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The cause of Patulous Eustachian Tube (Hypothesis)
Started by
Caravaggio
, Jan 25 2018 07:07 PM
patulous eustachian tube acetylcholine acetylcholinesterase
4 replies to this topic
#1
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
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 apossible caffeine-oestrogen interaction. This suggestion was based on the fact that theirfemale sample, who showed positive caffeine-related performance effects, were in fact testedonly during the menstrual cycle, to standardise hormonal influences. This is a particularlyinteresting result, then, in the light of the increased evidence for changes in cognitivecompetence as a consequence in oestrogen depletion in older female populations (e.g.Paganinihill & Henderson, 1994; Williams, 1998; Gibbs & Aggarwal, 1998). If oestrogen depletionis associated with memory impairment, that young women only show benefits of caffeine at thatpoint in their cycle when oestrogen levels take a substantive dip is entirely consistent with the viewthat, for the most part, healthy adults are working with optimized systems whose efficiency, interms of cognitive processes at least, can not be boosted significantly by stimulants.In fact, such potential interactions on memory measures between oestrogen and caffeine donot appear to have been systematically considered in the published literature. As summarisedearlier, there appear to be no age x caffeine interactions on subjective assessments of moodchange, despite a main effect of caffeine on mood. Many of these studies, however, were runon male only samples; where mixed sex samples were used, sex differences were notanticipated, and sex was rarely incorporated as a factor in the analyses. Similarly, onmeasures of memory, sex differences have rarely been systematically explored as a possiblesource of differential effects. Rees et al., (1999) tested a mixed older age sample of 24 malesand 24 females, and reported no significant effects of caffeine on digit span (a measure ofworking 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 onan immediate free recall task; there were no significant effects of caffeine on recall scores. Yuet al., (1991) tested 20 elderly volunteers on a paired associate learning task. They did notspecify the sex ratio of their sample, but again found no significant effects of caffeine oncognitive performance levels. It remains possible that these null results may mask sexdifferences in caffeine-related performance effects, and the interesting possibility that womenmay be substantially more sensitive to caffeine-induced performance benefits during themenstrual cycle.Oestrogen-related effects on memory have been associated with the modulatory effects of thishormone on the cholinergic neurotransmitter system, this being the neurotransmitter systemmost closely associated with effective acquisition and storage of new memories (see Everittand Robbins, 1997, for an excellent review). One study, Riedel, et al. (1995) explored thepharmacological basis of caffeine's cognitive-enhancing effects by testing its ability to reversethe robust impairments induced by the drug scopolamine. Scopolamine is a cholinergicantagonist which produces transient dose dependent impairments in both memory andattention when administered to healthy volunteers. It is commonly used as a model of ageanddementia-related changes in cognitive performance, since changes in efficiency of thecholinergic system are robustly associated with both age- and dementia- related cognitivedecline. (Riedel, et al. 1995) reported that moderate doses of caffeine (250 mg) reversed thescopolamine-induced deficit in immediate and delayed recall of unrelated word lists, whilehaving no effect on memory scanning times, visual search, simple, choice or incompatiblechoice RT measures. In a control condition, co-administration of nicotine (a cholinergicagonist) with scopolamine reversed the scopolamine-induced deficits in incompatible choiceRT and in immediate but not delayed recall. The authors conclude that the cognitiveenhancing properties of caffeine and nicotine are therefore distinct, and that while nicotinemay affect primarily speeded and sustained attentional processes, caffeine's effects appear tobe more memorial than attentional in nature. They conclude that caffeine may havecognitive-enhancing effects via its cholinergic connections, and not solely via its adenosineantagonism, 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.
#3
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
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.
#5
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
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.
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.
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).
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 asActivation of membrane Na+/K+-ATPase of mouse skeletal muscle by acetylcholine and its inhibition by α-bungarotoxin, curare and atropineHana 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
Also tagged with one or more of these keywords: patulous eustachian tube, acetylcholine, acetylcholinesterase
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