Considered Glutathione deficiency/ depletion?
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.
Thanks.