What this means is that my ongoing use of nicotine lozenges is helpful to me (but I do need to not overuse them) after having had a bad passive exposure illness in May 2021 with some relapses at other times of the year. Once sensitized it seemed that further exposures were more likely like an allergy getting worse. I did use KN95 masks when in medical settings or busy places. Confined with poor ventilation is highest risk, along with a setting where many jabbed people might be at (medical office or business giving jabs, for example).
The S1 subunit of the jabs seems even more of a nAChR inhibitor/paralytic than the infection, having had that in early 2020.
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.
There is a cobra toxin-like gene sequence in the chimeric spike protein of either the SARS-C0V-2 virus, or the CoV injection’s spike sequence. (1) It likely can paralyze the function of nAChR clolinergic receptors, (4), . . . and medical world seems to be ignoring or denying that.
The solution is simple, though controversial – just start nicotine – OOOH, BUT THEN -> ADDICT! True, better off -> dead?
The dysfunction may be involved in the excessive menstrual bleeding or severe colitis like diarrhea. The cholinergic receptors also help modulate immune function to not produce too many inflammatory cytokines.
Chimeric – made of many species. The SARS-CoV-2 spike protein, and the sequence used for the CoV injections, also have similar genetic sequences to a wasp toxin, and it has genes from HIV and MERS. Chimeric – like the many headed hydra of mythology – they can all bite, and all may need to be dealt with to achieve health.
Summary:
Spike protein or the S1 subunit have a snake venom toxin like sequence which can block nAChRs receptors, and it disrupts the function of the nAChRs. (1, 4)
Nicotine is protective of the function of nAChR receptors, it is an agonist, an activator. It is addictive, yes, so is health.
The alpha 7 nAChRs are involved in preventing cytokine storm over-immune reactions, (2) ;
nAChRs are also involved in: menstruation/endometrial tissue (3); regular bowel movements; sperm motility; and functioning nAChRs are critical for prenatal and child development of the retina and eyes, and throughout life for retinal health, (5); nAChRs are needed to be able to send nerve signals from the ears to the brain – ie – to be able to “hear”. (7)
TRP channels are also needed to be able to hear, they are in the inner ear hair cells. (10) They are also throughout the body, needed for fetal development, (11), and magnesium absorption in the intestines, ().
Reports of harm to vision & hearing of children have been reported to VAERS.
VAERS reports of adverse reactions involving CoV injections include reports of children going blind or deaf. (6) That may involve cholinergic dysfunction of the nAChR receptors. (5, 7)
Spontaneous abortion/miscarriage in the first trimester has also been reported for most women who received CoV injections during the first trimester. (ref to add)
Lack of magnesium due to TRP channel dysfunction in the GI tract may be a factor in risk to a fetus if the TRP channels’ function is loss – which resulted in death, in a genetic animal study.
“Genetic inactivation of Trpm7 in mice results in early embryonic death17, 19. Conditional tissue-specific inactivation of Trpm7 in mice showed that TRPM7 plays a critical role in morphogenesis of various internal organs19,20,21.” (12)
Hearing & TRP channels: Hearing loss likely also involves damage to the inner ear hair cells. The TRP channel’s ankyrin repeat domains can be affected by the spike protein. (10) TRP channels with long stretches of ankyrin repeat domains are abundant in inner ear hair cells as they form a coil like area that can sense mechanical pressure and activate the TRP channel if a strong enough force is exerted on it. (8, 9) The open area of the ion channel is usually formed as an empty space between two very large protein subunits – similar building blocks put together in a circular pattern that can leave an open channel in the middle.
Simple solution – soak in magnesium sulfate and it enters the body through hair follicle pores – larger than TRP channels.
Epsom salt soaks are the simple solution to bypass the poor absorption of magnesium in the digestive tract. Both the magnesium and the sulfate are protective to the inner ear hair cells and the rest of the body. The hydrated form of a bath or foot soak may aid in the absorption. Magnesium sulfate was well absorbed from a bath relative, based on change in blood levels of magnesium. There have been less good results seen in topical magnesium chloride studies.
