@RSandra266
@oliver_beldi
@__Acc_Deleted__
Absolut. Wir planen derzeit für Ende diesen Monats eine n=1 Bildgebungsstudie, bei der auch der SPG Verlauf unter Nikotingabe bewertet werden soll.
@mmeclouseau81
@Clautoffel
Mastzellen sind in ihrer Histaminproduktion durch hemmende nikotinerge Azetylcholinrezeptoren reguliert. Aus der Blockade der nAChRs erklärt sich die unregulierte Freisetzung von Histamin (MCAS). Das Pflaster sollte also das MCAS eher bessern als provozieren.
@_waldmeer_
@RSandra266
Beim Inhalieren von Zigarettenrauch entstehen 80fach höhere Konzentrationen von Nikotin im Vergleich zum Pflaster. Das setzt Dopamin frei, welches die Sucht macht. Pflaster decken den Nikotinhunger, setzen aber kein Dopamin frei = Sucht ausgetrickst
@EisenkraftFam
@useless_priest
The theory is that nicotinic acetylcholine receptors all over your body are blocked by SARS-CoV-2 impairing severely the communication between your cells. This is the pathological basis of LC.
@acjuelich
@petri_pellinen
@TMaritanoAquino
@danaparish
Since,the great majority of LC sufferers are nicotinnaiv individuals those should start with a partly covered 7.5mg patch an accelerate every second day.When 7.5mg are reached, at least 7 days this dosage.After long term LC better 2 up to 4 interruption
@internetuserf12
This is definitely not the case. All the money, my study has taken Was my own. I did so, exclusively for the millions of sufferers from LC/ME/CFS, which until now experience no financial, investigational and moral support from any side. My study refers exclusively to patches!
In the case of a post-vac syndrome the initial worsening is obviously far harder than in PCS/ME/CFS. If somebody with PVS is going to try, please reduce the initial dosage (1/4) and accelerate very slowly.
If the dosage acceleration takes part in a very protracted manner this might lead to virus liberation in a likewise bit by bit fashion. If this, below the threshold of your immune system’s activation, the initial worsening might take longer than 2 days.
@EisenkraftFam
@useless_priest
Since, nicotine has a far higher affinity to these receptors compared to acetylcholine it can extrude the virus from the receptor. Thus the diminished cellular communication is reestablished.
@Naomi_D_Harvey
from the blocked receptors. Along TNT it is not advisable to use both substances, since nicotine + increased AChR might provoke overexcitation to the system. After TNT one of these substances is probably smart to support the healing process.
@EisenkraftFam
@useless_priest
The first 2 days could be hard due to the set free virus particles and the physiological reaction time of your immune system. Since, nicotine has a very short halftime continuous application is essential. Otherwise, the virus re occupies the receptors.
@oliver_beldi
@__Acc_Deleted__
@RSandra266
Das stimmt. Ich gehe davon aus, dass diese Spikeproteinzirkulation unter der immunologischen Schwelle liegt. Wie die herx reaction zeigt/vermuten lässt, wird diese Schwelle bei Nikotinapplikation überschritten und eine immunologische Beseitigung des SGP ermöglicht.
Because nicotine has up to 30-fold higher affinity for nAChRs than the natural ligand (acetylcholine), transcutaneous nicotine application is a promising candidate to control the post COVID tragedy.
@peakstopac
@DYork1979
Palpitations are very common to nicotine usage and they feel really bad. To wait with dosage acceleration until they get better is a smart option
@TheNicotineTest
Both substances should be avoided along
#TheNicotineTest
whilst patch pasting. During the recovery phase (without nicotine patches) they may offer beneficial support to healing
@probablyautist
@ourcarly
Cholinergic agents are principally the right direction. Since, pure acetylcholine cannot displace the virus, these agents are of minimal effect before nicotine. Along nicotine they are ‚twice salt in the soup‘. After nicotine they are very good support. (opinion)
@jungleswatcher
@TheNicotineTest
@petri_pellinen
You‘ve got me wrong. nAChRs counteract clotting. Their blockade promotes hyperclotting. The release of SARS-CoV-2 from nAChRs results in fixing this problem. Therefore, nicotine should be the solution, not the problem. (understandable?)
@mmeclouseau81
@Clautoffel
Im Übrigen haben wir mittlerweile bei vielen neu aufgetretenen Nahrungsmittelunverträglichkeiten tolle Verläufe gesehen. Viel konnten wieder alles essen. Fazit: 3,5mg, wenn anfangs gut vertragen, weiter.
Manchmal sind herx, Nikotinnebenwirkung und MCAS schwer zu unterscheiden.
@TheNicotineTest
@illness_almanac
Actually, HBOT does not improve perfusion but oxygen supply due to increased partial pressure of oxygen in the blood. This means, despite bad perfusion due to microclots the oxygen supply increases because the blood carries far more oxygen than normal.
@noralove
@Canal1point5
@Fatigo_MECFS
Please, not the neck. Your inner ear is an extremely good perfused region.Transdermal nicotine from wherever is going to reach them.Within your neck one finds a plethora of extremely sensitive structures influenceable by nicotine, which might lead to very central reactions.
@Canal1point5
Imagine, some (or a lot) of the myofribrilles of each muscles are blocked: earlier anaerobic activity => lactate generation, weakness no need to explain, organism tries to compensate this with elevating acetylcholine (limited capacity to do so) => PEM after any action above this
@PaulineKevin5
@TheNicotineTest
ACE2 receptors are used by the virus to enter the cell along acute infection. After cell entry,those receptors are given free, because the actual target of the virus is host dna to replicate. nAChRs are blocked in chronic courses,where ACE2 receptors play not a prominent role
@leap_ryan
@BrendaBrenner3
@NickChambers2
@CortJohnson
You should take more time to judge your successes. In such a long lasting illness, it is advisable to consider more rounds (7 days) with strict interruptions (7days as well). We saw ME/CFS sufferers definitely improving after 4 rounds
@_trans4m8tion
@TMaritanoAquino
@rasxchelo
Antihistamines are absolutely not counterproductive. Keep the inhalers to feel safe. Mastcell activation is likewise controlled by acetylcholine receptors and their blockade is a reasonable explanation for MACS.
