Whenever I'm sick I hear people say "Don't eat sugar. Sugar feeds infection". It seems like a well-known concepts:

"Sugar feeds infection", "feeds infection and causes inflammation" and "contributes to a weakened defense against bacterial infection"

Recently, I had a throat infection, it seemed to be going away and I had a piece of (sugary, delicious) cake and got much, much worse.

But when I asked my doctor about it he said, "sugar doesn't feed infection and it was probably circumstancial".

Does sugar feed infection? For specificity, let's say refined cane sugar.


1 Answer 1


(In mice models,) it depends on the type of infection.

Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation (Wang et al)

Acute infections are associated with a set of stereotypic behavioral responses, including anorexia, lethargy, and social withdrawal. Although these so-called sickness behaviors are the most common and familiar symptoms of infections, their roles in host defense are largely unknown. Here, we investigated the role of anorexia in models of bacterial and viral infections. We found that anorexia was protective while nutritional supplementation was detrimental in bacterial sepsis. Furthermore, glucose was necessary and sufficient for these effects. In contrast, nutritional supplementation protected against mortality from influenza infection and viral sepsis, whereas blocking glucose utilization was lethal. In both bacterial and viral models, these effects were largely independent of pathogen load and magnitude of inflammation. Instead, we identify opposing metabolic requirements tied to cellular stress adaptations critical for tolerance of differential inflammatory states.

These researchers found (in mice) that for bacterial infections, fasting from sugar was beneficial, but for viral infections it was detrimental.

They assume the way this works is not by actually feeding or starving the actual pathogens, but by having an influence on the immune system / protective measures of tissue against the inflammation.

Unexpectedly, we found that these effects on mortality were largely independent of the degree of inflammation and pathogen clearance. In the case of viral inflammation, lethality subsequent to inhibition of glucose utilization appeared to be mediated by type I IFN signaling on target tissues—likely the brain—which require glucose to mitigate the ER stress response and CHOP-mediated cellular dysfunction. In the case of bacterial inflammation, lethality subsequent to glucose administration appeared to be mediated by suppression of ketogenesis, which led to impaired resistance to ROS-mediated damage in the brain (Figure 7). Thus, our results suggest that distinct inflammatory responses may be coupled with specific metabolic programs in order to support unique tissue tolerance mechanisms that, when uncoupled, lead to enhanced immunopathology, leading to death.

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