>>9908475 (lb)

May your friend rest in peace, anon. His life was cut far too short.

>https://www.diabetesselfmanagement.com/news-research/2020/04/30/covid-19-diabetes-and-high-glucose-related-to-longer-hospital-stay-higher-death-risk/

Researchers found that within this group of people with diabetes and elevated blood glucose levels, the in-hospital mortality rate was 29% — more than four times as high as in COVID-19 patients without diabetes or high blood glucose. Even more shocking was that among participants with no evidence or history of diabetes before their hospital stay, those that developed high blood glucose in the hospital had a mortality rate of 42% — seven times as high as in those without elevated glucose.

According to the study quoted below, this "covid" is behaving moar like a bacterial infection than a viral one in diabetics. You might want to do moar investigation.

>https://www.theatlantic.com/science/archive/2016/09/glucose-inflammation/498965/

Ruslan Medzhitov cares. He’s a distinguished professor of immunobiology at Yale. And in the journal Cell today, his team showed some dramatic benefits to starving a bacterial illness—but feeding a viral illness.

To be more precise, we do not feed or starve the bacteria or viruses themselves, but we may be able to modulate the different types of inflammation that these infections cause. “I want to be cautious here not to oversimplify and generalize,” Medzhitov warned. The most accurate and compelling way to put it, then, really: “Fasting has opposite consequences in different types of inflammation.”

When Medzhitov infected the mice with the influenza (flu) virus, the mice were more likely to survive if they were force fed. Denying them food—especially glucose, either by withholding it or administering the antagonist 2-deoxy-D-glucose—caused the mice to die. As the researchers write in the journal, in influenza infection, “inhibition of glucose utilization is lethal.” Whereas glucose was “required for survival in models of viral inflammation, it was lethal in models of bacterial inflammation.”