@Gmwetz
@realfrankbecker
Von unseren 10 Billionen Körperzellen kann theoretisch jede betroffen sein, so dass, je nachdem wo das Nikotin andockt, nicht gleich alle betroffenen Zellen Nikotin „abbekommen“.
@LenaLenaLund
@petri_pellinen
Almost perfect. Nicotines binds and kicks off the virus. After binding it stimulates what the virus did not. Then it breaks down due to its short halftime. Thus, the way is paved for physiological stumbling acetylcholine.
To be understood?
@EisenkraftFam
@useless_priest
The 7 days described in the article have proven to be fairly short. 14 up to 28 days are safer.
The patches cannot evoke addiction!
@buckleydebbie
@TheNicotineTest
You must differentiate between autoantibodies and SARS-CoV-2 related receptor blockade. Autoantibodies can appear to any target within your body along LC
@TheMurfDawg
@TheNicotineTest
@Canal1point5
I think it is better to await the bypassing fluvax reaction of you body, before starting nicotine. So, in best case you could start 3 day before C booster.
@TheNicotineTest
@petri_pellinen
The microclots lead to hypoxic metabolism in the perfusion areas after clot-occlusion. This metabolism without oxygen produces lactate.
@LenaLenaLund
@petri_pellinen
Guess so. It is not proven. But ME/CSF is more and more referred to prior virus infections. Meanwhile, some ME/CFS sufferers experienced clear improvement after nicotine.
@KristinaRevay
@TheNicotineTest
@kiss_my_kumquat
@candlelovers12
@Canal1point5
This conclusion, unfortunately, was a bit to short, since cholinergic neurotransmission is an extremely individual property of each organism, influenced by a huge, partly undeciphered, factors. I am afraid, there is no real alternative to individual dosage finding.
@akkadtr1
@TheNicotineTest
@tessfalor
@remissionbiome
@patientled
The released virus particles evoke an inflammation-like situation, which is experienced as „herx “. The sufficient immunological reaction of the organism takes its time. Since,nicotine releases the virus particles bit by bit, this situation is difficult to predict conc. endurance
@sarahga89137569
@TheNicotineTest
To my opinion pasting patches along acute infections is not an issue and might even ameliorate them.
I pasted patches to my father along his severe acute COVID-19 infection at our ICU and I am convinced (even if not provable) that this prevented him from ventilator treatment.
@Big_Appel
@ClausErnst
@PuzzleOfHealing
Nope.Rauchen erhöht die Blutspiegel von Nikotin in Sekunden auf exorbitante Werte, die genau so schnell wieder abfallen. Das erricht die Rezeptoren nicht nur nicht alle, sondern wird der Rezeptordynamik/-konformation nicht gerecht. Außerdem generiert Rauchen Sucht, Pflaster nicht
@MaryandBessie
@GillelandKristi
The mentioned receptors realise communication between all the cells in our body. SARS-CoV2 blocks these receptors leading to all the symptoms of LC after the acute phase of COVID. Transcutaneous nicotine can extrude the virus. The set free virus is eliminated by our immune system
@NickChambers2
@CiaraGlenville
Hi Nick, I think that this is absolutely possible. To provide a safety short nicotine patch intervention might be a very good bridge before permanent improvement, which could take time in the individual case. This, especially, since we saw cases with a rather prolonged response.
@007_siegel
There are currently 3 youngsters (~12 years) under reduced dosage and daily feedback to me under nicotine patch pasting. We need a little more time to see how they do
@PaulRKeeble
@theedifyingword
👍🏽 patches are fare superior to gums since the theory is made on the basis of constantly low nicotine blood levels until your immune system erased the entire SARS-CoV-2 residuals. Only this protects the acetylcholine receptors from viral re-occupation
@Gmwetz
@realfrankbecker
Zudem ist der nAChR allosterisch konfiguriert. Das heißt 5 der 6 AChR Bindungsstellen sind im Normalzustand gar nicht zugänglich. Wenn diese aber blockiert sind, ist der Weg für Nikotin „länger“
@_trans4m8tion
@__Acc_Deleted__
@RSandra266
Switching off ACE2 reduces the binding sites for the virus substantially. After knock out of ACE2 there are just AChRs for binding of SGP available. AChRs do not directly promote viral infection (indirectly via blocked antiinflammatory alpha7nAChRs), the result are LC symptoms.
@TheNicotineTest
@DSKnipp
I think, it is rather a question of time of application. Long term low dose agonist application leads to desensitised (1 of 3 functional states) acetylcholine receptors leading to pro-inflammatory action. Therefore, after a while an interruption may be beneficial
@kirstler31
@Canal1point5
@DominicMoss13
Absolutely. For eliminating residual virus particles you need constantly low blood levels of the substance. This is only guaranteed with patches. Any other application form could even prolong or worsen the symptoms due to very high blood levels disappearing in a very short time.
@acjuelich
@petri_pellinen
@TMaritanoAquino
@danaparish
The study author I was referring to (
@LeitzkeMarco
) now says that 3-4 weeks has crystallized to be the sufficient length of patch application for long time long haulers.
So it may depend on how long you’ve been sick, as well as other variables.