And by opposite, he means opposite, life and death. In that way, his new findings could change not just the way we eat when we come down with a common cold, but how doctors treat the end stages of infections—when they spread throughout the blood and becomes known as sepsis, a condition that kills thousands of people every year.

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It all starts with the idea that losing your appetite is a symptom of a lot of illnesses. Why? Wouldn’t it be best to fortify ourselves with all the nutrients we can?

A temporary loss of appetite is known to doctors as anorexia (not to be confused with anorexia nervosa). Medzhitov counts anorexia alongside other common but rather mysterious “sickness behaviors” including altered sleep patterns, depression, and social withdrawal. He has been fascinated with how these things might contribute to our survival. Should they be embraced—listen to what your body is telling you—or fought?

A popular idea behind temporary anorexia is that it seems to happen for a reason: it protects us against certain infections. We alter our metabolisms to deprive our invasive species of fuel. As nutrients and minerals become scarce, the infectious organism will starve before our bodies do. It’s a race to the bottom.

Consider the classic food-poisoning bacterium Listeria monocytogenes. Medzhitov’s team infected a bunch of mice with Listeria, and, predictably, the mice stopped eating. They eventually recovered. But when the researchers fed the mice the same food—force-feeding them, as they had no appetites—they died.

Why, exactly, would that happen? Was some specific element in the food keeping the infection alive?

To figure that out, the Yale team broke down the food by macronutrients (fats, lipids, and carbohydrates). And, indeed, it seemed that the mice could survive the illness when they were forcibly fed proteins or fats. What they couldn’t take was the sugar glucose.

(Glucose comes to us not just by way of what we traditionally think of as sugar, but from any starchy food like bagels or crackers where carbohydrate chains break down into glucose in our mouths and stomachs.)

To double-check that these negative effects of sugar were real, the researchers fed glucose to some mice and then administered a rescue drug (2-deoxy-D-glucose) that blocks the body’s ability to metabolize that glucose—and they survived. In the case of this infection, it could seem, the bacteria need to be starved of sugar.

This is the sort of misguided thinking that leads people to go on cleanses, to deprive themselves of food unnecessarily, and to risk making things even worse. The story is much bigger than avoiding sugar. In other diseases, glucose seems to be beneficial. Critical even.

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.”