One to two cups of Epsom salt for a half-full bath, soak for 20-40 minutes. One cup or so in a large bucket or bin so more than the feet can soak, and soak for 20-40 minutes. Depending on the severity of magnesium deficiency a soak 1-3 times per week may be needed to help prevent muscle cramps or anxiety/anger. Low magnesium can affect depression risk or psychosis also.
Blocking nAChRs may add to risk of excess cytokines -sepsis; they help prevent an over-active production.
The retina is the area in the back of the eye where light sensing rod and cone cells are located. Activating the alpha7 nAChR type of receptors lead to improved cell survival in a model of glaucoma, (5) possibly aided by the anti-inflammatory role.
“Retinal ganglion cells treated with the α7 nAChR agonist [such as nicotine] alone demonstrated a 28.0% (± 12.8%) increase in cell survival over untreated control.”
The cholinergic nAChR receptors are involved in modulating an inflammatory cytokine response – so that it isn’t excessive and producing an over-active amount of cytokines as seen in sepsis.
“Due to its role in the downregulation of the production of pro-inflammatory cytokines, 33–35, it has been suggested that the α7 nAChR may be involved in the hyper-inflammation response that can be caused by SARS-CoV-2. 9, 36” (2)
So the more obvious colitis or excessive menstrual bleeding symptoms experienced from being around recently CoV injected people, may be an indicator that other excessive inflammatory responses are also happening throughout the body – and the solution is the same: nicotine activates the nAChRs and is protecting them, taking up the open spot in the receptor so S1 or Spike protein can not lodge in the spot instead – blocking its immunomodulatory or other functions.
Snake toxin sequence more exposed on the freed S1 subunit portion of the chimeric spike protein.
The chimeric spike protein can split into parts and both parts of the main spike are able to interact with cell receptors, S1 and S2. The gene sequence that is similar to a snake and snail type of toxin becomes more exposed on the separate S1 subunit – meaning it is likely then more interactive with nicotinic Acetylcholine Receptors.
“Notably, the exposure of this motif and its close sequential neighbors is further accentuated in the S1 trimer (Fig. 2C) shed after cleavage by the human proteases (TMPRSS2 or furin) to enable the activation of the fusion trimer of S2 subunits.” (1)
The ability to split into parts, at the Furin Cleavage Site (FCS), is unique to the chimeric spike protein. Other coronavirus spike proteins do not have that capability.
Furin Cleavage Site
Chimeric spike protein is unlike any other CoV spike in that it can break into parts, subunits, at the Furin Cleavage Site (FCS), leaving S2 attached to the base part and freeing S1, both elongated halves of the spike: /\_ -> / and \_ .
The full spike can interact with ACE2 and various receptor types – and the S1 and S2 subunits can also, they are elongated. The base parts are smaller. Receptors are like a keyhole, & the spike, S1, & S2 are like a key that can fit in, but jam it -> no function, or dysfunction.
The S2 and base, \_ , stays attached to the human cell membrane if produced by a CoV injected person, (which would never happen in a real viral infection); or it would stay on the viral membrane in an CoV infection.
The S1, / , is freed, loose, floating in extracellular fluid… and the gene sequence that is cobra toxin like, PRRA, is more exposed on the freed S1, than it is in the full spike. The freed S1 could then travel to other areas of the person & block their nAChR receptors, or it might be excreted in sweat or breathed out.
The fact that un-CoV-injected people are getting symptoms after being around CoV-injected people suggests that it is an aerosolized risk. Standard fabric face masks would not be protective but better quality KN95 masks seem helpful.
People getting menstrual bleeding symptoms after being around recently injected people is likely because S1 exposure in a large enough load to be paralyzing the function of nAChR receptors in endometrial tissue (uterus). That link mentioned smokers are less at risk for endometreosis (excess menstrual blood but internal clotting), & that nAChR agonists might be a therapy to consider. (3)
Health Aids for Special Times – foods, phytonutrients and nutrients, and some lifestyle habits that may help protect against chimeric protein issues.
