Why Young Men Die from Covid and from the Vaccine
(Updated: 07/02/22)
(this is an opinion piece that benefits from a lifetime of study and experience. It is not an attempt at diagnosis or treatment)
We have heard lately about apparently very fit young men suffering severe heart inflammation, including death following either catching COVID-19 or, more often, from having the mRNA vaccine. I am aware of one very fit young man who may require a heart transplant following the jab. They tell us these are rare medical mysteries, but they are far from being mysteries. Are they rare because hardly any get reported?
Please read this article:
and this one:
Heart issues aside, the younger a person is, the lower their risk of harm from COVID-19. For example, in New Zealand, the average age of death from COVID is about 82 years, while worldwide statistics show youngsters are very unlikely to die. How come?
The younger a person is, the lower their risk of harm from COVID-19.
Why do these patterns exist?
Let me explain.
Firstly, read these two science abstracts:
(Read the last couple of sentences of each abstract if you can't be bothered wading through the lot).
Abstract:
"Glutathione (GSH) plays a central role in coordinating the synergism between different lipid- and aqueous-phase antioxidants. We documented 1) how exogenous GSH and N-acetylcysteine (NAC) may affect exhaustive exercise-induced changes in tissue GSH status, lipid peroxides [thiobarbituric acid-reactive substances (TBARS)], and endurance and 2) the relative role of endogenous GSH in the circumvention of exercise-induced oxidative stress by using GSH-deficient [L-buthionine-(S,R)-sulfoximine (BSO)-treated] rats. Intraperitoneal injection of GSH remarkably increased plasma GSH; exogenous GSH per se was an ineffective delivery agent of GSH to tissues. Repeated administration of GSH (1 time/day for 3 days) increased blood and kidney total GSH [TGSH; GSH+oxidized GSH (GSSG)]. Neither GSH nor NAC influenced endurance to exhaustion. NAC decreased exercise-induced GSH oxidation in the lung and blood. BSO decreased TGSH pools in the liver, lung, blood, and plasma by approximately 50% and in skeletal muscle and heart by 80-90%. Compared with control, resting GSH-deficient rats had lower GSSG in the liver, red gastrocnemius muscle, heart, and blood; similar GSSG/TGSH ratios in the liver, heart, lung, blood, and plasma; higher GSSG/TGSH ratios in the skeletal muscle; and more TBARS in skeletal muscle, heart, and plasma. In contrast to control, exhaustive exercise of GSH-deficient rats did not decrease TGSH in the liver, muscle, or heart or increase TGSH of plasma; GSSG of muscle, blood, or plasma; or TBARS of plasma or muscle. GSH-deficient rats had approximately 50% reduced endurance, which suggests a critical role of endogenous GSH in the circumvention of exercise-induced oxidative stress and as a determinant of exercise performance."
https://pubmed.ncbi.nlm.nih.gov/7868431/
Abstract:
"The novel COVID-19 pandemic is affecting the world’s population differently: mostly in the presence of conditions such as aging, diabetes and hypertension the virus triggers a lethal cytokine storm and patients die from acute respirato