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Nicotine

Videos

The Strange Health Benefits Of Nicotine - YouTube

DE-DEMONIZING NICOTINE | Ending Fear to Promote Benefits
Know About the Pathophysiology of Nicotine Withdrawal
Scientists look at smokers' brain activity before and after quitting
Joe Rogan on NICOTINE (nootropic properties, not addictive)

Joe Rogan on NICOTINE (nootropic properties, not addictive) - YouTube

Dr. Bryan Ardis reveals BOMBSHELL findings about reptilian VENOM PEPTIDES in popular weight loss drugs, and role of NICOTINE in healing “long COVID”

Nicotine is a cholinergic agonist. Therefore, it is an important inhibitor of pro-inflammatory cytokines acting through the cholinergic anti-inflammatory pathway via α7-nAChRs. Nicotine inhibits TNF, IL-1, IL-6 and HMGB1 while it does not inhibit anti-inflammatory cytokines such as IL-10. In vivo animal models have found nicotine to be protective against lipopolysaccharide-induced ARDS by reducing leukocyte infiltration and pro-inflammatory mediators in bronchoalveolar lavage fluid. Such effects are relevant to COVID-19 since cytokine storm appears to be the hallmark in severe cases.

SARS-CoV-2 is known to use the angiotensin converting enzyme 2 (ACE2) as a receptor for cell entry. ACE2 has well-established vasodilatory, anti-inflammatory and antioxidant properties. Studies on smoking and ACE2 have reported contradictory findings. Studies published before the COVID-19 pandemic reported that smoking and nicotine down-regulate ACE2. However, more recent studies suggest that they up-regulate ACE2. There is currently no evidence to suggest that up-regulation of ACE2 is associated with increased COVID-19 susceptibility or severity. In fact, up-regulation of ACE2 appears to be protective against tissue damage caused by SARS-CoV-2. ACE2 has been found to protect mice from developing ARDS. Data from SARS experimental studies suggest that continuous SARS-CoV-2 infection and replication induces immediate down-regulation of ACE2 that may be implicated in organ damage and disease severity. Further support for the beneficial role of ACE2 comes from data that estrogens appear to up-regulate ACE2 while children and younger adults have higher ACE2 levels compared to older people. At the same time, women, children and young people have milder COVID-19 symptoms. If accurate and verified, the recently-observed ACE2 up-regulation in smokers is probably induced as a defence mechanism to counteract the effects of angiotensin II. There is probably a dynamic balance between ACE and ACE2, which is continuously changing, depending on stressors and stimuli. Thus, there is uncertainty on whether nicotine affects COVID-19 progression through the renin-angiotensin-aldosterone axis and there is no known interaction between ACE2 and nAChR receptors.

Importantly, ACE2 is expressed in several regions in the brain. The regions where vagal afferent fibers terminate and vagal efferent fibers originate exhibit ACE2 expression. Neuroinvasion is a common feature of coronaviruses. Anosmia and ageusia have been reported by COVID-19 patients. SARS-CoV-2 may enter the CNS either through the blood stream or via the olfactory nerve across the cribriform plate. A case series of 214 patients reported that 36.4 % had neurological manifestations. Thus, it is possible that the virus might infect the terminal areas of vagus afferent fibers or the origin of vagus efferent fiber causing down-regulation of ACE2 and resulting in local inflammation that could disrupt the cholinergic anti-inflammatory pathway and dysregulate the inflammatory response. Nicotine could have protective properties against possible brain inflammation caused by SARS-CoV-2, mediated through α7-AChRs. Source

VIDEOSThis is a neuron under nicotine

Articles/Studies

This study demonstrates a sex-dependent effect of nicotine on gut microbiome community composition, functional bacterial genes, and the fecal metabolome.

Behavioural and pharmacokinetic studies on nicotine, cytisine and lobeline.

Nicotine changes how nicotinic receptors are grouped on brain cells

In vivo modulation of the behavioral effects of nicotine by the coumarins xanthotoxin, bergapten, and umbelliferone.

Nicotine’s Influence on Reward and Aversion

Risk Factors

The lethal dosage for nicotine for an adult is 40-100mg, although this can be considerably elevated through habituation (with smoking Tobacco, 2 to 7 g, one cigarette contains 10mg nicotine, of which 1 to 2 mg are inhaled during smoking).

Symptoms of acute poisoning include dizziness, salivation, vomiting, diarrhea, tremling of the hands and feelings of weakness in the legs; very high dosages can lead rapidly to spasms, unconsciousness, cardiac arrest and respiratory failure. Poisonings occur in particular through the ingestion of cigarettes y children, the handling of insecticides containing nicotine (through skin contact), and in connection with the harvesting of Toacco (also through cutneous resorption). Nicotine patches also represent a danger for children. See Tobacco, for Overdose treatment.

Benefits

Texas A&M: Nicotine can protect aging brains against Parkinson's, Alzheimer's disease

Protection from Nicotine Toxicity

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