This document includes a lengthy section titled Excessive Menstrual Bleeding with information about nicotine, and colitis related to spike exposure may also be related to nAChR disruption and benefit from nicotine treatment – that is the problem it helped me with. The document also has information on Sleep and Iodine/Thyroid, in addition to chimeric protein related aids. When many types of receptors can be disrupted – they all need to be protected ideally. My website jenniferdepew.com has page Nutrients and page Cofactors with dosing details about a variety of other nutrients not specified in the document.
Disclaimer: This information is being shared for educational purposes within the guidelines of Fair Use. It is not intended to provide individual medical guidance. Please seek a health care provider for that purpose, such as a functional health nutritionist or practitioner.
Reference List
Mary Hongying Cheng, She Zhang, Rebecca A. Porritt, Magali Noval Rivas, Lisa Paschold, Edith Willscher, Mascha Binder, Moshe Arditi, Ivet Bahar. Superantigenic character of an insert unique to SARS-CoV-2 spike supported by skewed TCR repertoire in patients with hyperinflammation. Proceedings of the National Academy of Sciences. Sep 2020, 202010722; DOI: 10.1073/pnas.2010722117 https://www.pnas.org/content/early/2020/09/25/2010722117
Oliveira, A., Ibarra, A. A., Bermudez, I., Casalino, L., Gaieb, Z., Shoemark, D. K., Gallagher, T., Sessions, R. B., Amaro, R. E., & Mulholland, A. J. (2020). Simulations support the interaction of the SARS-CoV-2 spike protein with nicotinic acetylcholine receptors. bioRxiv : the preprint server for biology, 2020.07.16.206680. https://doi.org/10.1101/2020.07.16.206680 https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7386492/
Wu Y, Wang LP, Pan JQ. Nicotinic acetylcholine receptor agonists may be a novel therapy for endometriosis. Med Hypotheses. 2011 Nov;77(5):745-7. doi: 10.1016/j.mehy.2011.07.028. Epub 2011 Aug 10. PMID: 21835554. https://pubmed.ncbi.nlm.nih.gov/21835554/
Farsalinos, K.; Eliopoulos, E.; Leonidas, D.D.; Papadopoulos, G.E.; Tzartos, S.; Poulas, K. Nicotinic Cholinergic System and COVID-19: In Silico Identification of an Interaction between SARS-CoV-2 and Nicotinic Receptors with Potential Therapeutic Targeting Implications. Int. J. Mol. Sci.2020, 21, 5807. https://doi.org/10.3390/ijms21165807 https://www.mdpi.com/1422-0067/21/16/5807/htm
Moglie Marcelo J., Marcovich Irina, Corradi Jeremías, et al., Loss of Choline Agonism in the Inner Ear Hair Cell Nicotinic Acetylcholine Receptor Linked to the α10 Subunit. Frontiers in Molecular Neuroscience. 14 (2021) pp 5, DOI=10.3389/fnmol.2021.639720 https://www.frontiersin.org/articles/10.3389/fnmol.2021.639720/full
Phelps CB, Huang RJ, Lishko PV, Wang RR, Gaudet R. Structural analyses of the ankyrin repeat domain of TRPV6 and related TRPV ion channels. Biochemistry. 2008;47(8):2476-2484. doi:10.1021/bi702109w https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3006163/
Halim Maaroufi, Interactions of SARS-CoV-2 spike protein and transient receptor potential (TRP) cation channels could explain smell, taste, and/or chemesthesis disorders. 15 Jan 2021, https://arxiv.org/abs/2101.06294
TRPM7 channels are needed in embryo development and also have an ankyrin repeat sequence. Jingjing Duan, Zongli Li, Jian Li, et al., Structure of the mammalian TRPM7, a magnesium channel required during embryonic development. Proceedings of the National Academy of Sciences Aug 2018, 115 (35) E8201-E8210; DOI: 10.1073/pnas.1810719115 https://www.pnas.org/content/115/35/E8201
Ferioli, S., Zierler, S., Zaißerer, J., et al. TRPM6 and TRPM7 differentially contribute to the relief of heteromeric TRPM6/7 channels from inhibition by cytosolic Mg 2+ and Mg ATP. Sci Rep 7, 8806 (2017). https://doi.org/10.1038/s41598-017-08144-1 https://www.nature.com/articles/s41598-017-08144-1
Notes related to specific health aids that may protect against epigenetic changes, or in other ways.
