the scopolamine-induced deficits in incompatible choice
RT and in immediate but not delayed recall. The authors conclude that the cognitive
enhancing properties of caffeine and nicotine are therefore distinct, and that while nicotine
may affect primarily speeded and sustained attentional processes, caffeine's effects appear to
be more memorial than attentional in nature. They conclude that caffeine may have
cognitive-enhancing effects via its cholinergic connections, and not solely via its adenosine
antagonism, as has generally been assumed (Yu et al., 1991; Nehlig, Daval, & Debry, 1992). 

 

This could be the reason why more women than men suffer from PET and why hormonal contraception worsens PET.

 

A quote from an article of Raymond Peat:

 

Estrogen, which was promoted so intensively as prevention or treatment for Alzheimer's disease, was finally shown to contribute to its development. One of the characteristic effects of estrogen is to increase the level of growth hormone in the blood. This is just one of many ways that estrogen is associated with cholinergic activation. During pregnancy, it's important for the uterus not to contract. Cholinergic stimulation causes it to contract; too much estrogen activates that system, and causes miscarriage if it's excessive. An important function of progesterone is to keep the uterus relaxed during pregnancy. In the uterus, and in many other systems, progesterone increases the activity of cholinesterase, removing the acetylcholine which, under the influence of estrogen, would cause the uterus to contract.

Progesterone is being used to treat brain injuries, very successfully. It protects against inflammation, and in an early study, compared to placebo, lowered mortality by more than half. It's instructive to consider its anticholinergic role in the uterus, in relation to its brain protective effects. When the brain is poisoned by an organophosphate insecticide, which lowers the activity of cholinesterase, seizures are likely to occur, and treatment with progesterone can prevent those seizures, reversing the inhibition of the enzyme (and increasing the activity of cholinesterase in rats that weren't poisoned) (Joshi, et al., 2010). Similar effects of progesterone on cholinesterase occur in menstrually cycling women (Fairbrother, et al., 1989), implying that this is a general function of progesterone, not just something to protect pregnancy. Estrogen, with similar generality, decreases the activity of cholinesterase. DHEA, like progesterone, increases the activity of cholinesterase, and is brain protective (Aly, et al., 2011).

http://raypeat.com/a...plessness.shtml

 

So progesterone, pregnenolone (as a precursor to progesterone) and DHEA could ameliorate PET.



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#3 Asta

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Posted 22 February 2018 - 03:29 AM

This is all very interesting. I'm going to bookmark it to read it in full when I have a second to myself. 



#4 Caravaggio

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Posted 26 March 2018 - 07:01 PM

There is also another substance that inhibits AChE. It's mercury, which is constantly released from amalgam tooth fillings, coal plants and also found in some vaccines as ethylmercury (which is now generally replaced with aluminium as the adjuvant) and in larger fishes.

 

If you happen to have amalgam fillings or had them removed think about on which side you have the PET as the teeth are very close to the medial pterygoid nerve which controls the tensor veli palatini muscle.

 

 

FEBS J. 2007 Apr;274(7):1849-61. Epub 2007 Mar 12.
Mechanisms of cholinesterase inhibition by inorganic mercury.
Frasco MF, Colletier JP, Weik M, Carvalho F, Guilhermino L, Stojan J, Fournier D.
 
Huan Jing Ke Xue. 2006 Jan;27(1):142-5.
[Effect of chronic exposure by mercury contaminated rice on neurotransmitter level changes in rat brain].
Ji XL, Jin GW, Qu LY, Cheng JP, Wang WH.

https://www.ncbi.nlm...pubmed/16599137

 

J Environ Sci (China). 2005;17(3):469-73.
Effect of methylmercury on some neurotransmitters and oxidative damage of rats.
Cheng JP1, Yang YC, Hu WX, Yang L, Wang WH, Jia JP, Lin XY.
 
Folia Haematol Int Mag Klin Morphol Blutforsch. 1989;116(1):151-5.
Effect of mercury and combined effect of mercury and dimethylsulphoxide (DMSO) on the activity of acetylcholinesterase (AchE-E.C. 3.1.1.7) of rat lymphocytes during in vitro incubation.
Miszta H, Dabrowski Z.

 

Folia Haematol Int Mag Klin Morphol Blutforsch. 1984;111(5):632-7.
Effects of mercury on acetylcholinesterase (E.C. 3.1.1.7.) activity of erythrocytes and bone marrow in rats.
Miszta H.
 
Exp Pathol (Jena). 1978;16(1-6):267-75.
Cerebral changes in the course of intoxication with mercury phenylacetate.
Kozik MB, Wigowska-Sowińska J.
 
Environ Health Perspect. 1975 Dec;12:127-30.
Methylmercury-cholinesterase interactions in rats.
Hastings FL, Lucier GW, Klein R.

 


Edited by Caravaggio, 26 March 2018 - 07:01 PM.


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#5 Caravaggio

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Posted 18 May 2018 - 09:05 PM

The cause could be a defect in the sodium–potassium pump (Na+/K+-ATPase).

 

How Ion Channels Regulate Muscle Contraction

Attached File  coreofccd_1.jpg   87.23KB   0 downloads
Acetylcholine leaves the nerve fiber and docks on receptors in the muscle fiber membrane, causing parts of the fiber to become slightly more positively charged.

Attached File  coreofccd_2.jpg   74.9KB   0 downloads
Sodium channels open in response to this small change, permitting a huge flow of positively charged sodium ions to enter the fiber and change the voltage.

Attached File  coreofccd_3.jpg   81.38KB   0 downloads
The voltage change in the fiber is sensed by calcium channels located on indentations of the membrane. They then signal the calcium release channels (ryanodine receptors), which allow calcium to flow out from internal storage areas. The released internal calcium causes the filaments of the muscle fiber to slide over each other (contract).

Attached File  coreofccd_4.jpg   81.95KB   0 downloads
To relax, all the above processes have to reset, with the internal calcium re-entering the storage areas and the release channels closing.

 

 

Pictures and text from http://quest.mda.org...etting-core-ccd

 

I don't quite get yet how the sodium-potassium pump fits in there as it moves both sodium and potassium in the same channel.

 

 

Physiol Rev. 2003 Oct;83(4):1269-324.

Na+-K+ pump regulation and skeletal muscle contractility.
Clausen T.

https://www.ncbi.nlm...pubmed/14506306

 

Am J Physiol Endocrinol Metab. 2016 Jul 1;311(1):E1-E31. doi: 10.1152/ajpendo.00539.2015. Epub 2016 May 10.

Na,K-ATPase regulation in skeletal muscle.
Pirkmajer S, Chibalin AV.

https://www.ncbi.nlm...pubmed/27166285

 

Acetylcholine doesn't seem to be the causal factor it just seems to be involved due to the activation of the sodium-potassium pump.

 

Pflügers Archiv

May 1979, Volume 380, Issue 1, pp 101–104 | Cite as
Activation of membrane Na+/K+-ATPase of mouse skeletal muscle by acetylcholine and its inhibition by α-bungarotoxin, curare and atropine
Hana DlouháJ. TeisingerF. Vyskočil

https://link.springe...1007/BF00582620

 

My blood sodium and potassium are normal but the blood doesn't show the amount of it in tissues.

 

A hair mineral test showed that I have very low sodium and potassium levels.

 

The problem with the sodium-potassium pump could be either genetically or by some substance that interferes with it, maybe this:

 

Am J Physiol. 1992 May;262(5 Pt 2):F830-6.

Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism.
Anner BM, Moosmayer M, Imesch E.

https://www.ncbi.nlm.../pubmed/1317120







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