Cholinergic inhibition and breathing.

“Activation of Nicotinic Cholinergic Receptors Prevents Ventilator-Induced Lung Injury in Rats” (Bregeon, et al., 2011)

Pair that headline with this one:

“Weakened Diaphragm May Contribute to Long COVID Dyspnea” … “Whether patients had received ventilation treatment or not, twitch trans-diaphragmatic pressure following posterior cervical magnetic stimulation was significantly impaired in COVID survivors 15 months after hospitalization compared with healthy controls. Furthermore, this measure of diaphragm weakness correlated with severity of dyspnea on exertion.”

Interestingly, the body of the article refutes the title:

“Spiesshoefer's group reported that at 15-month follow-up, 28% of COVID survivors reported experiencing mild to no exertional dyspnea, 48% reported moderate exertional dyspnea, and 32% reported severe exertional dyspnea.

Their hypothesis that diaphragm dysfunction may also be related to exertional dyspnea after COVID-19 illness was not supported in the present report. Diaphragm dysfunction was identified via ultrasound in 80% of the study's participants, and did not differ by dyspnea severity or receipt of mechanical ventilation during the index hospitalization.” […]

“Nevertheless, "regardless of the specificity of COVID-19, the extent of diaphragm muscle weakness and its clear association with otherwise unexplained persistent dyspnea is a significant finding, particularly because the large number of post-COVID patients worldwide are likely to impose a considerable burden on modern healthcare systems," they maintained.” (medpagetoday.com)

So - bypassing the misleading title - and no treatment options are suggested besides exercise maybe, gentle breathing exercises maybe. The article reassures readers that it is nice to have more of a causal handle on the issue - yet the hypothesis that the dyspnea would be linked to more weakness of the diaphragm muscle was not supported by the study findings. Diaphragm dysfunction was more universal for post CoV no matter vent history or dyspnea comorbid symptoms . . . suggesting something else about CoV is involved in the diaphragm dysfunction too.

Nicotinic acetylcholine receptor blocking by the injection version S1 subunit of the chimeric spike protein is my theory.

Coincidentally nAChRs have a regulatory role over respiration pattern - the rhythm of our breathing. (Shao, Feldman, 2009) Interesting factoids interest me. Alpha -7-nAChrs have a regulatory role over inspiratory contractions of the diaphragm muscle. (Dehkordi, et al., 2004) Another #Coincidence.

“These findings suggest that nicotinic cholinergic regulation of the chest wall pumping muscles may occur at multiple levels of the central nervous system.” (Dehkordi, et al., 2004)

Cholinergic blocking toxins like Conotoxin and snake venom toxin are used as paralytics because they are cholinergic inhibitors of nAChRs. Generally, not a good thing for health.

A study found that the original SARS-CoV-2 spike, S1 and S2 did not affect nAChRs -https://www.pnas.org/doi/10.1073/pnas.2204242119 however the injection version is different and is when we first heard of passive exposure leading to menstrual irregularities even in post-menopausal or pre-menstruation age females (girls and babies). Something fishy is going on and it smells more like escargot to me, <snail pun>, (which smells like garlic and is delicious).

Photo by Sereina on Unsplash

Conotoxin is from a marine snail and conotoxin and other pathogenic sequences have been found in urine samples of CoV patients. (Citation somewhere among my posts) The snake venom toxin in the water video didn’t help - the gene sequence produces a similar effect to snake venom or conotoxin more than “being” “snake venom toxin”. It seems to be acting like a cholinergic blocker and specifically, the jab version seems to be producing the effect, more than the original CoV infection in earlier stages of illness.

Critical thinking involves not believing the press releases and creatively using the search engine to find answers in older research.

More info in this post:

• Catecholamine-mediated stress myocarditis, spike S1 and alpha 7 nAChRs. Can we please talk about solutions yet? Nicotine lozenges are one, and I linked to more in an older post. (substack.com)

Yes, nicotine has some negatives, even the lozenges. Cancer is not necessarily one though. Rh. arthritis is a risk, related directly to nicotine itself and excess can cause nausea and jitteriness and even a racing heart. The lozenges are minty and sweet and can be easy to overdo. Overall, I liked their effect for my ADHD though. I try to cut back occasionally on how often I am having a tiny piece (often). Life isn’t always easy to figure out. I rub black seed oil on my knuckles. Osteoarthritis and bone spurs are already a thing for me and it is a concern. Clear-headed alertness is nice though.

What seems definite is that more research is needed than breathing exercises for patients with exertional dyspnea as the main treatment focus.

Patient: “Doctor, doctor, I’m having trouble breathing!”

Doctor: “Well, you should practice harder then. You need more exercise to strengthen your weak muscles.”

What if the “weak muscles” are not being innervated - not being told to contract? Then they would get weaker and weaker as they contract less and have less nerve stimulation which promotes growth stimulating factors.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes. 

Reference List

(Bregeon, et al., 2011) Brégeon, F., Xeridat, F., Andreotti, N., Lepidi, H., Delpierre, S., Roch, A., et al., (2011). Activation of Nicotinic Cholinergic Receptors Prevents Ventilator-Induced Lung Injury in Rats, PLOS One, August 8, 2011, https://doi.org/10.1371/journal.pone.0022386

(Dehkordi, et al., 2004) Dehkordi O, Haxhiu MA, Millis RM, Dennis GC, Kc P, Jafri A, Khajavi M, Trouth CO, Zaidi SI. (2004). Expression of alpha-7 nAChRs on spinal cord-brainstem neurons controlling inspiratory drive to the diaphragm. Respir Physiol Neurobiol. 2004 Jul 12;141(1):21-34. doi: 10.1016/j.resp.2004.03.006. PMID: 15234673. https://pubmed.ncbi.nlm.nih.gov/15234673/

(Shao, Feldman, 2009) Shao XM, Feldman JL. Central cholinergic regulation of respiration: nicotinic receptors. Acta Pharmacol Sin. 2009 Jun;30(6):761-70. doi: 10.1038/aps.2009.88. PMID: 19498418; PMCID: PMC4002383. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4002383/