Beta-glucan – epigenetic protection factor in mushrooms and Nutritional yeast flakes: Novakovic, B., Habibi, E., Wang, S. Y., Arts, R., Davar, R., Megchelenbrink, W., Kim, B., Kuznetsova, T., Kox, M., Zwaag, J., Matarese, F., van Heeringen, S. J., Janssen-Megens, E. M., Sharifi, N., Wang, C., Keramati, F., Schoonenberg, V., Flicek, P., Clarke, L., Pickkers, P., … Stunnenberg, H. G. (2016). β-Glucan Reverses the Epigenetic State of LPS-Induced Immunological Tolerance. Cell, 167(5), 1354–1368.e14. https://doi.org/10.1016/j.cell.2016.09.034 https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC5927328/
Herbacetin, isobavachalcone, quercetin 3-β-d-glucoside and helichrysetin were found to block the enzymatic activity of MERS-CoV 3CLpro. https://pubmed.ncbi.nlm.nih.gov/31436895/
Xiong, J., Ma, F., Ding, N., Xu, L., Ma, S., Yang, A., Hao, Y., Zhang, H., Jiang, Y. (2021). miR-195-3p alleviates homocysteine-mediated atherosclerosis by targeting IL-31 through its epigenetics modifications. Aging Cell, 00, e13485. https://doi.org/10.1111/acel.13485 https://onlinelibrary.wiley.com/doi/10.1111/acel.13485
via “Don’t have a CVA” – James V. Kohl, “Our findings shed new light on the involvement of miR-195-3p in macrophage inflammation, which might provide a potential therapeutic strategy for atherosclerosis induced by Hcy.” https://twitter.com/microRNApro/status/1443965887514562560?s=20
Unusual gene insertions within the SARS-CoV-2 viral gene sequence were found that resemble the protein structure and genetic code of a snake venom toxin. That is the bad news. The good news is that an anti-clotting snake venom anti-toxin medication was found helpful in the treatment of patients with severe COVID19. The anti-clotting medication is Tirofiban/Aggrastat, see image, and Dr. Fauci was emailed about the success of the treatment on April 27, 2020. It would have been nice of Dr. Fauci to let the rest of us know the good news last year.
*7-6-21 – addition – that was sarcasm and sarcasm is no longer adequate – it was Dr. Fauci’s job to let the US public know of effective remedies rather than obstruct investigations and use of early treatment. He and Ralph Baric and their team need to be investigated by an independent (non US corrupt) group and be charged with global homicide – seriously. We can’t just joke about bioweapons or gain of function ‘vaccine’ research that accidentally gets out, gets covered up, and early treatments suppressed for the apparent purpose of pushing emergency approval through for an inadequately tested experimental genetic manipulation treatment.
Image via Dr. Tau Braun, on Facebook.
The other good news is that nicotine is protective, by blocking access to the toxic spike protein to nicotinic Acetylcholine Receptors (nAChRs) which both nicotine and the neurotransmitter acetylcholine can activate (agonists of the receptor type, rather than antagonists).
“Based on the clinical observation of low prevalence of smoking among hospitalized COVID-19 patients, we examined and identified a “toxin-like” amino acid (aa) sequence in the Receptor Binding Domain of the Spike Glycoprotein of SARS-CoV-2 (aa 375–390), which is homologous to a sequence of the Neurotoxin homolog NL1, one of the many snake venom toxins that are known to interact with nicotinic acetylcholine receptors (nAChRs).” (1)
Anyone feeling a little tired? – a similar type of nerve toxin from a cone snail: Neurotoxin homolog NL1: “Antagonist [inhibitor] of muscle and neuronal nicotinic acetylcholine receptors (nAChR) with highest affinity for neuronal alpha-7/CHRNA7 nAChRs.” (9)
The Cholinergic System
The Cholinergic System effects health and cognition in many ways: “The cholinergic system is the network of acetylcholine receptors clustered within certain brain regions which the activation of, or inhibition of, in total effects most of our actions. More specifically effecting the cholinergic system might cause symptoms of “dry mouth, tachycardia or bradycardia [rapid or slow heart rate], drowsiness, sedation, and short-term memory loss,”…” Low levels of acetylcholine can cause difficulty forgetting traumatic memories, while higher levels help with the formation of new memories. (The Cholinergic & Dopaminergic Systems: previous post)
Formaldehyde – a neurotoxin that also inhibits acetylcholine receptors.
