Why COVID-19 hits smokers harder

Apr 10, 2020
1
0
10
This article is contradictory to CDC data and numerous studies based on real COVID-19 patients:

According to CDC data, only 1.3% of hospitalized patients have been current smokers. About 10 times lower than the prevalence of smoking in the general US population.

Meta-analysis of 13 studies found no link between smoking and Covid-19.

A systematic research of the literature (PubMed) was performed on April 1. Out of 432 studies, we identified 13 studies examining the clinical characteristics of a total of 5960 hospitalized COVID-19 patients that presented data on the smoking status. No study reported e-cigarette use among COVID-19 patients. The prevalence of current smoking ranged from 1.4% to 12.6%. The random effect pooled prevalence of current smoking was 6.5% (95%CI: 4.9-8.2%). This preliminary analysis does not support the argument that current smoking is a risk factor for hospitalization for COVID-19. Instead, these consistent observations, which are further emphasized by the low prevalence of current smoking among COVID-19 patients in the US (1.3%), raises the hypothesis that nicotine may have beneficial effects on COVID-19. This could be attributed to its immunomodulatory effects and its interaction with the renin-angiotensin system.
Earlier, similar results from China were published in The Lancet:

 
Apr 13, 2020
2
1
10
Oxidative stress-inducing effects of nicotine is modulated by glutathione .

A personal observation is that of glutathione deficiency in all underlying conditions seen in COVID-19 mortality, which is true in relation to the elderly. I am not an expert in the field, but given the crisis I have been trying to find a link among those who have succumbed to the disease in the hope to add to the existing body of knowledge.
There is evidence to suggest that glutathione depletion results in H2O2 accumulation and resulting 'cytokine storm', inflammation of lung parenchyma, lung fibrosis, microcirculatory dysfunction, progression to refractory hypotension and fatal septic shock.
Could more efficient cellular viral entry through increased ACE2 receptors in COVID-19 patients on ARBs and ACEi, mean more rapid depletion of already deficient glutathione reserves? Could the morbidity of COVID-19 in addition to atypical RAS signalling, be the accummulation of H2O2 and xenobiotic stress as a result of glutathione depletion? Could environmental conditions, lifestyle and dietary choices add to xenobiotic stress in symptomatic COVID-19 patients. Some of which could include carbon-monoxide exposure, cigarette smoking (low glutathione), narcotic abuse, excessive use of acetaminophen (? Tylenol), ibubrophen use, asbestos exposure, mercury exposure, mycotoxin exposure (black mould), aflatoxin contaminated food and milk (endemic in certain areas of the globe).
Symptoms of Glutathione depletion:
- Shortness of breath
- Cough
- Sepsis
- Nitric oxide deficiency
- Refractory hypotension
- Lung injury
- Fibrosis
Perhaps simple substances that boost glutathione reserves like N-acetylcysteine (mucolytic, reduces fibrosis and pneumonia); alpha lipoic acid, L-glutamine; L-glutathione etc. could improve outcomes of symptomatic patients and prevent adverse reactions in high-risk population.
I may have gone off on a tangent or perhaps this theory has substance.
 
May 23, 2020
5
3
535
Smokers are very much less likely to be infected with covid-19 , as is becoming clear from study data, but the few that do, are more likely to have serious symptoms. It was ASSUMED early on that smoking would make anyone more susceptible due to immune system weakness or upregulation of ACE2 but it appears the latter is protective not susceptive.
 

ASK THE COMMUNITY