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Despite current controversies, some reports show a paradoxical mitigating effect associated with smoking in individuals with symptomatic COVID-19 compared to the general population. To explain the potential mechanisms behind the lower number of hospitalized COVID-19 patients, it has been hypothesized that cigarette smoking may reduce the odds of cytokine storm and related severe inflammatory responses through cholinergic-mediated anti-inflammatory mechanisms. Japanese scientists have recently identified a potential mechanism behind the lower numbers of COVID-19 cases amongst smokers compared to non-smokers. However, we believe that this mitigative effect may be due to the relatively high concentration of deposited energy of alpha particles emitted from naturally occurring radionuclides such as Po-210 in cigarette tobacco. Regarding COVID-19, other researchers and our team have previously addressed the anti-inflammatory and immune-modulating effects of low doses of ionizing radiation. MC-simulation using the Geant4 Monte Carlo toolkit shows that the radiation dose absorbed in a spherical cell with a radius of .9 μm for a single 5.5 MeV alpha particle is about 5.1 Gy. This energy deposition may trigger both anti-inflammatory and anti-thrombotic effects which paradoxically lower the risk of hospitalization due to COVID-19 in smokers.
A team of Japanese scientists demonstrates that treatment with AHR agonists decreases expression of ACE2 via AHR activation, resulting in suppression of COVID-19.
Researchers have identified two drugs that mimic the effect of chemicals in cigarette smoke to bind to a receptor in mammalian cells that inhibits production of ACE2 proteins, a process that appears to reduce the ability of the SARS-CoV-2 virus to enter the cell.
Results: The percentages of current smokers (4.1% vs 16%, p = .00003) and never smokers (71.6% vs 56.8%, p = .0014) were significantly different between COVID-19 and non-COVID 19 patients. COVID-19 patients had lower mean age (69.5 vs 74.2 years, p = .00085) and were more frequently males (59.2% vs 44%, p = .0011). In the logistic regression analysis, current smokers were significantly less likely to be hospitalized for COVID-19 compared with nonsmokers (odds ratio = 0.23; 95% confidence interval, 0.11-0.48, p < .001), even after adjusting for age and gender (odds ratio = 0.14; 95% confidence interval, 0.06-0.31, p < .001).
Conclusions: We reported an unexpectedly low prevalence of current smokers among COVID-19 patients hospitalized in nonintensive care wards. The meaning of these preliminary findings, which are in line with those currently emerging in literature, is unclear; they need to be confirmed by larger studies.
Implications: An unexpectedly low prevalence of current smokers among patients hospitalized for COVID-19 in some Italian nonintensive care wards is reported. This finding could be a stimulus for the generation of novel hypotheses on individual predisposition and possible strategies for reducing the risk of infection from SARS-CoV-2 and needs to be confirmed by further larger studies designed with adequate methodology.
This association is strongest for venous thromboembolic disease, but the risk of myocardial infarction (MI) is approximately doubled in the 7 days after COVID-19 diagnosis.1 Multiple studies have suggested worse outcomes in patients with COVID-19 and MI, with direct effects of the virus on endothelial cells, increased propensity for vascular thrombosis, and deficient care delivery all mechanistically implicated
Conclusion
Smoking seems to be associated with a favourable outcome post myocardial infarction. The phenomenon of ‘smoker’s paradox’ is in fact a reality in our patients population. The definitive explanation for this unexpected protective effect of smoking remains unclear.
However, only a low proportion of smokers suffered from SARS-CoV-2 infection [52]. This is referred to as the “smokers’ paradox” [53]. Although smoking cannot be recommended as a protective measure for COVID-19, the underlying mechanism for the smokers’ paradox may give a clue for our consideration of preventing SARS-CoV-2 infection.
Farsalinos et al. proposed that nicotine intake could be the reason for the low prevalence of smoking among hospitalized patients [51], whereas Hedenstierna et al. hypothesized that the short burst of concentrated NO (approximately 250 to 1350 ppm per puff) contained in cigarette smoke may prevent SARS-CoV-2 infection [54], an explanation similar to that given for why asthmatic patients are less likely to contract COVID-19.
The antiviral activity of NO has been reported for many types of viruses, most typically, DNA viruses such as murine poxvirus, herpesviruses, and some RNA viruses [55].
The direct action of NO as an antiviral agent involves the inhibition of viral replication and viral entry into the host [70,71]. In 1999, Saura et al. demonstrated that the in vitro replication of the RNA virus coxsackievirus is suppressed by NO-dependent S-nitrosylation that causes the inactivation of viral cysteine protease, an enzyme necessary for replication [72]. The S-nitrosylation of the cysteine-containing enzymes of viruses is thought to be a general mechanism for the antiviral activity of NO [73].
SARS-CoV-2 is a positive-sense RNA virus belonging to the family Coronaviridae, which includes severe acute respiratory syndrome coronavirus (SARS-CoV), the pathogen that caused the SARS outbreak. In 2005, Akerstrom et al. reported that the NO chemical donor SNAP inhibits the in vitro replication cycle and the protein and RNA synthesis of SARS-CoV [74].
Subject: Although not technically a medical treatment, nicotine and menthol could possibly be used to treat COVID-19. At a molecular level, nicotine may help prevent a cytokine storm from COVID-19 and menthol may have a synergistic relationship with nicotine that boosts this effect. Below is information from the NIH on nicotine and menthol.
originally posted by: nugget1
I was just reading yesterday a gov. sanctioned blurb showing statistically how smokers suffered from severe cases of covid at a much higher rate than non-smokers.
My kids got covid; SIL (smoker) only tested because he lost his sense of smell-for two days. NO other symptoms! Daughter (non-smoker) was sick for a week, on meds and didn't fully recover lung function for a couple of months.
As with everything related to covid, flip a coin and go with your gut.
originally posted by: MichiganSwampBuck
Have a look at the second post in this forum thread . . .
Subject: Although not technically a medical treatment, nicotine and menthol could possibly be used to treat COVID-19. At a molecular level, nicotine may help prevent a cytokine storm from COVID-19 and menthol may have a synergistic relationship with nicotine that boosts this effect. Below is information from the NIH on nicotine and menthol.
DDZ Link
when man first crawled out of the sea a lived in caves,
they learned to control fire for heating and cooking/ As result, our lungs developed and evolved in heavy smoke and where toughened to air-borne pollutants.
originally posted by: TiredofControlFreaks
a reply to: infolurker
Actually smoker's paradox is not funny. scientists have long known the cause. when man first crawled out of the sea a lived in caves, they learned to control fire for heating and cooking/ As result, our lungs developed and evolved in heavy smoke and where toughened to air-borne pollutants.
When man stopped heating their homes with oil, coal and wood and switched to clean burning natural gas, guess what happened, chilhood asthma rose by an astrnomical 800 %, COPD rose and all sorts of allergies. Gues whose children fared better....that right, homes where children were exposed to smoke.