Formaldehyde has an inhibitory effect on acetylcholine receptors as it leads to increased break down of acetylcholine, so excess amounts of it may worsen symptoms of spike toxicity. Increased formaldehyde levels leads to an increase in levels of the enzyme that breaks down acetylcholine, resulting in less of the neurotransmitter being available for stimulating the acetylcholine receptors of nerve cells. (12)
Formaldehyde is found in smoke toxins whether you are the smoker, or there is fresh secondhand smoke, or a long term lingering thirdhand smoke on the walls & surfaces of everything in the home. Formaldehyde is also breathed in from smog or air pollution, and may off-gas (be released) from vinyl or other environmental sources. More bad news – we also make our own formaldehyde when our stress level is elevated. (References & more info, The Cholinergic & Dopaminergic Systems – also has dietary tips for Parkinson’s Disease: previous post)
Formaldehyde is a chemical used to embalm corpses. No need to make it for ourselves.
Peace – tranquility – focus on the now, not the worries of the future or the regrets of the past. By focusing on the present we can take decisive action steps towards a different future.
Jumping ahead to my own present time – I am using a half a nicotine patch per day (= 10.5 mg), for the last few days and it has helped my health, after a colitis like flair-up that was lingering longer than ever before. To me three weeks of colitis is three weeks too many – however some people suffer from it most days for years. It can end lives prematurely. I lost 30 pounds in three weeks during my initial problem – extreme stress was happening at that time. of the nicotinic Acetylcholine Receptors can be involved in Inflammatory Bowel Disease. (2)
Nicotine activates most types of nAChRs.
Nicotine activates most of the subtypes of nicotinic Acetylcholine Receptors, except for two subtypes, which it inhibits: “Nicotinic receptors are so named because they are activated by the tobacco plant alkaloid nicotine, but curiously, α9 and α9α10 nAChRs are not activated by nicotine and instead are inhibited by this ligand [8,13,25].” (2) Those two types have not been identified within the gastrointestinal tract, although many other subtypes are found there. (Table 1, 2)
Where are they found? It is the standout details that provide clues.
“Upon its release, acetylcholine activates a nicotinic acetylcholine receptor (nAChR) composed of α9 and α10 subunits14,15,16,17. In vertebrates the expression of these 2 subunits is limited mainly to the cochlear and vestibular end organs14,15,18,19. ” (3)
>>> “Neurons of the medial olivary complex inhibit cochlear hair cells through the activation of α9α10-containing nicotinic acetylcholine receptors (nAChRs).” (3)
Vertigo & Tinnitus can result from cochlear hair cell damage.
Vertigo and tinnitus might be related to something affecting the cochlear hair cells. They are very delicate and prone to irreversible damage. Dehydration, certain medications, and lack of magnesium may all be risk factors in addition to very loud noise, particularly if typically on one side more than the other – so one set of cochlear hair cells are damaged and the other is still okay – leaving the person off balance in perception and causing vertigo or tinnitus. The conditions have been reported as symptoms of COVID19 and as adverse reactions following CoV injection.
Magnesium is needed to protect cochlear hair cells.
“... intravenous administration of magnesium sulfate improved hearing recovery…” (4)
Epsom salt soaks provide a topical source of magnesium and sulfate which is absorbed through skin pores, bypassing any potential intestinal malabsorption.
Nicotine activates nAChRs, except for the type found in the inner ears.
