Q: What is the hypothesis behind low testosterone and severity under Covid-19 infection?
A: Low testosterone and hypogonadism in particular, is accompanied by visceral fat.
Muscle wasting costs in lower BMR, that in turn develops adipose tissue.
Omental fat is among the factors of metabolic syndrome (midsection>95cm) and increases
insulin resistance (HbA1C>5.5%).
It releases inflammatory cytokines, known as Interleukin 6 (IL6) & Tumor Necrosis Factor
(TNF).
These chemicals participate in the inflammatory cascade of the Covid-19 infection.
Another reason why coved patients are characterized by low testosterone is their age.
Their average age is over seventy and most likely tare to be of low testosterone under
andropause.
Moreover the Intravenous (IV) administration of corticosteroids and dexamethazone
particularly, costs in Hypothalamic-Pituitary-Testicular Axis (HPTA).
Cortisone is inhibitory to testosterone synthesis.
Furthermore, the overall physical and mental stress under Intensive Care Unit (ICU)
hospitalization, increases cortisol and prolactin, that are suppressive to endogenous
testosterone production.
Men are of higher mortality rate that women and have a greater tendency to develop severe
ARDS under Covid-19 infection.
The reason is that testicles possess the so called ACE2 receptors, to where the virus is
attached.
The take home message is that eugonadal men and optimal testosterone levels, are
protective to the disease prognosis.
Men with higher testosterone levels are less likely to have visceral fat that has deleterious
effects in the escalate of inflammation.
TESTOSTERONE AND COVID-19 INFECTION