Bath time over – back to the subtypes of nicotinic Acetylcholine Receptors – toxins can be very specific to subtype. Conus imperialis snails have a toxin that affects only the α7 subtype, making it useful in research of the brain’s cholinergic system. “It has no effect on nAChRs composed of α2/ß2, α3/ß2, α4/ß2, α2/ß4, α3/ß4, or α4/ß4 subunits.” (5)
That doesn’t rule out an effect on the α9 and α10 subunits, does it? Do the snake venom like toxin on the spike protein effect the α9 and α10 subunits? Based on reports of tinnitus and vertigo, it seems likely that they are effected by the spike protein.
Nicotine for better hearing and balance? Odd world today. Though, the nicotine doesn’t activate the α9 and α10 subunits so it might not protect them – bath time is fun according to Ernie from Sesame Street.
What other nutrients might help the inner ear cochlear hair cells?
Antioxidants and polyphenols and other NfKB inhibitor phytonutrients would also help protect the hair cells of the inner ear. Supplements of the antioxidant/metabolite CoQ10 and vitamin E have been found beneficial for tinnitus patients. (4) Nrf2 promoting foods have the double bonus of increasing our own antioxidant production and inhibiting the inflammatory NfKB. See: Nrf2 Promoting Foods for nutrient and foods that might be helpful.
“The levels of nitric oxide, peroxynitrite, oxidative stress, nuclear factor kappa-beta (NF-kappa), glutamate receptor (N-methyl-D-aspartate), and calcium are elevated in patients with tinnitus.12,13 About 21% to 42% of tinnitus cases are induced by exposure to noise.14 About 34% of tinnitus patients have post traumatic stress disorder (PTSD), suggesting there may be some linkage of neuronal mechanisms that cause both tinnitus and PTSD.15 Evidence for increased oxidative stress and chronic inflammation has also been found in patients with PTSD.” (4)
*Adequate levels of acetylcholine is needed to help forget things like trauma memories. (The Cholinergic & Dopaminergic Systems: previous post)
Reducing glutamate in the diet and use of glutamate inhibitors may be protective as excess glutamate is formed as a result of damage to hair cells.
“When hair cells become damaged, gluta-mate—an excitatory neurotransmitter responsible for converting vibrational sound into electrical signal—is produced in excessive amounts. Excessive amounts of gluta-mate are very toxic to neurons. Damage to peripheral auditory and somatosensory systems causes imbalance between excitatory and inhibitory neurotransmitters in the mid-brain auditory cortex and brainstem. This imbalance causes hyperactivity in the auditory cortex leading to the perception of phantom sounds (tinnitus).” (4)
Avoiding loud noise also protects the hair cells, which are motion sensitive and can be broken by physical pressure change. Loud noises do cause a change in the air pressure as the sound wave passes by – the vibration of a loud concert has the beat of the music.
From an old post:
A review of the negative side effects possible with an excess intake of the hormone calcitriol: [drugs.com]
Ringing in the ears and inner ear pressure is not mentioned on the list but – I am personally and professionally pretty sure that tinnitus can be part of the cluster of symptoms that might occur from a calcitriol overdose. The symptom list would be similar to a list of magnesium deficiency symptoms. The symptoms won’t go away simply by taking a magnesium supplement alone however. The intake of the vitamin D would continue to signal the bones to release calcium into the blood if it is being converted into hormone D. When excess of the calcitriol/hormone 1,25-D is present the intestines preferentially absorb calcium and magnesium is wasted in the kidneys and is poorly absorbed in the intestines.
An Epsom salt bath or foot soak can help relieve physical and mental symptoms and slightly reduce the ringing in the ears. Zinc, inositol and B vitamins seem to be involved in the tinnitus – magnesium alone doesn’t make it go away. B1 and zinc seem to be involved with the risk of cardiac arrhythmia as well as adequate supplies of taurine, an amino acid that can be converted from the more common cysteine but in the elderly that conversion can malfunction.
α9 and α7 are structurally similar, bad news doesn’t stop does it?
Back from the search engine – Structurally 7 and 9 are similar, (9 is curvier, haha): “Despite the recent upsurge in research interest in these subunits, there is much unknown about their functions and the underlying molecular mechanisms. They are most similar to the α7* nAChR; α-bungarotoxin and strychnine are antagonists of α7* and α9* receptors and α7* and α9* highly permeable to calcium. Recent evidence suggests a functional interaction of the subunits and potentially a structural association.” (6)
The alpha 9 and 10 subunits are not found within the brain’s cholinergic system, just in the inner ear, at the post-synapse area of the nerve connections – however the 9 and 10 subunit types are found throughout the rest of the body and immune system:
“There is an emerging literature that the distribution of the α9 and α10 subunits in peripheral tissues is widespread and non-synaptic, regulated in disease states, and may not always be assembled as heteromeric receptors. One or both subunits are expressed in most immune cells, dorsal root ganglion, keratinocytes, brain glioblastoma, colon, human breast cancer. Their expression levels may be prognostic in cancer and osteoporosis, and recent evidence suggests they may be involved in immune regulation. Importantly, they are potential targets for treatment of pain, cancer, and inflammatory diseases.” (6)
The alpha-7 type of receptors are found in the colon and are involved in glutamate release. They may be involved in pain relief. “Additionally, α7 nAChRs located on DRG neuron terminals in the dorsal horn of the spinal cord modulate the release of glutamate and have been proposed to be involved in nicotine mediated analgesia [34].” (2)
A computer modeling image shows the α7 receptor being blocked by a snake toxin, (7), the receptor is made of five similar subunits that form a channel through the cell membrane. Once activated the channel allows certain minerals to pass through, such as calcium. Excess can cause overactivity to the point of cell death.
Figure 4. Structural model of the α7 receptor–α-Cbtx complex. The five subunits of the receptor are depicted with their β-sheets colored blue and the apical helices colored red and yellow. One toxin molecule is shown at an arbitrary subunit interface with its β-sheet in yellow and its backbone in red. (A) Top view of the model. (B) The receptor is seen perpendicularly to the 5-fold axis with the toxin in an equatorial position. (Fruchart-Gaillard et al, 2002) (7)
“How can this situation explain the antagonistic property of the snake toxin? Small ligands also bind at the interface of two α7 subunits (10–13) on loops A, B, C, D, and F for ACh, nicotine or DHβE and A, B, C, and E for conotoxin ImI (α-ImI). This and previous (13) pairwise analyses indicate that α-ImI and α-Cbtx clearly bind to overlapping sites. Even both toxins possess an arginine residue that seem to establish homologous cation π interactions with the α7 receptor. ” (7)
Nicotine is a strong agonist of the α7 subunits, and activating that type of receptor helps reduce inflammation. (10, 13)
“We examined the anti-inflammatory effect of nicotine, a potent α7 nicotinic acetylcholine receptor (α7nAChR) agonist, with regard to TLR expression and signaling during sepsis.” (10)
Nicotine for prevention of snake venom-like poisoning? Odd world today.
Lobeline sulfate is chemically similar to nicotine, but less potent of an activator of the nicotinic Acetylcholine Receptors. (8)
“Where there is a will, there is a way,”
– as my mother always said. And when the first attempt doesn’t work, you try something else until something works. That is the stick-with-method. Try, try again.
Feeling a little better, rather than worse, may be the goal – sorry. Autoimmune conditions may have occurred.
There are no guarantees in life and trying dietary solutions or any treatment may not restore full health. Infections or other traumatic damage can increase risk of autoimmune antibodies developing – and there is often ups and downs rather than any true cure like resolution. Once autoimmune antibodies are formed the memory immune cells remember. Avoiding any dietary chemicals that were similar to the one the body is reactive against can help reduce the level of antibodies that are currently being produced rather than a memory cell type waiting to be needed again. Wheat gluten is similar to the thyroid hormone for example.
Demyelination conditions such as the autoimmune like condition Multiple Sclerosis may involve misfolded proteins too.
Multiple sclerosis also has been found to likely involve misfolded proteins. “MS may be a transmissible protein misfolding disorder, study suggests. SAN DIEGO – Multiple sclerosis appears to be a transmissible protein misfolding disorder like Alzheimer’s and Parkinson’s diseases, results of a new study suggest. ” (11)
Strategies that support myelination and prevent demyelination may also be helpful for protecting against a prion like toxin that does other damage too. Malnutrition is a risk factor for demyelinating conditions of which MS is one, however excess calories and carbohydrates may also be a risk factor. Our body needs to get hungry in order for the cellular debris mechanisms to function. When we are eating a lot of food, the body is busy using or storing those nutrients and there is no time or need to scavenge for extra tangled piles of misfolded proteins. Niacin, B vitamins, C, magnesium, CoQ10, are all needed for energy production in our mitochondria and also may help with the cellular debris functin.
Other tips for promoting good myelin coating around the long axons of nerve cells are on this webpage: G12. Demyelination.
See previous posts for more about the potential prion like risks of the spike protein:
Excess free iron is a frequent problem. Vitamin C would help, quercetin, resveratrol, artemisinin, lactoferrin, and possibly turmeric might all help as an iron chelator to protect against some of the vascular risks and excessive level of inflammatory cytokines.
“Artemisinin is an iron chelator and helped me right away with post recovery fatigue. In 1-2 days had more energy. Took am & pm. Still using 1/day. It felt like anemia of chronic infection – standard body response to move iron out of pathogen risk.” (one of my Tweets) -> (artemisinin-arteannuin-b-and-covid-19/)
Anemia of chronic infection or inflammation (post) is a natural immune response of the body, which seems to be an over-response in the case of COVID19 and LongCovid. Iron is stored as ferritin instead of being made into new hemoglobin for immature red blood cells. Less oxygen carrying capacity is in the blood – but also less potential nutrients for a pathogen. This condition is readily reversible with vitamin C and iron chelators – and address the underlying chronic infection that is causing the immune response. – And in the meantime avoid high altitudes such as mountain drives or airplane flights as hypoxia and loss of consciousness may result. Airplane pilots have experienced some problems post CoV injections.
“(Reuters) – United Airlines and its pilots’ union have reached an agreement to prohibit the airline from mandating COVID-19 vaccinations to its pilots, the Air Line Pilots Association said. “Pilots who elect not to be vaccinated will not be subject to any discipline,” “ – @GillianMcKeith. (ref)
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
Farsalinos K, Eliopoulos E, Leonidas DD, Papadopoulos GE, Tzartos S, Poulas K. Nicotinic Cholinergic System and COVID-19: In Silico Identification of an Interaction between SARS-CoV-2 and Nicotinic Receptors with Potential Therapeutic Targeting Implications. Int J Mol Sci. 2020;21(16):5807. Published 2020 Aug 13. doi:10.3390/ijms21165807 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7461543/
Lola Rueda Ruzafa, José Luis Cedillo, and Arik J. Hone. Nicotinic Acetylcholine Receptor Involvement in Inflammatory Bowel Disease and Interactions with Gut Microbiota. Int. J. Environ. Res. Public Health2021, 18(3), 1189; https://doi.org/10.3390/ijerph18031189 https://www.mdpi.com/1660-4601/18/3/1189/htm
Fruchart-Gaillard C, Gilquin B, Antil-Delbeke S, et al. Experimentally based model of a complex between a snake toxin and the alpha 7 nicotinic receptor. Proc Natl Acad Sci U S A. 2002;99(5):3216-3221. doi:10.1073/pnas.042699899 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC122499/
Tae-Hoon Kim, So-Jin Kim, Sun-Mee Lee, Stimulation of the α7 Nicotinic Acetylcholine Receptor Protects Against Sepsis by Inhibiting Toll-like Receptor via Phosphoinositide 3-Kinase Activation, The Journal of Infectious Diseases, Volume 209, Issue 10, 15 May 2014, Pages 1668–1677, https://doi.org/10.1093/infdis/jit669 https://academic.oup.com/jid/article/209/10/1668/855517
Zendehdel R, Fazli Z, Mazinani M. Neurotoxicity effect of formaldehyde on occupational exposure and influence of individual susceptibility to some metabolism., Environ Monit Assess. 2016 Nov;188(11):648. Epub 2016 Oct 31. parameters. https://www.ncbi.nlm.nih.gov/pubmed/27796833
de Jonge WJ, Ulloa L. The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation. Br J Pharmacol. 2007;151(7):915-929. doi:10.1038/sj.bjp.0707264 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042938/
